Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareOXIDATIVE STRESS BIOMARKERS IN RATS EXPOSED TO BROMOXYNIL
English0106Ahmed K. SalamaEnglish Khaled A. OsmanEnglish Ahmed S. El-BakaryEnglish Maher S. SalamaEnglishAim: The present study was designated to evaluate the oxidative stress biomarkers in male rat following oral repetitive administration of 0.1 LD50 of the herbicide bromoxynil. Methodology: Animals were orally received four doses of 0.1 LD50 of bromoxynil every other day. Twenty-four hours after the last oral dosing, all rats were killed by decapitation. Blood, brain, liver, and kidneys were taken for determination of TBARS, lactic dehydrogenase, catalase and alkaline phosphatase. Results: TBARS were found to be significantly increased in the liver, kidneys and brain where they were 390.20, 293.80, and 287.03% of control, respectively. In case of serum it was insignificantly increased to 162.88% of control value. Lactic dehydrogenase activity was significantly enhanced in serum and liver comparing with the control values (119.49 and 114.12%) and insignificantly enhanced in kidneys and brain (105.17 and 107.40%). Catalase activity was increased in all tissues where the enhancement was significant in both of serum and liver (122.68 and 119.99%, respectively) and insignificant in case of kidneys and brain (112.55 and 105.12%, respectively). Alkaline phosphatase activity in serum, liver, kidneys and brain was found to be elevated. These values were significant in liver and kidneys (113.47 and 121.14%, respectively) while they were insignificant in serum and brain (109.91 and 114.46%, respectively). Conclusion: Therefore, the herbicide bromoxynil could produce significant alteration in the lipid peroxidation and activities of some antioxidant enzymes and producing cellular oxidative damage in male rats following repetitive oral dosing.
EnglishBromoxynil, Oxidative stress, Rat, Biomarkers, Antioxidant, EnzymesINTRODUCTION Pesticides are used to prevent, control and eliminate unwanted pests and associated diseases. However, large amounts of these compounds caused environmental and public health concerns (Bhanti et al, 2007). Pesticide intoxication induces a derangement of certain antioxidant mechanisms in different tissues, including alterations in antioxidant enzymes and the glutathione redox system (Ahmed et al, 2001). Exposure to pesticides can induce oxidative stress by the induction of reactive oxygen species (ROS) as byproducts of detoxifying metabolism, by alteration in antioxidant defense mechanisms, including detoxification and scavenging enzymes, or by increasing lipid peroxidation as a result of the interaction between reactive oxygen species (ROS) and cellular or subcellular membranes (Abdollahi et al., 2004).
These mediate a wide variety of toxic effects such as DNA damage or genotoxicity (Ryter et al, 2007 and Franco et al, 2009). Overproduction of reactive oxygen and nitrogen species can result from exposure to environmental pollutants (Poljsak and Fink, 2014). Oxidative stress arises if detoxification systems and antioxidants are compromised or if ROS production is excessive, resulting in DNA, protein and lipid oxidation (Ryter et al, 2007, West and Marnett, 2006, Franco et al, 2007). A more recent pilot study has pointed out that oxidative stress and DNA damage are possibly linked to pesticides-induced adverse health effects in agricultural workers (Muniz, 2008). Bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) is used for the post-emergence control of annual broad-leaved weeds in cereals, maize, sorghum, flax, allium species, mint, and grass seed crops (Roberts, 1998).
Bromoxynil is active as mitochondrial uncoupler (Tomlin, 2000). Bromoxynil is highly toxic to mammals and birds. The data for the acute oral LD50 in rats range from 190 mg/kg up to 440 mg/kg (Krieger et al, 2001). Recently, data indicate that the toxic action of pesticides may include the induction of oxidative stress and accumulation of free radicals in the cell. A major form of cellular oxidation damage is lipid peroxidation, which is initiated by hydroxyl free radical through the extraction of hydrogen atom from unsaturated fatty acids of membrane phospholipids (Farber et al., 1990). As a consequence, these compounds can disturb the biochemical and physiological functions of cells in blood and liver (Akhgari et al., 2003).
The increased oxidative stress resulted in an increase in the activity of antioxidant enzymes such as superoxide dismutase and catalase. The enhancement of release of lactate dehydrogenase (LDH) is also indicative of cellular and membrane damage, while inactivation of superoxide dismutase and catalase are expected to enhance the generation of reactive oxygen species (ROS) and consequently, pose an oxidative stress upon the system (Tabatabaie and Floyed, 1996). The production of ROS can initiate lipid peroxidation and cause intracellular excess of malondialdehyde (MDA) (Peluso et al, 2010). Astiz et al (2011) found that thiobarbituric acid-reactive substances were increased in the exposed workers group of professional sprayers to various agrochemicals for about 10 years.
Our previous studies investigated the ability of many different groups of pesticides to induce oxidative stress in animals (Osman, 1999, Osman et al, 2000, Salama et al, 2005 and Salama et al 2013). The aim of the present study was to investigate the effect of the herbicide bromoxynil on producing alteration in the lipid peroxidation and activities of some antioxidant enzymes and producing cellular oxidative damage in male rats following repetitive oral dosing.
MATERIALS AND METHODS Chemical Bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) was supplied by Chem Service, West Chester (99% purity). All other chemicals used in this study were obtained either from Sigma or BDH Companies and they were of the highest grade available. Animals Male rats, Ratus norvegicus, weighing an average of 110 g were obtained from the High Institute of Public Health, Alexandria University. Animals were randomly separated and housed in stainless steel cages (5 per cage) and left two weeks under the laboratory conditions. Animals were provided rodent chow and tap water ad libitum through the study. Treatment of animals Male rats were divided into two groups, five rats each. The first group was orally received four doses of 0.1 LD50 of bromoxynil every other day.
The second group received corn oil as the same manner of pesticide treated animals and served as vehicle control. Twenty-four hours after the last oral dosing, all rats were killed by decapitation. Blood samples were taken using non-heparinized tubes. Blood was centrifuged at 5000 rpm for 5 min at 4 °C to separate serum for analysis of oxidative stress biomarkers. Brain, liver, and kidneys were excised rapidly, weighed, placed in glass vials and stored at -20 °C until determination. Preparation of tissue homogenate Selected tissues were homogenized in saline solution (1:10 w/v) using a polytron homogenizer. The homogenates were used for determination of thiobarbituric acid reactive substances (TBARS), lactic dehydrogenase, catalase and alkaline phosphatase. Lipid Peroxidation assay The determination of lipid peroxidation was based on the formation of thiobarbituric acid-reactive substances (TBARS) (Uchiyama and Mihara, 1978).
To 0.5 ml of the homogenate, 3 ml of 1% phosphoric acid and 1 ml of 0.6% thiobarbituric acid aqueous solution were added. The mixture was heated for 45 min in a boiling water bath and then cooled. n-Butanol (4 ml) was added to the above mixture and mixed vigorously. The butanol layer was measured was separated by centrifugation and the absorbance was measured at 532 and 520 nm. Malondialdehyde (MDA) was employed as the standard and the molar absorptivity constant of 1.56 x 10-5 M cm-1 was used. Lipid peroxidation is expressed as nmole MDA/mg protein. Lactic dehydrogenase assay The determination of lactic dehydrogenase (LDH) was based on the conversion of lactate to pyruvate or pyruvate to lactate (Moss et al, 1986). The rate of NADH oxidation is proportional to LDH activity. Twenty microliter of tissue homogenate was added to 1ml of 50 mM phosphate buffer pH 7.5 containing o.6 mM sodium pyruvate, 0.9 g/L sodium azide and 0.18 mM NADH. The mixture was gently mixed and incubated at 30 °C. The rate of NADH oxidation was measured at 340 nm. LDH activity is expressed as unit.mg protein-1.
Catalase assay Catalase activity was assayed by the method of Aebi (1984). The decrease in absorbance was measured at 240 nm. The enzyme activity was expressed as unit of catalase .mg-1 protein. One unit of catalase was defined as the amount of enzyme necessary to reduce 1 µmole of H2 O2 per minute. Alkaline phosphatase assay Alkaline phosphatase activity was estimated according to McComb et al (1966) using sodium p-nitro phenyl phosphate as a substrate.
Determination of protein The protein contents were determined by the method of Lowry et al (1951), using bovine serum albumin as standard. Statistical analysis Data were calculated as mean ±S.D. and analyzed using analysis of variance technique (ANOVA) followed by Least Significant Difference (LSD). Probability of 0.05 or less was considered significant. All statistical analysis was done with Costat Program (1986) on a personal computer.
RESULTS Effect of bromoxynil on lipid peroxidation Lipid peroxidation levels were determined in different tissues of male rats following oral administration with repetitive doses of 12.9 mg/kg b.wt. (0.1 LD50) of bromoxynil. The concentrations of thiobarbituric acid-reactive substances (TBARS) in male rats intoxicated with bromoxynil are presented in Table (1). TBARS concentrations were significantly increases in the liver, kidneys and brain where they were 390.20, 293.80, and 287.03% of control, respectively. While in case of serum it was insignificantly increased to 162.88% of control value. Effect of bromoxynil on the activity of lactic dehydrogenase (LDH) Lactic dehydrogenase activity in serum, liver, kidneys and brain were measured following bromoxynil administration and presented in Table (2).
The results clearly indicate that bromoxynil induced oxidative stress, where serum and liver LDH activities were significantly increased comparing with the control values. They were 119.49 and 114.12% of control in serum and liver, respectively. Lactic dehydrogenase activity also insignificantly increased in kidneys and brain. The values were 105.17 and 107.40% of control in kidneys and brain, respectively. Activity of catalase The increased oxidative stress resulted in an increase in the activity of antioxidant enzymes such as catalase is indicative of cellular and membrane damage. Catalase activity in different tissues of male rat was assayed following oral administration with repetitive doses of 12.9 mg/kg of bromoxynil (Table 3).
Our findings indicated that the catalase activity was increased in all tissues where the enhancement was significant in both of serum and liver (122.68 and 119.99%, respectively) and insignificant in case of kidneys and brain (112.55 and 105.12%, respectively). Activity of alkaline phosphatase The repetitive oral administration of 12.9 mg/kg of bromoxynil to male rats caused an enhancement of alkaline phosphatase activity in serum, liver, kidneys and brain. These values were significant in liver and kidneys (113.47 and 121.14%, respectively) while they were insignificant in serum and brain (109.91 and 114.46%, respectively) (Table, 4).
DISCUSSION The obtained results indicate that the repetitive exposure to the herbicide, bromoxynil lead to the generation of oxygenated reactive species (ROS) which affects the activity of the scavenging enzyme system. Overproduction of reactive oxygen and nitrogen species can result from exposure to environmental pollutants, including pesticides (Poljsak and Fink, 2014). The production of ROS can initiate lipid peroxidation and cause intracellular excess of malondialdehyde (MDA) (Peluso et al, 2010). The potential of ROS to damage tissues and cellular components is known as oxidative stress.
Astiz et al (2011) found that thiobarbituric acidreactive substances were increased in the exposed workers group of professional sprayers to various agrochemicals for about 10 years. In our study, lipid peroxidation, lactic dehydrogenase, catalase and alkaline phosphatase were assayed and considered as good biomarkers for oxidative stress. The results indicate that the toxic action of pesticides include the induction of oxidative stress and accumulation of free radicals in the cell. A major form of cellular oxidation damage is lipid peroxidation, which is initiated by hydroxyl free radical through the extraction of hydrogen atom from unsaturated fatty acids of membrane phospholipids (Farber et al., 1990). As a consequence, these compounds can disturb the biochemical and physiological functions of cells in blood and liver (Akhgari et al., 2003). Our results concerning the lipid peroxidation levels indicate that the level of MDA increment is pesticide dependent. Evidence from in vivo studies with many toxicants including pesticides supports the concept that free radicals e.g. hydroxyl radicals .
OH, H2 O2 and others, are important mediators of tissue injury and formation of these radicals result in increased lipid peroxidation (Farber et al., 1990; Akhgari et al., 2003, Jaiswal et al, 2014). Shvedova et al (2003) studied the oxidative stress, inflammatory biomarkers, and toxicity in mouse lung and liver after Inhalation exposure to diesel emissions. They showed that the degree of cytotoxicity/tissue damage and inflammation was evaluated by assessing the LDH and they observed a significant increase in the levels of LDH compared to control. The increased oxidative stress resulted in an increase in the activity of antioxidant enzymes such as catalase.
The enhancement of release of lactate dehydrogenase (LDH) is also indicative of cellular and membrane damage (Tabatabaie and Floyed, 1996, Osman, 1999, Osman et al, 2000, Salama et al, 2005 and Salama et al 2013). Catalase detoxifies H2 O2 in the biological systems. Hermes-Lima (2004) indicated that catalase activity often increase due to the regulation by ROS. Alkaline phosphatase is involved in trans phosphorylation reactions. The increase in this enzyme activity is attributed to its release from ruptured cells due to the effect of pesticides exposure (Shaffi, 1980).
CONCLUSION The current study indicates that the repetitive exposure to bromoxynil herbicide could produce significant alteration in lipid peroxidation and some antioxidant enzyme activities such as lactic dehydrogenase, catalase and alkaline phosphatase. The results demonstrated that intoxication with Bromoxynil induced significant damage of the serum, brain, liver and kidneys tissues leading to imbalance in enzymes activities in different organs and could produce oxidative damage.
ACKNOWLEDGEMENT Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12TechnologyDELAY ANALYSIS OF ADHOC NETWORK USING NS 2.34
English0711Samiksha NikamEnglish B. T. JadhavEnglishAd hoc network is popular nowadays due to the easy disposition and self-configuring nature. Hence, routing related issues encounter challenges in the ad hoc network. Such network is mainly used for transmission of text, picture and video data. The speed of data delivery decides the quality of service of the network. The quality of service depends upon the protocol used for data transmission. Efficient routing protocol improves the quality of service. The efficiency of the protocol is decided by evaluating different performance parameters like throughput, delay, packet drop, routing load, packet delivery ratio etc. The end to end delay is one of the most important performance parameter sofad-hoc network. It plays a major role in deciding the quality of service. The delay is measured as total time is taken by the packet to reach the destination. Delay in ad hoc network gets affected by the mobility of nodes, and a number of nodes connected to the network. The objective of this research paper is to analyze delay of ad hoc network for DSDV routing protocol. The delay is measured in high and low mobility scenario by changing various parameters of ad hoc network such as a number of nodes, pause time, speed, and connections between the nodes. Network simulator ns2.34 is used for this.
EnglishAd-hoc Network, DSDV, NS2.34, Performance Measurements, DelayINTRODUCTION In ad hoc network nodes can enter and leave a network as per their wish. Hence, routes may break or new route forms during data communication process. Various routing protocols are designed for the ad hoc mobile network. The mobility of the nodes is major challenges researchers have to face while designing routing protocols. [2][12]. Due to self-organized nature of ad hoc network, it is very much popular nowadays. Most of the people using the adhoc network for transmission of multimedia data. The requirement for such transmission is that delay should be minimum. Delay in ad hoc network depends on the factors such as node density, the number of connected nodes, and the speed and mobility of the nodes. In this research paper researcher analyses the delay of ad hoc network in two different scenario such as, 1. By assigning maximum and minimum values for network parameters and running a simulation to evaluate delay for various combinations. 2. The delay is measured in low and high mobility scenario by changing number of nodes and speed of nodes.
DESTINATION-SEQUENCED DISTANCE-VECTOR (DSDV) PROTOCOL It is a first table driven ad-hoc network protocol. It is a hop by hop table distance vector routing protocol. In this protocol, each node maintains arouting table that contains all possible destinations within network and number of routing hops to each destination. The information in the routing table is updated by increasing sequence number which avoids counter to infinity problem. The sequence number shows freshness of route and route with higher sequence number are favorable. Each mobile node of ad hoc network maintains a routing table which stores information about all available destinations, the number of hops and a sequence number. Using this routing table packets are transmitted between the nodes. Routing tables can be exchanged between neighbors at regular interval to keep an up to date view of network topology. The tables are also forwarded if a node observes a significant change in local topology [4] [7][12].
PERFORMANCE METRIC The delay is the important performance parameter of ad hoc network. A network’s delay is defined as the time required forsuccessful delivery of data packets to the destination node. [1][7]. Delay performance parameter is an important entity to decide efficiency of the routing protocol. In DSDV protocol routes are already stored in routing table hence route establishment time is negligible. However due to the mobility of nodes routes get fail and this increases the delay in the network. In this research paper delay is measured by changing various network parameters in a different scenario.
SIMULATION PROCESS The simulations were performed using Network Simulator (NS2.34). Fig 1.2 shows various steps used in the simulation. Initially scenario and traffic files are generated. These files are used as input for TCL script. After execution of TCL script, two files are created i.e. NAM file and trace files. Trace files are used to analyze the behavior of the network. Trace files are analyzed using AWK scripts. Detailed simulation process steps are as follows. 1. Generate scenario and topology files using cbrgen and setdest commands. 2. Write TCL script (.tcl Extension file) 3. Execute TCL script (Use ns Command) 4. Generate Trace and NAM file. 5. Select performance parameters. (Delay). 6. Execute AWK script to measure performance parameter delay of protocol. 7. Plot a graph. Experiment No.1. The goal of the experiment is to examine and compute delay of ad hoc network when DSDV routing protocol is used.
To evaluate the delay of ad hoc network we consider 10 random simulation runs to generate 10 random scenario patterns. The result is calculated by taking an average of those 10 outputs. To carry out simulation experiment parameter values set to maximum and minimum levels as shown in table 1.1. As four input parameters are selected total 2^4 = 16 combinations are possible. Table 1.2 shows a simulated experimental reading for sixteen combinations of four input parameters.
ANALYSIS OF EXPERIMENT 1 Case 1: Pause time means the amount of time for which node remains stable in the network. The pause time term relates with mobility of the nodes. Low pause referred as high mobility and high pause time referred as low mobility. In first case network mobility is high (P.T. = 0).It is observed that in high mobility scenario to maintain low delay in the network number of connections in between the nodes should below. Case 2: The mobility of the nodes plays an important role to maintain delay in ad hoc network. It is observed from Table1.3 that in a low mobility scenario delay is maintained at moderate level (i.e.10 to 20 ms). This is because in low mobility situation frequency of route failure is less and in DSDV protocol routes are already stored hence less time is required for route discovery. This reduces delay. Case 3: In the third case it is observed that in high mobility scenario as the number of connections between the nodes increased it will increase the delay significantly.
EXPERIMENT NO 2: In the previous experiment, we consider maximum and minimum values for the parameters and calculate delay. It is observed that delay depends on mobility and number of connections between the nodes depicted in table 1.3. To strengthen the collective analysis perform in the first experiment second experiment is performed. In this experiment simulation is run for case 1 and case2. Here case 3 is not considered because low delay always desirable in networking Case 1: In this case mobility is high i.e. P.T. =0.A number of nodes and speed of the nodes is variable. Nodes vary from 15 to 60 and speed of nodes changes from 10 to 50 ms. A number of connections between the nodes are5 and 10 respectively. The reading of the experiment is shown in table 1.4. either 5 or 10 respectively. The experimental data is stored in table 1.5
Analysis of Experiment 2: It is observed from table 1.4 that in high mobility scenario when a number of connections in between the nodes is 5 delays is less than 10 ms. When the number of connections between the nodes increases to the number10 delay increases more than 10 ms. This shows that a number of connections between the nodes affect the delay of ad hoc network. To maintain low delay in ad hoc network when DSDV protocol is used for routing try to keep a number of connections in between the nodes minimum. It is observed from table 1.5 that in low mobility scenario when a number of connected nodes are either 5 or 10 then delays maintain between 10 to 20 ms. It is concluded that delay depends on mobility and connection between the nodes of ad hoc network. By regulating these parameters low delay can be preserve in the ad hoc network.
EXPERIMENT NO 3: To scrutinize effect of a number of connections on delay in ad hoc network this experiment is performed. In this experiment speed of the nodes is kept constant at 40ms. And a number of nodes are 100. Connections between the nodes vary from 5 to 75 and delays measured in high and low mobility scenario. The reading is shown in table1.6.
Analysis of Experiment No 3 It is observed that as the number of connections increases delay is increasing in both the cases. However in low mobility case delay maintain at a lower level than high mobility scenario. In high mobility scenario nodes are continuously moving. In DSDV protocol, each node maintains a routing table which contains information of other nodes in a range. The continuous movement of nodes requires frequent updating of routing tables this increases the delay in the network.
CONCLUSION This simulation-based study is conducted to analyze delay of ad hoc network when DSDV routing protocol is used. Ad hoc network has dynamic topology which raises various performance issues. The delay is important parameters for performance measurement. It is observed from the first experiment that in high mobility scenario if a number of nodes and speed of nodes are variable and other parameters are constant then delay in ad hoc network become unstable. The parameters Pause time and number of connections in between the nodes helps to reduce delay in ad hoc network. In the second experiment, we set parameters in combination and it is observed that mobility plays a significant role to maintain low delay in the network. Low mobility scenario helps to maintain moderate delay. In high mobility scenario if a number of nodes are kept minimum then delay can be maintained at a lower level. It is observed that delay dependson more than one factor hence, the researcher suggested using fuzzy logic to maintain low delayin an ad hoc network.
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13. S.Y. Wang, C.L. Chou, C.H. Huang, C.C. Hwang, Z.M. Yang, C.C. Chiou, and C.C. Lin,”The Design and Implementation of the NCTUns 1.0 Network Simulator”.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareDERMATOGLYPHICS IN MENTALLY RETARDED CHILDREN
English1216Anjana P. GaikwadEnglish Swati R. PandhareEnglishObjective: This study was undertaken to evaluate the dermatoglyphic features in children belonging to primary mental retardation and co-relating the findings with previous workers. Methods: Dermatoglyphics obtained from the palm and finger tips in 72 children of primary mental retardation were compared with the similar studies in 72 normal children. These cases were from special institution for mentally retarded children in Pune. Results: The features which showed significant variations included: reduced whorl pattern and increases in ulnar loop on the finger tip, increase frequency of pattern in thenar / I1 and I3 area with distal displacement of axial triradius, higher atd angle, and increase incidence of simian crease. Conclusion: Dermatoglyphics features were noticed in the mentally retarded groups. These are increase ulnar loops on finger tips, decrease in whorl on finger tip, thenar / I1 and I3 area showed significant increase in pattern, higher atd angle, distal shift in axial triradius. It can be assumed that the cases of primary mental retardation could be dermatoglyphically varied from the normal, though the number of cases studied is not enough to make a definite statement.
EnglishAtd angle, Axial triradius, Simian creaseINTRODUCTION The human body is a wonder. Because of innumerable gifts offered by the nature, man is superior to the rest in animal kingdom. As the skin on the palmar and plantar surfaces of man also the tips of fingers shows characteristic. It has ridges which form configurations that are unique to every individual1 . This fact has been known for centuries and its use was made for purposes of personal identification. It also attracted the attention of both scientists and layman alike for the purpose of study. This study of prints came to be termed as ‘dermatoglyphics’. The word dermatoglyphics is derived from the Greek word ‘Derma’ means skin and ‘glyphae’ meaning carving. The term was introduced by Cummins and Midlow in 1926.1
As the scientists studied this particular branch, they found that dermatoglyphic features once formed remain unchanged throughout life. They also observed that these patterns are heritable traits and influenced by a number of genes during their formation. Being genetically inherited, the pattern is highly influenced by insults during early fetal life. Hence genetically related disorders may be studied by this method. This study was undertaken to evaluate the dermatoglyphic features in children belonging to primary mental retardation. Varied causes of mental retardation are antenatal, natal and postnatal. Antenatal causes of mental retardation are highly related to genetic factors and therefore affect dermatoglyphic features as well.
MATERIAL AND METHODS: In the present study, the dermatoglyphic features were studied in 72 mentally retarded children of both sexes between age groups 3yrs-18yrs. These children were from special institutions for mentally retarded children in Pune. All these children were thoroughly investigated and diagnosed as mentally retarded with I.Q. less than 70. The children with exogenous or extrinsic causes were excluded from the study. Similar studies were conducted in 72 normal school children of the same age groups control.
The dermatoglyphic studies were carried out by the means of palm and finger print. These prints were taken by using Ink-method. In each case the dermatoglyphic patterns were studied using the following parameters. 1) Finger tip patterns e. g. whorl, loop, arch, 2) Patterns in four interdigital areas i.e. I1 , I2 , I3 , and I4 . (Fig I) 3) Patterns in Thenar, Hypothenar areas. (Fig I) 4) Position of axial triradii designated as‘t’. (Fig I) 5) atd angles (Fig II) 6) Type of palmer flexion creases. (Fig. III and Fig. IV) (Simian crease and Sydney line)
STATISTICAL METHODS
The results were compared statistically to find out significant variation between the mentally challenged retarded group and controls (together for males and females) by using chi square test.
RESULTS
Table I shows the number of cases studied and their sexwise distribution. Table II shows percentage of frequency of patterns distribution on fingertip. There is a significant increase in ulnar loop pattern and reduction of whorl pattern in mentally retarded as compared to the normal children. There is incidence of pattern in interdigital areas including thenar and hypothenar. Table III shows percentage wise incidence of the presence of some pattern on five main interdigital areas in control and mentally retarded children comparatively. In Thenar / l1 and l 3 areas showed a significant increase in pattern in mentally retarded as compared to normal. The site of actual triradius– The position of axial triradius was noted according to t, t’, t’’ nomenclature basis.
Table IV shows percentage distribution of the site. The distal displacement of axial triradius (t’’) were observed in mentally retarded, whereas the normal children showed a significant proximal axial triradius (t). There was a widening of atd angle in mental retarded children as compared to the normal children (Fig. III). Palmar crease pattern – Number of cases having simian crease (Fig. III) and Sydney line (Fig. IV) are compared in table V. It shows a significant increase in simian crease in mentally retarded as compared to normal. The decrease in the Sydney line in mentally retard was not significant.
DISCUSSION The study of various dermatoglyphic features, when considered with other clinical signs and symptoms may serve as a supportive investigation. Our study which considered of 72 mentally retarded children included cases with primary cause which were microcephaly-16, Down syndrome-10, cerebral palsy-32, mucopolysaccharoidosis-1, epilepsy and hydrocephalus-13. Cases with exogenous causes were excluded from study. Previous Work 1. Alter M and Bruhl H (1967) (376 idiopathic cases): Increase frequency of pattern in I2 on right hand and Simian Crease in males2 . 2. Kher M.B. (1971) (200 mentally retarded cases): Significant decrease in percentage of whorls, increase in percentage of loops and arches3 . 3. Purandare and Hema, Atre P.R. (1978) (50 idiopathic mentally retarded children) and: Low TRC in male, higher atd angle, increase frequency of hypothenar pattern and higher incidence of tibial arch4 . 4. Pote Anand, Herekar N.G (1994) (52 mentally retarded children): increase frequency of ulnar loops, decrease frequency of radial loops, I2 area showed decrease and I3 and I4 area showed higher frequency of pattern with distal displacement of axial triradius and higher incidence of palmar crease pattern.5 5.
Present study (1996) (72 mentally retarded children): Increase frequency of ulnar loop decrease in whorls on fingertip. Thenar/I1 , I3 area showed significant increase in pattern, higher atd angle, Distal shift in axial triradius with increased frequency of simian crease. As seen from Table VI, the increase in ulnar loop pattern in our study is similar to the findings of Kher M. B. and Pote. There was increase in pattern in I2 , I3 and I4 areas. Higher atd angle and shift of axial triradius is similar to the finding by Purandare. Presence of simian crease can be co-related with finding by Alter M. Few of the differences in the findings in our study and other workers could be due to the difference in causes of mental retardation.
It would therefore require a large and selective sample to make a definitive statement regarding mentally retarded cases on basis of dermatoglyphic. Thus dermatoglyphic can serve to strengthen diagnostic impression and is useful in screening device for further extensive investigation.
CONCLUSIONS The following dermatoglyphic features were noticed in the mentally retarded groups.
Increase ulnar loops on finger tips
• Decrease in whorl on finger tip
• Thenar / I1 and I3 area showed significant increase in pattern
• Higher atd angle.
• Distal shift in axial triradius.
ACKNOWLEDGEMENTS Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
ETHICAL CLEARANCE: Before the study conducted, ethical clearance was taken from institute’s ethical committee. Informed Consent: These children were from special institutions for mentally retarded children in Pune. Hence prior to the study, informed consent has been taken from head of the institute. Source of Funding: To conduct this study there is no any external source of funding. Conflict of Interest: Here I declare that, there is no any conflict of interest related to this study.
Englishhttp://ijcrr.com/abstract.php?article_id=267http://ijcrr.com/article_html.php?did=2671. Cummins H and Midlow C. Finger prints, palm and sole. An introduction to dermatoglyphics.1961; Dover publication. Inc New York.
2. Alter M, and Bruhl H. Dermatoghlyphic in idiopathic Mental Retardation, Amer Jr of disease od Children. June 1967; 113: 702-706.
3. KherM.B, Indurkar M. B., Lokur U.V. Dermatoglyphics in Pediatric Practice. Ind Jr Med Science. 1971; 25:618.
4. Purandare H, Atre P. R. (1978): Dermatoglyphic features in mentally retarded chidren. Anat Soc India. 1978; 27 (3): 127.
5. Pote A, Herekar N. G. (Dec. 1994): Dermatoglyphic trait in mentally retarded children. Abstract from 42nd National conference of the Anatomical Society of India. Vol. 27, No. 3: 127.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareMETASTATIC OVARIAN CYSTOSARCOMA PHYLLOIDES OF BREAST
English1720Papa DasariEnglish Haritha SagiliEnglish Priyanka Yoga PuraniEnglishBackground: Cystosarcoma Phylloides is a rare breast neoplasm constituting ≤ 1% of all breast neoplasms. These are mostly benign and reccur. Malignant cystosarcoma Phylloides can recur and metastasize to lung, bone and abdominal viscera. Metastasis to Ovary is not reported in literature. Case Report: A 46 year old multiparous lady was diagnosed with a recurrent cystosarcoma of right breast and a large Ovarian mass which was causing her dyspnoea. The mass was of 30 weeks size and was firm and tender. CECT showed a large solid abdominopelvic mass with irregular enhancing septate extending from pelvis to infracolic area with minimal free fluid. Uterus and Ovaries could not be delineated. FNAC from the mass was reported as low-grade malignant mesenchymal tumour. CA 125 was within normal range. Laparotomy revealed a large fleshy mass with jelly like material which was adherent to intestines and pelvic and parietal peritoneum. Right ovary is not visualized. Left ovary parially visualised and incorporated into the mass. Excision of the mass with TAH and BSO was carried out. There was diffuse ooze from the pelvic and peritoneal cavity which was managed by packing, blood product transfusion and tranexamic acid. She received massive transfusion and survived. Later she developed haemoptysis and underwent tracheostomy and feeding ileostomy and was managed in ICU for 8 weeks. Palliative mastectomy and adjuvant Radiotherapy and chemotherapy were differed by Oncologists and hence she was discharged after 4 months of admission. Conclusion: Managing ovarian metastasis from cystosarcoma phylloids can be challenging and the quality of life is poor when the primary disease is not managed adequately.
EnglishMetastatic ovarian cystosarcoma phylloides, Breast, Large solid abdominopelvic mass, Ovarian tumourINTRODUCTION Phylloid tumours account for less than 1% of breast masses and occur rarely. They affect women at young and middle age unlike adenocarcinomas which occur at a later age. .They most often reccur locally and 20% to 40% develop distant metastasis. The most common sites of distant metastases are lung, bone and abdominal viscera1 .The abdominal visceral metastasis is reported in duodenum and Pancreas.2 Metastasis to ovaries is not found in literature. Hence this rare case is reported.
CASE REPORT A 46-year-old para2 live 2 whose child birth was 14 years back underwent simple mastectomy for a right sided breast mass one month ago at a private hospital, the histopathology was consistent with cystosarcoma phylloids. The breast mass re-appeared at the same site with in one month of surgery. FNAC from the recurrent breast mass revealed cystosarcoma phylloids with stromal elements. She also developed sudden onset of pain abdomen and distension of abdomen of one month duration and decreased urine output, difficulty in breathing and constipation of 12 days duration. CT scan of abdomen and pelvis reported a large solid mass in abdomen and pelvis with minimal free fluid in pelvis.
The mass is not separately seen from uterus and ovaries. She was referred to our Institute with a diagnosis of recurrent cystosarcoma phylloids with Ovarian tumour. Her Obstetric and gynecological history revealed that she had 2 normal deliveries and underwent tubectomy 14 years back and there was no family history of malignancies. She had polymenorrhea .She gave history of loss of weight and loss of appetite for the past 6 months.She also had urinary retention and hence she was on continuous bladder drainage for one week. She complained of fever with chills of 10 days duration. On examination she was emaciated, tachypnoeic, febrile, pulse was 108/min regular, BP 100/60 mm Hg. No significant lymphadenopathy. There was a hard mass of 10x6x3 cm in size on the lateral aspect of right breast with local rise of temperature and tenderness. Left breast was normal. Respiratory system was normal.
Cardiovascular system was normal except for tachycardia. Abdomen was grossly distended in sub- umbilical and umbilical region. There was a hard immobile tender mass of 30 weeks size arising from pelvis. Bowel sounds were normal. General surgical opinion was recurrent or residual cystosarcoma phylloides (as the resected margins were reported positive) with Ovarian tumour and advised to manage the ovarian tumour first. Her abdominal USG was reported as a large abdominopelvic complex mass with minimal ascites displacing the bowel loops laterally suggestive of Ovarian mass. Her CECT at our Institute after one week of admission reported as a large abdominopelvic dense mass with irregular enhancing septate extending from POD to infra colic areas.
Ovaries are not visualized separately. FNAC from the abdominal mass was reported as a low grade malignant mesenchymal tumour. She was taken up for laparotomy 2 weeks after admission after surgical oncologist opinion. On laparotomy there was hemorrhagic ascites of more than 500ml. There was a large fleshy mass with jelly like material with a breach on the surface suggesting tumour rupture. The mass was of 28 week size occupied pelvis and lower abdomen and extended up to the root of the mesentery and covered by small bowels which were closely adherent. There was lot of mucoid material within the mass appearing like myxoid degeneration (Fig1a). Both ovaries incorporated in to the mass and right ovary could not be recognised and left ovary was only partially recognized (Fig 1b) Both fallopian tubes were free. Uterus was 10 weeks size and anterior to the mass which was densely adherent to POD, lateral pelvic walls and rectosigmoid.
The mass was separated from the intestines and excised with the help of surgical oncologist. Total abdominal hysterectomy with bilateral salphingo opherectomy was carried out. There was lot of oozing from the intestinal surfaces and peritoneal surfaces of POD. Multiple haemostatic sutures were taken and bilateral internal iliac arteries were ligated. As the oozing persisted from the peritoneal surfaces , pelvis and abdomen was packed. Blood loss was 1000 ml and she received 5 units of FFP, 4 packed cells. In view of poor general condition she was ventilated and was kept on SIMV mode. Abdominal pack was removed after 48 hours under general anaesthesia. She was monitored in post-operative ward and received 22 units of FFPs, 4 units of platelets,3 units of Packed cells, 12 units of cryoprecipitate over a period of 8 days. She also received intravenous tranexamic acid during surgery and for 48 hours following surgery.
Mastectomy was deferred at the time of laparotomy though it was planned to do earlier by the surgical oncologist. She could be started on oral fluids after a week and was shifted to ward after 10 days of surgery. On 14 th postoperative day she developed sudden dyspnoea and was managed conservatively with oxygen and sedation. Her fever persisted despite of 3 broad spectrum intravenous antibiotics. She had superficial wound gaping and developed dyspnoea again with decreased saturation. She was kept on mechanical ventilation. X Ray chest P/A revealed minimal left sided effusion with basal atelecatsis. She underwent tracheostomy after 4 days as prolonged ventilation was required . She produced thick sputum which required mucolytic and frequent suctioning. After 10 days she was weaned off ventilator and was maintaining 100% saturation.
The histopathological report was metastatic malignant cystosarcoma Phylloids to ovary and parametrium. Fallopian tubes and uterus and cervix were free of tumour. Tumour showed high cellularity and moderate nuclear atypia and high mitosis 16/10 high power field with extensive myxoid change. (Fig 2 a, b,and c) This was consistent with previously diagnosed and treated malignant phylloids. Her haematological parameters were with in normal limits. She was given one course of Ifosphamide and MESNA which she tolerated well. She was given total parenteral nutrition for almost one month. After seven days of receiving chemotherapy she became dyspnoeic and right sided air entry decreased and she was shifted to RICU(Respiratory Intensive care Unit) under care of the anaesthetists. Her abdominal wound healed by secondary intention. She was given ICU care and underwent feeding jejunostomy . She was decanulated after 8 weeks of tracheostomy. The breast mass increased in size 20x10 cms, infected and displaced to right lateral side of chest. Surgical Oncologists deferred in doing any kind of palliative surgery and medical oncologists and Radiation Oncologists deferred in giving chemotherapy and radiation therapy. She was in RICU for 6 weeks and received antibiotics as per the sensitivity of the organisms from wound swab, tracheal swab, infected breast mass swab etc.,.
The organisms were Acenetobacter, klebsiella, pseudomonas .The abdomen was scaphoid and there was no evidence of fluid or mass. She was asked to take over by Gynaecologists. As there was no gynaecological treatment necessary and the surgical Oncologists deferred in performing palliative surgery she was explained the inability to give further supportive treatment and discharged home.
local excision the resected margin should be free of tumour for 1 cm. Local recurrence is expected in 15 % of cases even with this modality of treatment3 . Cystosarcoma Phylloids are diagnosed to be benign, borderline and malignant based on histopathological characteristics and a clinical diagnosis of malignant variety is not made as recurrence and even metastasis can occur in benign tumours. A study correlating histopathological features with clinical presentation in 187 cases , found local recurrence in 27%, 32% and 26% of benign, borderline and malignant tumours respectively. Metastasis was present in two borderline and six malignant tumors out of 100 (8%). There were no specific histological features that correlated with local recurrence and metastasis but cytological atypia of stromal cells, stromal overgrowth and mitotic figures of >15 per 50 high power fields were present in those who showed metastasis.4 Flow cytometric analysis of s fractions greater than 0.05 was found to be a useful predictor of clinical outcome along with histological features of stromal overgrowth and and infiltrating margins5 . A literature review in 1999 to find out the predictors of recurrence after conservative surgery of cystosarcoma phylloids concluded that wide local exicision is also a suboptimal modality of treatment for borderline and malignant phylloid tmours because the recurrence rate is high (29% for borderline and 36% for malignant).6
The most common site of metastasis is lung7 and other sites reported are spine, brain, parotid gland, nasal cavity, forearm and mandible. The metastatic sites in the abdomen reported are pancreas, duodenum, jejunum and liver. Metastasis to genital organs is very rare and only one case report of metastasis to vulva 8 and another to Brenner tumour of ovary is found in literature9 . The metastasis to vulva occurred along with pulmonary metastasis a year after the management of primary by surgery and local radiation. The diagnosis in their case was made by PET-CT as the metastatic nodule was only 2x2cm and the diagnosis was confirmed by fine needle aspiration8 . The metastasis to ovary could not be diagnosed prior to laparotomy by fine needle aspiration in the present case. This is because FNAC has very high false negative rates in diagnosing cystosarcoma phylloids.10 Adjuvant therapy for management of metastatic Phylloids includes chemotherapy and Radiotherapy. Response to chemotherapy was observed in lung metastasis and abdominal metastasis but not in bone metastasis. Single agent and combined regimens have been used and response is long lasting with increase in progression free survival when Ifosfamide is used11. Radiotherapy has a role for loco regional control in recurrent benign as well as malignant Phylloids. However the control of primary tumour is important when metastasis had been taken care of to improve the survival rates as well as the quality of life.
The present case though she survived after laparotomy and complete removal of the large ovarian metastasis, she continued to suffer as the primary was not taken care of. Palliative surgery, chemotherapy and radiotherapy were deferred in the present case even after repeated discussions saying there is no role for surgery of primary in metastatic disease. But in this case the Ovarian metastasis was taken care of almost completely by surgery. Aggressive palliative surgery in metastatic Phylloids is reported to improve survival as well as quality of life. The physical and mental well being was improved after radical surgery for repeated recurrence that occurred twice . and this improved the nutritional status and immunity to undergo further treatment with chemotherapy7 .
The present case was unable to get up from the bed because of the weight of the tumour mass (breast) that progressed to large size and also because of poor nutritional status. Palliative breast surgery and palliative Radiotherapy under high risk consent may have improved her quality of life. A recent study which assessed the predictive factors for the local recurrence and distant metastasis of phylloides tumours of the breast in 192 cases concluded that histopathological type and margin status were independent predictors of distant metastasis- free survival and overall survival and it is essential to reduce the local recurrence to prevent distant metastasis.12
CONCLUSION Managing ovarian metastasis from cystosarcoma phylloids can be challenging and the quality of life is poor when the primary disease is not managed adequately. When an abdominal mass and a breast mass co-exist , metastasis from the breast mass to be considered as the first etiology rather than an association of different pathology until proved otherwise. Conflicts of Interests: None Sources of Funding: Nil
ACKNOLEDGEMENTS The authors acknowledge the immense help received from the scholars whose articles are cited and included in the manuscript. The authors are also greatful to authors/editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=268http://ijcrr.com/article_html.php?did=2681. Parker SJ, Harries SA, Phylloid tumours. Postgrad Med J 2001;77:428–435
2. Ang TL Leong Ng VW, Fock KM, Teo EK, Chong CK. JOP. J Pancreas 2007; 8(1):35-38.
3. Chen WH, Cheng SP, Tzen CY, Yang TL, Jeng KS, Liu CL, Liu TP. Surgical treatment of phyllodes tumors of the breast: retro-spective review of 172 cases. J Surg Oncol. 2005 ;91(3):185- 194.
4. Grimes MM. Cystosarcoma phyllodes of the breast: histologic features, flow cytometric analysis, and clinical correlations.Mod Pathol. 1992;5:323-329..
5. Palko MJ1 , Wang SE, Shackney SE, Cottington EM, Levitt SB, Hartsock RJ. Flow Cytometric S fraction as a predictor of clinical outcome in Cystosarcoma Phylloides. Arch Pathol Lab Med. 1990 Sep;114(9):949-52.
6. Bharat RJ Jr. Histologic features predict local recurrence after breast conservating therapy of Phylloid tumours.. Breast Cancer Res Treat. 1999 ;57(3):291-5.
7. Kapali AS, Singh M, Deo SVS, Shukla NK, Muduly DK. Aggressive palliative surgery in metastatic Phylloids tumor: Im pact on quality of life.Ind J Palliat Care. 2010; 16 (2):101-104.
8. Khangembam BC, Sharma P,Singla S,Shingal A,Dhull VS, Bal C,Kumar R. .Malignant Phylloides tumour of the Breast metastasing to the Vulva.18 F-FDG PET-CT demonstrating rare metastasis from a rare tumour Nucl Med Mol Imaging .2012 46:232–233
9. Hines JR, Gordan RT, Widger C, Kolb T.Cystosarcoma Phylloids metastatic to a Brenner tumour of the ovary. Arch Surg 1976;111(3):299-300.
10. Jacklin RK, Ridgway PF,. Ziprin P,, Healy V, Hadjiminas D, and . Darzi A, “Optimising preoperative diagnosis in phyllodes tumour of the breast,”. J Clin Pathol, 2006; 59(5):454–459.
11. Hawkins RE,Wiltshaw E,Fisher C McKinna JA..Ifosphamide is an active drug for chemotherapy of metastatic Cystosarcoma Phylloides.Cancer.1992;69:2271-2275.
12. Wei J,Tan Yu-T, Cai Yu C, Yuan Z-Yu, Yang D, Wang SS.Predictive factors for local recurrence and distant metastasis of Phylloides tumours of the breast: a retrospective analysis of 192 cases at a single centre. Chin J Cancer; 2014; 33 (10):492- 500.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareCOMPARATIVE ANALYSIS OF SENSITIVITY AND SPECIFICITY OF CARDIAC SPECIFIC TROPONIN I AND CK-MB FOR DIAGNOSIS OF ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
English2125Sandipkumar R. PatelEnglish Hariom SharmaEnglish Bhavika VananiEnglishBackground: Study is designed to see correlation of cardiac specific Troponin I and Creatine Kinase-MB level to diagnose ST segment elevation myocardial infarction. Aim and Objectives: To access the diagnostic importance of cardiac specific Troponin I over Creatine Kinase-MB in patient of ST-segment elevation myocardial infarction. Materials and Methods: A comparative study was carried out in 100 patients, having ST segment elevation myocardial infarction. A group of 100 normal healthy individuals, age and sex matched from the same population served as controls. Troponin I and Creatine Kinase-MB levels were estimated in both the groups. Results: Results of present study shows that cardiac specific Troponin I and CK-MB levels were significantly higher in STEMI patients compared to healthy subjects with ‘p’ value of EnglishTroponin I, ST-segment elevation myocardial infarction (STEMI), Creatine Kinase – MB (CK-MB)INTRODUCTION Acute myocardial infarction occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis and is the most common contributor of morbidity and mortality worldwide. Slowly developing, high-grade coronary artery stenoses do not typically precipitate ST-segment elevation myocardial infarction (STEMI) because of the development of a rich collateral network over time. [1] In India, incidence of cardiovascular diseases was about 7% in 1970 and increased up to 32% in 2011 and 31.7% of deaths occur due to myocardial infarction. The huge burden of coronary artery disease in Indian subcontinent is the consequence of large population and high prevalence of cardiovascular risk factors like smoking, tobacco chewing, alcohol, low fruit and vegetable intake, lack of physical activity, obesity, high blood pressure, abnormal lipid levels and diabetes. [2]
Cardiac specific troponin I is present in three isoforms namely cardiac, skeletal slow-twitch and skeletal fast-twitch, encoded by three separate genes. However, cardiac specific Troponin I is expressed as a single isoform in adult heart but not in skeletal muscle. [3] Creatine Kinase, which is a cytosolic carrier protein for high-energy phosphates, has three isoenzymes: CK-MM (skeletal muscle), CK-BB (brain), and CK-MB (heart and skeletal muscle). Creatine Kinase - MB is most abundant in the heart. [4] Jagannadha Rao Peela et al. reported that troponins have ushered in a new era of highly specific and sensitive cardiac markers for diagnosis of myocardial infarction.[5] So, the present study was designed to measure and compare the changes in Creatine Kinase – MB and Troponin I level in patients of ST-segment elevation myocardial infarction.
MATERIALS AND METHODS The present study was conducted at Department of Biochemistry, Government Medical College and Sir Takhtsinhji General Hospital, Bhavnagar in which 100 cases of ST-segment elevation myocardial infarction were included. The myocardial infarction patients were primarily diagnosed by cardinal symptoms like chest pain and 12-lead ECG (Echocardiogram). A group of 100 normal healthy individuals, age and sex matched from the same population served as controls. Inclusion criteria were both male and female above 18 years of age. Exclusion criteria were age less than 18 years and patients, not willing to give informed consent.
The study was reviewed and approved by Human Ethics Committee of Government Medical College, Bhavnagar. Venous blood sample was collected in plain vacutainer from patients of ST-segment elevation myocardial infarction and from healthy controls and after centrifuging, were analyzed for CK-MB and Troponin I. CK-MB was estimated by using Fully auto analyzer I-Lab 650. Troponin I was estimated by using iMark Micro plate Absorbance Reader (Elisa Reader). Quality controls were done before analyzing both parameters. Methods of estimating CK-MB: Immuno-Inhibition method, Troponin I: ELISA (The enzyme-linked immunosorbent assay) method.
STATISTICAL METHODS Results of the present study were analyzed by using Graph Pad in Stat version 3.0. In data analysis, comparison of these parameters for ST segment elevation myocardial infarction patients were carried out by applying unpaired t-test and their correlation were studied by applying Pearson Correlation test. Interpretation of the test result was done according to p value (p < 0.05 – significant, p < 0.001 – highly significant and p ≥ 0.05 – not significant).
RESULTS Present study includes 100 healthy controls and 100 STEMI patients. Control subjects include 34% females and 66% males, while STEMI patients comprise 23% females and 77% males. Mean age in STEMI patients was 47.33 ± 9.949 years which include 31 patients (31%) between30-40 years, 36 patients (36%) between 41-50 years, 25 patients (25%) between 51-60 years and 8 patients (8%) between 61-70 years of age. The maximum number of patients belongs to age group between 41-50 years. In healthy control mean of age was 46.66 ± 13.10 years which include 44 patients (44%) between 30-40 years, 16 patients (16%) between 41-50 years, 26 patients (26%) between 51-60 years and 14 patients (14%) between 61-70 years of age.
The maximum number of patients belongs to age group between 30-40 years. (Table – 1) The mean level of Troponin I was 1.428±0.960 ng/ml in STEMI patients and 0.0492±0.022 ng/ml in healthy subjects. The mean level of CK-MB was 99.48±41.33 U/L in STEMI patients and 28.67±9.219 U/L in healthy subjects. STEMI patients have significantly higher Troponin I and CK-MB level than healthy subjects. (Table – 2, 3) Troponin I and CK-MB levels in STEMI patients were statistically highly significant with ‘p’ value of Englishhttp://ijcrr.com/abstract.php?article_id=269http://ijcrr.com/article_html.php?did=2691. Harrison’s Principles of Internal Medicine, Volume 1, 18th edition, chapter 245: ST-Segment Elevation Myocardial Infarction. McGraw Hill Education; p. 4082.
2. Sushma Pandey, Suresh Pandey, Purushottam Jhanwar, Anshul Jhanwar. A prospective study of Myocardial Infarction patients admitted in a tertiary care hospital of south-eastern Rajasthan. Int J Biol Med Res. 2012;3(2):1694-96.
3. Gary Ross, Frank N. Bever, Zi Uddin, Elaine M. Hockman. Troponin I sensitivity and specificity for the diagnosis of acute myocardial infarction. JAOA 2000;100:29-32.
4. Harper’s Illustrtaed Biochemistry, 28th Edition, chapter 7:Enzymes: Mechanism of Action, pp 127-28.
5. Jagannadha Rao Peela, Abdalla M. Jarari, Abdul Hai, Avinaash K. Rawal, Shoba Devi Kolla, Shakila Sreekumar et al. Cardiac Biomarkers: The Troponins and CK- MB. Ibnosina Journal of Medicine and Biomedical Sciences 2010;2(5):190-97.
6. Denis Xavier, Prem Pais, P J Devereaux, Changchun Xie, D Prabhakaran, K Srinath Reddy et al. Treatment and outcomes of acute coronary syndromes in India (CREATE): a prospective analysis of registry data. Lancet 2008;371:1435–42.
7. S Joarder, M Hoque, M Towhiduzzaman, AF Salehuddin,N Islam, M Akter et al. Cardiac Troponin-I And CK-MB for Risk Stratification in Acute Myocardial Infarction (First Attack): A Comparative Study. Bangladesh J Med Biochem 2011;4(1):10- 15.
8. Allan S. Jaffe, Jan Ravkilde, Robert Roberts, Ulf Naslund, Fred S. Apple, Marcello Galvani et al. It’s Time for a Change to a Troponin Standard. Circulation 2000;102:1216-20.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcarePREVALENCE OF THYROID DISORDERS IN A TERTIARY CARE CENTER
English2630Deokar PGEnglish Nagdeote ANEnglish Lanje MJEnglish Basutkar DGEnglishBackground: Thyroid disorders are a widespread endocrinological problem, but data on its prevalence in India is scanty. Aims and Objective: The aim of the present study was to assess the proportion of various thyroid disorders in subjects attending a tertiary care center. Material and Methods: This retrospective hospital based study involved 2076 patients who underwent thyroid function test, in the central clinical biochemistry. Thyroid function tests were performed on Siemens Centaur immunoassay analyzer. Statistical analysis was performed by SPSS version 16 software. Results: We found 22.16% subjects having thyroid dysfunction in our study population. Out of these, 4.24% were overt hypothyroid, 9.44% were subclinical hypothyroid, 2.5% overt hyperthyroid and 5.97% were found to be subclinical hyperthyroid. Conclusion: Our study suggested that the prevalence of thyroid disorders in our study population is high and hypothyroidism is more common than hyperthyroidism. Highest prevalence of thyroid disorder was found in 30-49 years age group. The mean TSH concentration increased with age in euthyroid, hypothyroid (both overt and subclinical) and hyperthyroid (both overt and subclinical) groups studied. The highest TSH concentration was seen in the age group 60- 69 years and lowest TSH was seen in age group 10 – 19 years.
EnglishHypothyroidism, Hyperthyroidism, TSHINTRODUCTION
Diseases of the thyroid gland are among the most abundant endocrine disorders worldwide second only to diabetes, India is no exception. Recent report shows that 300 million people in the world are suffering from thyroid disorders and among them about 42 million people reside in India.1 Thyroid disorders are more common in women than in men. One in every eight women during their life time has risk for thyroid disorder. The exact reason is not known. The higher prevalence in females may be associated with estrogen and progesterone.1 Our understanding of the effects of thyroid hormones under physiological circumstances, as well as in pathological conditions, has increased dramatically during the last two centuries and it has become clear that overt thyroid dysfunction is associated with significant morbidity and mortality. Both hypothyroidism and hyperthyroidism have been linked with increased risk from cardiovascular disease and the adverse effects of thyrotoxicosis in terms of osteoporosis risk are well established. Hypothyroidism itself contributes to morbidity from osteoporosis, hyperlipidemia, hypercholesterolemia, cardiovascular and neuropsychiatry disease in the population. The seriousness of thyroid disorders should not be underestimated as thyroid storm and myxedema coma can lead to death in a significant number of cases.2, 3 Furthermore the prevalence and pattern of thyroid disorders depends on sex, age, ethnic and geographical factors and especially on iodine intake. After successful salt iodinisation adopted by the Indian government, World Health Organization assessment status classified India as having optimal iodine nutrition in 2004. Still thyroid disorders especially hypothyroidism, both subclinical and overt, contributes significantly to burden of thyroid disorders in India. Data available on the prevalence of hypothyroidism and hyperthyroidism for Indian population is scanty.4, 5
The present study aimed to carry out hospital based study on the proportion of various thyroid disorders. We therefore evaluated cases with high suspicion of thyroid disorders over a six month period to estimate proportion of various thyroid disorders in subjects attending our tertiary care centre.
MATERIAL AND METHODS
Serum of individuals with suspicion of thyroid dysfunction was subjected to thyroid profile (Total T4, Total T3, Free T4, Free T3 and TSH) using Siemens Centaur immunoassay analyzer. The TSH levels of serum samples were analyzed using a 3rd generation chemiluminescence sandwich immunoassay. The analytical sensitivity was 0.004 μIU/ml. The T3, T4, FT4 and FT3 levels were also analysed by chemiluminescent immunoassay using Siemens Centaur immunoassay analyzer. The laboratory’s reference values were TSH: 0.55- 4.78 µIU/ml; fT3: 2.3- 4.2 pg/ml; fT4: 0.89- 1.76 ng/dl; T3: 60 -181 ng/dl and T4: 4.5- 12.60 µg/dl. Analytical sensitivity was 0.004 μIU/ml for TSH, 0.4 µg/dl for T4, 35 ng/dl for T3, 0.05 ng/dl for FT4 and 1.0 pg/ml for FT3. Coefficient of variation was < 10% for TSH, T4, T3, FT4 and FT3. Hypothyroidism was classified as clinical (overt) if TSH was ≥ 4.78 μIU/ml and FT4 ≤ 0.89 ng/dL or T4 ≤ 4.5 µg/dl and subclinical if TSH was ≥ 4.78 μIU/ml and FT4 / T4 was within the reference range. Hyperthyroidism was classified as clinical (overt) if TSH was ≤ 0.55 μIU/ml and FT4 ≥ 1.76 ng/dL or T4 ≥ 12.6 µg/dl and subclinical if TSH was ≤ 0.55 μIU/ml and FT4 and T4 was within the reference range.
Statistical Analysis The data collected were analyzed using Excel 2007, R2.8.0 Statistical Package for Social Sciences (SPSS) for windows version 16.0 (SPSS Inc.; Chicago, IL, USA). We calculated the odds ratio (OR) and their 95% Confidence Interval (95% CI). The study was carried out over a period of 6 months (June 2014- November 2014). 2076 subjects (250 males; 1826 females) formed part of the study.
RESULTS
The current study was a retrospective hospital based study, carried out from June 2014 – November 2014 (6 months) involving 2076 subjects (250 males and 1826 females) with suspicion of thyroid disorder who were subjected to thyroid function assay. The highest number was in the 20- 29 age group (34.29 %) and lowest number in the 60-69 age group (5.1%). Out of 2076 with suspected thyroid disorder, 77.84% (n=1616; 1442 F and 250 M) were categorized as euthyroid.
The distribution of various thyroid disorders is depicted in fig 1. The overall frequency of thyroid disorders along with percentage and 95% CI are described in Table 1 and table 2 while gender wise distribution given in Table 3 and table 4. Subclinical hypothyroidism was detected in 9.44% subjects (n=196; 164F and 32M). 4.24% (n=88; 66F and 22M) individuals were overt hypothyroid with elevated levels of TSH and low levels of total T3 / fT3 and total T4/ fT4 in serum. 2.5% (n=52; 40F and 12M) cases had hyperthyroidism and the laboratory findings of thyroid profile showed significant elevation of total T3/ fT3, total T4/ fT4 in serum and low levels of TSH. Subclinical hyperthyroidism was detected in 5.97% (n=124; 114F and 10M). The study cohort was divided in six age groups to determine the occurrence of various thyroid disorders in different age groups (Table 4). The age group division was 10-19 years, 20 to 29 years, 30 to 39 years, 40-49 years, 50-59 years and 60-69 years. In the age 10-19 years age group, out of 106 cases (6 M,100 F), 92 (86.79%) were euthyroid, 6 (5.66%) were subclinical hypothyroid, 4(3.77%) were clinically hypothyroid, 2(1.88%) were subclinical hyperthyroid whereas 2(1.88%) were clinically hyperthyroid. The 20-29 years age group comprised our largest group with suspicion of thyroid disorders. This group consisted of 712 cases (52 M, 660 F), 616 (86.51%) were euthyroid, 46(6.46%) were subclinical hypothyroid, 18(2.52%) were clinically hypothyroid, 20(2.80%) were subclinical hyperthyroid whereas 12(1.68%) were clinically hyperthyroid. In the age 30-39 years age group, out of 612 cases (62 M,550 F), 470(76.79%) were euthyroid, 62 (10.13%) were subclinical hypothyroid, 22 (3.59%) were clinically hypothyroid, 38(6.20%) were subclinical hyperthyroid whereas 20 (3.26%) were clinically hyperthyroid. In the age 40-49 years age group, out of 364 cases (58 M,306 F), 248 (68.13%) were euthyroid, 56 (15.38 %) were subclinical hypothyroid, 22(6.04%) were clinically hypothyroid, 32 (8.79%) were subclinical hyperthyroid whereas 6(1.64%) were clinically hyperthyroid. In the age 50-59 years age group, out of 176 cases (42 M,134 F), 128 (35.16%) were euthyroid, 14 (3.84%) were subclinical hypothyroid, 12 (3.29%) were clinically hypothyroid, 16 (4.39%) were subclinical hyperthyroid whereas 6 (1.64%) were clinically hyperthyroid. In the age > 60 years age group, out of 106 cases (30 M, 76 F), 62 ( 58.49%) were euthyroid, 12(11.32%) were subclinical hypothyroid, 10 (9.43%) were clinically hypothyroid, 16(15.09%) were subclinical hyperthyroid whereas 6 (5.66%) were clinically hyperthyroid. The mean TSH concentration increased with age in euthyroid, hypothyroid (both overt and subclinical) and hyperthy- roid (both overt and subclinical) groups studied. The highest TSH concentration was seen in the age group 60- 69 years and lowest TSH was seen in age group 10 – 19 years.
DISCUSSION
Thyroid disorders are amongst the most common endocrine diseases in India. However data on the prevalence of thyroid disorders in India is relatively scanty. This retrospective hospital based study was carried out from June 2014 – November 2014 (6 months) involving 2076 subjects (250 males and 1826 females) with suspicion of thyroid disorder who were subjected to thyroid function assay. We found 22.16% subjects having thyroid dysfunction in our study population. Rebecca et al6 reported prevalence of 15.8 % of thyroid dysfunction in a study conducted on 505 women in Pondicherry whereas Arindam Bose et al5 found prevalence of 15.35% in central India in their study. Various studies have reported variable prevalence of subclinical hypothyroidism. We found 9.44% of our population having subclinical hypothyroidism. The Rotterdam study2 reported an overall prevalence of 10.8% and Rebecca et al found 9.5% prevalence which was very similar to our finding. In females above 55 years of age, the prevalence was much higher 12.5% as reported by Rebecca et al (our study 9.52% women above 50 years had subclinical hypothyroidism). Colorado study7 and NHANES III8 study found 9.5% (TSH >5.1 μIU/ml) and 4.3% prevalence of subclinical hypothyroidism respectively. Other studies reported prevalence of 9.4% 9 , 11% 10, 6.31%5 .The prevalence of overt hypothyroidism in our study population was 4.24%. Rebecca et al reported 2%, a study from Cochin on 971 adults revealed 3.9%9 subjects to be hypothyroid whereas Rotterdam study and study by Arindam Bose et al reported 1.1% and 7.45% respectively. Our study population revealed 5.97% subjects to be subclinical hyperthyroid whereas 2.5% were overt hyperthyroid. Rebecca et al reported 1.8% of their study population to be hyperthyroid out of which 1.2% were overt hyperthyroid and 0.6% were subclinical hyperthyroid. Arindam Bose et al reported 1.79% as hyperthyroid in their study whereas the Hoogendoorn11 study found 0.4% o and 0.8% prevalence of overt and subclinical hyperthyroidism respectively. Our study suggested that the prevalence of thyroid disorders in our study population is high and hypothyroidism is more common than hyperthyroidism. The prevalence of subclinical hypothyroidism (9.44 %) as well as subclinical hyperthyroidism (5.97%) is much higher than overt hypothyroidism (4.24%) or overt hyperthyroidism (2.5%). Various studies have shown female preponderance in thyroid disorders. However we found male preponderance (24.7% vs. 18.2%). We believe this bias was introduced in the study since more number of females with complaints of menstrual irregularity, PCOS, infertility were subjected to thyroid function test as a part of routine protocol. However, only those males with suspicion of thyroid disorders were subjected to TFT. Also, we found that highest no of subjects with hypothyroidism (both overt and subclinical) was between 30-49 years age group. Other studies like Arindam Bose et al (19-45 years), Vanderpump MP et al12 (34 years and above) have reported similar age groups. The mean TSH value was found to increase with age in euthyroid, hypothyroid (both overt and subclinical) and hyperthyroid (both overt and subclinical) subjects. Similar finding was reported by Rebecca et al. Several other workers have reported an increase in TSH with age however Hoogendoorn et al12 found decrease in mean TSH level with age.2,7,12,13,14
CONCLUSION
Our study suggested that the prevalence of thyroid disorders in our study population is high and hypothyroidism is more common than hyperthyroidism. Highest prevalence of thyroid disorder was found in 30-49 years age group. The mean TSH concentration increased with age in euthyroid, hypothyroid (both overt and subclinical) and hyperthyroid (both overt and subclinical) groups studied. The highest TSH concentration was seen in the age group 60- 69 years and lowest TSH was seen in age group 10 – 19 years. We found male preponderance (24.7% vs. 18.2%). We believe this bias was introduced in the study since more number of females with complaints of menstrual irregularity, PCOS, infertility were subjected to thyroid function test as a part of routine protocol. However, only those males with suspicion of thyroid disorders were subjected to TFT. The finding that a large number of subjects unknowingly have laboratory evidence of thyroid dysfunction supports the usefulness of screening of thyroid function after age of 30 years, for early detection and treatment to reduce the ill effects of thyroid dysfunction.
ACKNOWLEDGEMENT
The authors are grateful to the dean for permitting to publish this article. Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Source of funding: Study is not supported by any organisation.
Conflicts of interest: There are no conflicts of interest.
Englishhttp://ijcrr.com/abstract.php?article_id=270http://ijcrr.com/article_html.php?did=2701. Nimmy N.J ET AL.A Survey on the Prevalence of Thyroid Disorder Induced by Demography and Food Habits in South Indian Population. Indian Journal of Pharmacy Practice. Apr-Jun 2012;5(2):49-52.
2. Hak AE, Pols HAP, Visser TJ, Drexhage HA, Hoffman A, Witteman JCM. Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: The Rotterdam Study. Ann Intern Med 2000; 132:270- 78.
3. Morris MS, Bostom AG, Jacques PF, Selhub J, Rosenberg IH. Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third U.S. National Health and Nutrition Examination.
4. Unnikrishnan AG, Kalra S, Sahay RK, Bantwal G, John M, Tewari N. Prevalence of hypothyroidism in adults: An epidemiological study in eight cities of India. Indian J Endocrinol and Metab. 2013. 17(5):647-652.
5. Arindam Bose, Norman Sharma, Nanda Hemvani, Dhananjay.S.Chitnis. A Hospital Based Prevalence Study on Thyroid Disorders in Malwa region of Central India. Int. J. Curr. Microbiol. App.Sci(2015) 4(6): 604-611.
6. Rebecca Abraham, V Srinivasa Murugan, P Pukazhvanthen and S K Sen. Thyroid disorders in women of Puducherry. Indian Journal of Clinical Biochemistry, 2009 / 24 (1) 52-59.
7. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado Thyroid Disease Prevalence Study. Arch Intern Med 2000; 160: 526-34.
8. Hollowel JG, Staehling NW, Flanders DW, Hannon WH, Gunter EW, Spencer CA, et al. Serum TSH, T4 and Thyroid Antibodies in the United States Population (1988 – 1994): National Health and Nutrition Examination Survey (NHANES III). J ClinEndocrinolMetab 2002; 87:489-99.
9. Usha Menon V, Sundaram KR, Unnikrishnan AG, Jayakumar RV, Nair V, Kumar H. High prevalence of undetected thyroid disorders in an iodine sufficient adult south Indian population. J Indian Med Assoc 2009; 107(2):72-77.
10. Verma A, Jayaraman M, Kumar HK, Modi KD. Hypothyroidism and obesity.Cause or effect? Saudi Med J. 2008; 29(8):1135-8.
11. Hoogendoorn EH, Hermus AR, de Vegt F, Ross AH, Verbeek ALM, Kiemeney LALM et al. Thyroid function and prevalence of Antithyroperoxidase Antibodies in a population with Borderline Sufficient Iodine Intake: Influences of Age and Sex. ClinChem 2006; 52:104 – 11.
12. Vanderpump MP, Turnbridge WM. Epidemiology and prevention of clinical and subclinical hypothyroidism. Thyroid 2002;12(10):839-47.
13. Sawin CT, Castelli WP, Hershman JM, McNamara P, Bacharach P. The aging thyroid.Thyroid deficiency in the Framingham Study. Arch Intern Med 1985; 145:1386-8.
14. Bjoro T, Holmen J, Kruger Q, Midthjell K, Hunstad K, Schreiner T, et al. Prevalence of thyroid disease, thyroid dysfunction and thyroid peroxidase antibodies in a large unselected population. The Health Study of Nord-Trondelag (HUNT). Euro J Endocrinol 2000; 143:639-47.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareEVALUATION OF GROWTH PROGRESS AMONG MALNOURISHED CHILDREN ATTENDING VILLAGE CHILD NUTRITION CENTRE (VCNC) UNDER THE PROGRAMME 'MISSION BALAM SUKHAM' IN A TRIBAL AREA OF WESTERN INDIA
English3139Dhara I. ZalavadiyaEnglish Suraj I. KuriyaEnglish Vihang S. MazumdarEnglish Sangita V. PatelEnglish Rajendra K. BaxiEnglishBackground: Government has started a programme “Mission Balam Sukham” to combat the malnutrition with 3 tier approach including Village Child Nutrition Center (VCNC), Child Malnutrition Treatment Center (CMTC) and Nutrition Rehabilitation Center (NRC). Present study was conducted with the aim to evaluate this programme at VCNC level in a tribal area of western India.Methods: Hundred malnourished children according to weight for age criteria by WHO, were selected from 10 VCNCs. Their growth progress was recorded and compared with other 100 malnourished children attending anganwadies from the area nearby, where the programme was not yet launched. VCNC intervention was done for 1 month. Children were followed for 3 months.
Results: There was 2 times higher chances of malnutrition grade improvement among VCNC children as compared to anganwadi children with relative risk at the end of 1 month (95% CI =1.2609 to 3.5662) (P-value< 0.05). After completion of 3 months malnutrition grade improvement was similar in both the groups. The difference in growth progress was not statistically significant at the end of 3 months (P = 0.8656).
Conclusions: The result suggests that VCNC intervention was not able to give sustained result over 3 month of period. VCNC intervention only gives short term benefits in improving malnutrition grades of borderline malnourished children.
EnglishMalnutrition, VCNC, EvaluationBACKGROUND
According to NFHS 2005-06 in India, 48 % of children under 5 years of age are stunted and 43 percent are underweight.1 In Gujarat state ongoing interventions to tackle the problem of malnutrition are mainly through Anganwadi centers under the “Integrated Child Development Services” (ICDS) Scheme. Malnourished children are provided 800 kilocalories and 20-25 grams of protein per day according to ICDS norms. Government of Gujarat has started “Mission Balam Sukham” to combat the malnutrition in which integrated management of malnourished children is done through – 3 tier approach including Village Child Nutrition Center (VCNC), Child Malnutrition Treatment Center (CMTC), Nutrition Rehabilitation Center (NRC).2 At village level VCNC runs at anganwadi centers managed by Anganwadi worker (AWW), Anganwadi helper (AWH) and Accredited Social Health Activists (ASHA). Severe acute malnutrition (SAM) and moderate acute malnutrition (MAM) children aged 6 months to 6 years without any medical complications are enrolled for 30 days. Nutrition supplements are given as per standard protocol including micronutrients like Vitamin-A, Iron, folic acid and Zinc. Malnourished Children are provided 5 meals per day including 2 ICDS meals containing total 1000 kcal and 30 grams of proteins for 6 to 36 months age and 1270 kcal and 40 grams of proteins for 3-6 years of children. Parents of malnourished children are also counselled for home based care, health and sanitation3 . The present study was undertaken to know the effect of this programmes on malnutrition status of children aged 6 months to 6 years and to record and compare the growth progress in ICDS anganwadies and VCNCs. METHODS It was a Prospective Cohort study conducted during the period from February 2014 to December 2014 in a tribal area of Gujarat as the programme was initiated in tribal area. Sample size Assuming significant weight gain as a malnutrition grade improvement according to WHO Growth chart over 1 month, and assuming 20% of malnourished children would improve their malnutrition grade at anganwadi level and 40% of malnourished children would improve their malnutrition grade at VCNC, 80% power and 95% Confidence Interval sample size comes to 91 for each group. Considering 10% drop out rate or loss to follow up sample size came to be 100 for each group. Study setting and population Exposed (VCNC) group: 100 children of 6 months to 6 years of age having moderate to severe malnutrition according to WHO growth chart from selected VCNC from Naswadi block acted as a study group to know the effect of VCNC on improvement in malnutrition as it is a newer initiative and provide additional supplementary nutrition to malnourished child. VCNCs under Mission Balam Sukham work thrice in a year for 1 month every time in anganwadies. After that anganwadies continue to work as guideline under ICDS. So in VCNC group, VCNC food and medicines were provided for 1 month only. After that VCNC group was provided food and services same as anganwadies under ICDS. Unexposed (Anganwadi) group: 100 children of 6 months to 6 years of age having moderate to severe malnutrition from selected anganwadi of Sankheda taluka acted as control group. Sankheda was selected for anganwadi as control group because it is near Naswadi so there was environmental, geographical, occupational, cultural similarity which helped to remove possible confounders. Matching was done for grades of malnutrition, age and sex to the nearest possible level. Inclusion exclusion criteria All the children included were within the age range of 6 months to 6 years, malnourished and permanent residents of the area. Children above the age of 6 years or having any disease or complication at the time of survey were excluded from study. Those children whose parents were not permanent residents of the area were excluded from study. Those children whose parents refused to give consent were also excluded from study. Sampling technique Considering the final calculated sample size of 100 children, 10 anganwadi from Sankheda block and 10 VCNC from Naswadi block were selected. From each anganwadi and VCNC average 10 malnourished children of age 6 months to 6 years were selected randomly. Anganwadies and VCNCs were selected by systemic sampling technique. Data questionnaire Data was collected by using semi-structured questionnaire. All the information was collected from the immediate caregivers, who were usually the mothers and anganwadi workers. Questionnaire included Introduction of child, age, sex, immunization detail, History of micronutrient given or not and anthropometric measurements including weight, height and MUAC. Anthropometric measurements were taken using standard methods and instruments4 . Salter spring balance (Model 235 PBW) was used for weighing 1 to 6 years age children. For children less than 1 year infantometer was used. Vertical measuring non stretchable tape was used for height measurement. For infants and children under 2 years of age, recumbent length was measured. Arm circumference is measured with special circumference measuring tapes called Shakir’s strip. Follow up of same individuals was done after 1 month to check growth progress in exposed and unexposed group as VCNC services provided mainly for first 1 month in VCNC group. Further follow up after 2 and 3 month was done for both groups to ascertain the continued progress or otherwise. Data management and statistical analysis The Data collected was entered in Microsoft excel worksheet and analyzed using WHO Anthro and Medcalc software. The Z-score of anthropometric data was calculated using the new international reference population released by the WHO (ONIS 2006) and accepted by Government of India. The relative risk and attributable risk of all anthropometric parameters was calculated within the Anganwadi and VCNC group. Chi-square test was used to assess the difference between the frequency distributions. Z-test was used to compare difference between the means. Consent At the time of data collection, the purpose of study was clearly explained to the guardians/parents. Parental/ guardian consent for assessment of nutritional status of child was taken. As it is not an interventional study, there was minimal or less than minimal risk to the children involved in study. Anganwadi children who are not getting extra benefit were natural control because government had not implemented the programme in the area. RESULTS In the exposed group, 100 malnourished children from 10 VCNCs were selected and their baseline data was collected. Follow up was done for next 3 months to evaluate growth progress every month. Out of them 2 were lost to follow up. In the unexposed group, 100 malnourished children from 10 anganwadies were selected for baseline data collection. 5 children out of 100 could not be followed up till the end in unexposed group. So the final analysis was done for 98 children in VCNC group and 95 children in Anganwadi group. For comparisons of growth progress, children in both the group should be comparable at baseline. Growth progress among malnourished children depends on their age, sex and malnutrition grade which were taken in to consideration during baseline data collection. Matching was done for age, sex and malnutrition grade according to weight for age WHO growth standards as much as possible in both VCNC and Anganwadi groups. Table-1 suggests that there was no statistically significant difference in age, sex or malnutrition grade in both groups. There was no statistically significant difference for other factors associated with malnutrition like education of mother, socio-economic class, immunization status, birth order, birth weight, exclusive breast-feeding for 6 months given or not and age of starting complementary feeding. The analysis of the nutritional status of children in this study is based on a new international reference population released by the WHO (Onis 2006) and accepted by the Government of India. The nutritional status indicator is expressed in standard deviation (SD) units (Z-scores) from the median of the reference population. Children whose weight for age Z-score is below the three standard deviations (Englishhttp://ijcrr.com/abstract.php?article_id=271http://ijcrr.com/article_html.php?did=2711. NFHS-3 Reports. 2005-06.
2. Guidelines for Management of Severe Acute Malnutrition (SAM) Children at Nutrition Rehabilitation Center. Department of Health and Family Welfare, Government of Gujarat; 2012.
3. Guidelines on Management of Bal Shaktim Kendra (Village Child Nutrition Center) at the level of Anganwadi. Health and family welfare department, Government of Gujarat; 2012.
4. WHO child growth standard; Methods and development. WHO; 2006.
5. Ashworth A. Efficacy and effectiveness of community-based treatment of severe malnutrition. Food and nutrition bulletin. 2006;27(3 Suppl):S24-48. Epub 2006/11/02.
6. Sanghvi J, Mehta S, Kumar R. Predicators for weight gain in children treated for severe acute malnutrition: A prospective study at nutritional rehabilitation center. ISRN Pediatrics. 2014:5.
7. Brown R, Brown J, Teeter R. Evaluation of a nutrition center program in rural Africa. J Trop Pediatr. 1980;26.
8. Ojofeitimi EO, Teniola SO. Evaluation of nutrition rehabilitation centre in Ile-Ife, Oyo State, Nigeria. World Rev Nutr Diet. 1980;35:87-95.
9. Stanton B, Phillips N, Clemens J, Wroot B, Gafur Z, Fleischman J, et al. An urban nutrition education and rehabilitation centre: a description of the programme and change in nutritional status of children who were enrolled. Trop Geogr Med. 1987;39.
10. Fronczak N, Amin S, Laston SL, Baqui AH. An evaluation of community-based nutrition rehabilitation centers. 1993.
11. Chapko M, Prual A, Gamatie Y, Maazou A. Randomized clinical trial comparing hospital to ambulatory rehabilitation of malnourished children in Niger. J Trop Pediatr. 1994;40:225-30.
12. Monte C, Ashworth A, Sa M, Diniz R. Effectiveness of nutrition centers in Ceara state, northeastern Brazil. Rev Panam Salud Publica. 1998;4:375-82.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareJOB SATISFACTION AMONGST POST GRADUATE STUDENTS AT TERTIARY CARE TEACHING INSTITUTE IN CENTRAL INDIA- A CRITICAL APPRAISAL
English4044Vaidya A.English DUA H.English MUJAWAR N.English NANOTI G.EnglishMultifaceted psychological retorts towards one’s job covering cognitive, affective and behavioural modalities is collectively known as “job satisfaction”.
Aims and objectives: To study the level of job satisfaction amongst Post Graduate (PG) students at tertiary health care teaching Institute in Central India.
Materials and methods: The present study was a cross sectional hospital based study, which included 199 PGs of all faculties of medical field.
Results: Out of total 169 PGs, 56 were from 1st year (junior resident I/JRI), 61 were JR II and 52 were JR III. Response rate was 85%. Amongst responses, majority of the participants had low level of satisfaction (43.1%), followed by 72 (42.6%) and 24 (14.2%) for average and high level of satisfaction, respectively. The major factors contributing to the job dissatisfaction were job not according to the interest and abilities, adverse working conditions, less opportunities for development and promotion and decreased autonomy.
Conclusion: The high levels of dissatisfaction amongst PGs in our study is alarming sign, which should be taken into account by every medical institute while decision making, because PGs are major component of health care in tertiary health care teaching hospital and it is safe to infer that highly satisfied physician will more likely work to his/her full potential.
EnglishJob satisfaction, PG studentshttp://ijcrr.com/abstract.php?article_id=272http://ijcrr.com/article_html.php?did=272Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2017May12HealthcareMORPHOLOGICAL STUDY OF THE TIBIAL TUBEROSITY IN THE POPULATION OF SOUTH KARNATAKA, INDIA
English4547Rashmi BhatEnglish Ramya RathanEnglish Neha SamapriyaEnglish Shakuntala PaiEnglishObjective: To estimate the prevalence of various morphological types of Tibial Tuberosity and to determine the side and gender differences.
Methods: 170 randomly collected tibiae of unknown sex were analysed to evaluate the shapes and the gender differences in the tibia. The prominence of the Tibial Tuberosity and the gender differences of the bone was determined
Results: Type 2 TT was the most common type seen in 34% bones followed by type 3 in 17% of the bones. Type 2 TT was the most common type seen on right side (31%) as well as on the left side (39%). Type 2 was the most common type of TT seen in both males (32%) and females (35%).
Conclusion: The present study shows variations in shape may be due to developmental reasons. There were no statistical differences in the side and gender differences. The knowledge of the present study will help further researchers in evaluating anterior knee pain syndromes.
EnglishTibia, Tibial Tuberosity, Shape, GenderINTRODUCTION
The Tibial tuberosity(TT) is a bony landmark present at the proximal end of the tibia. It is one of the bony points to measure the Quadriceps angle (Q angle) for assessing patellofemoral mechanics. The TT is an apophysis and develops in traction.1 Development of the tubercle has been divided into four stages: cartilaginous, apophyseal, epiphyseal, and bony.2 The TT begins ossification at between seven and nine years as a distal focus. This progressively enlarges proximally and anteriorly, while the proximal tibial epiphysis concomitantly expands downward into the tuberosity.3 The TT projects only a little and is divided into distal rough and a proximal smooth region. The patellar tendon is attached to the proximal smooth area while the distal end is palpable.4 The morphology of the TT has received scant attention by researchers. Variations in the morphology of the TT could cause errors in determining its precise location. The shape and the position of the TT influences the value of the Q angle and also has impact on patellofemoral biomechanics. According to Van Eijdn et al(1987)5 ,a TT which is anteriorly placed increases the length of the contact paths on both patellar and femoral articulating surfaces, produces a lengthening of the moment arm of the patellar ligament force which may either decrease or increase the ratio between patellar ligament force and quadriceps muscle force.5 An abnormal lateral position of the TT causes distal malalignment of the extensor mechanism of the knee and can lead to lateral tracking of the patella which causes anterior knee pain or objective patellar instability and is mainly characterised by recurrent dislocation.( Koetar S et al, 2007)6. The methods used to determine the position of the TT include clinical assessment7 , conventional radiography using marking wires8 and CT scan.6,7,8,9,10 Of these methods, measurements done on CT scans appear to be the most reliable.6 However, a survey of the literature did not reveal any study that used direct bony measurements. This information is likely to be useful to the clinician in evaluating anterior knee pain syndromes. With reference to the above literature the main objective of the current study is to estimate the prevalence of various morphological types of TT and to determine the side and gender differences.
MATERIALS AND METHODS
The material for the present study comprised of one hundred and seventy adult human tibia bones. The tibias were collected from the department of Anatomy from various Medical colleges in the Southern region of Karnataka. 170 tibiae were studied of which 101 belonged to right side and 69 to left side. The bones were first selected by using inclusion criteria and were numbered. The Prominence of the TT was assessed by analysing the end on frontal view photos with Adobe Photoshop version 5.0 (vide infra).
SUBJECTIVE SEXING OF THE TIBIA: was done to determine the gender differences in the above measurements. The criteria used were
• Weight and the length: measured by Electronic balance and Osteometric Board
• Mid-shaft circumference: First, the midpoint of the total length of tibia was marked. Then the midshaft circumference was measured using measuring tape.
• Width at the proximal and distal end: Were measured using digital callipers at the widest region.
• Minimum girth of the shaft: measured at the junction of middle and lower third using measuring tape.
• The bones were then classified as males or females using the demarking points given by Singh and Singh et al.11
RESULTS
The TT was classified into 5 types based on the shape of the ridge separating the proximal and distal parts of TT. The prevalence of the 5 types of TT is shown in table 1. Type 2 TT was the most common type seen in 34% bones followed by type 3 in 17% of the bones. Type 5 TT was the least common type. Table 2 shows that Type 2 TT was the most common type seen on right side (31%) as well as on the left side (39%). Type 1 was seen to be more common on right side than on left and type 3 was more common on the left side than on the right, however both were not statistically significant. Type 5 TT was the least common type. Type 2 was the most common type of TT seen in both males (32%) and females (35%) and is present in table 3. It’s of interest to note that a ridge on TT was always present in male tibiae when compared to female tibiae which was statistically significant.
DISCUSSION
In review of literature it was noticed that there are no documented works on classification of TT based on shape of the ridge separating the proximal and distal parts of TT. Hence, comparison with other studies could not be done. This ridge across the TT marks the distal limit of the proximal tibial growth plate.3 In the present study it was noticed that the oblique shape of the ridge was most common (34%) while absence of ridge on TT was the least common (6%). This suggests that the shape of the ridge is influenced by the proximal epiphyseal pull. When analysed for side differences it was observed that that there was no significant difference between the right and left in the prevalence of morphological types of TT. If paired right and left tibia of the same cadaver were available this difference could have been analysed better. Gender difference in the morphological types of TT was further analysed. For this purpose the subjective classification of the tibia according to various parameters was done. It was noted that there was no significant difference. Of interest here to note is the constant presence of the ridge on the TT in male tibiae where as about 10% of female tibiae lacked this ridge suggesting the differential amount of force applied to this proximal epiphyseal plate in males and females. The difference was statistically significant.
CONCLUSION
The present study shows variations in shape may be due to developmental reasons. There was no statistical differences in the side and gender. The present study will help further researchers in evaluating anterior knee pain syndromes.
AKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Source of funding: NIL Conflict of Interest: NIL.
Englishhttp://ijcrr.com/abstract.php?article_id=273http://ijcrr.com/article_html.php?did=2731. Ogden JA, Southwick WO. Osgood–Schlatter’s disease and tibial tuberosity development. Clin Orthop Relat Res 1976; 116:180–189.
2. Ehrenborg G, Engfeldt B. The insertion of the ligamentum patellae on the tibial tuberosity. Some views in connection with the Osgood–Schlatter lesion. Acta Chir Scand 1961; 121:491–499.
3. Ogden JA. Radiology of postnatal skeletal development. X. Patella and tibial tuberosity. Skeletal Radiol 1984; 11(4): 246-57.
4. Standring S, Borley NR, Collins P, Crossman AR, Gatzoulis MA, Healy JC et al, editors. Gray’s anatomy: The Anatomical basis of clinical practice. 40th ed. UK, Elsevier Ltd; 2008. p. 1412-15.
5. Van Eijden TMGJ, Kouwenhoven E and Weijs WA. The influence of anterior displacement of the TT on patellofemoral biomechanics. International Orthopaedics.1987; 11(3): 215-221.
6. Koetar S, Diks MJ, Anderson PG, Wymenga AB. A modified tibial tubercle osteotomy for patellar maltracking: result at two years. J Bone Joint Surg Br. 2007 Feb; 89(2): 180-5.
7. Shakespeare D, Fick D. Patellar instability- canthe TT-TG distance be measured clinically? Knee. 2005 Jun; 12(3): 201-4.
8. Nagamine R, Miura H, Urabe K, Matsuda S, Chen WJ, Matsunobu T. Radiological assessment of the position of the tibial tuberosity by means of a marking in knees with patellofemoral arthritis. Skeletal radiol. 1999 Jan; 28(1): 27-32.
9. P. Schoettle, M. Zanetti, B. Seifert, C. Pfirrmann, S. Fucentese, J. Romero. The tibial tuberosity–trochlear groove distance; a comparative study between CT and MRI scanning. The Knee.2006 ;13(1): 26-31.
10. Jones RB, Barlett EC, Vainright JR, Carroll RG. CT determination of tibial tubercle lateralization in patients presenting with anterior knee pain. Skeletal Radiol. 1995 Oct; 24(7): 505-9.
11. Singh G, Singh S, Singh SP. Identification of sex from tibia. J Anat Soc India 1975;24(1).
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareLEPTIN: A DRIVING FORCE BEHIND THYROID PROBLEMS
English4852Singla GesuEnglish Bedi GKEnglish Sandhu HSEnglish Vij ChittranjanEnglishIntroduction: Apart from diabetes mellitus, thyroid dysfunction is one of the most common endocrine disorders encountered in adults, affecting up to 10% of the UK population Leptin is a 16kDa protein hormone that plays a key role in regulating energy intake and energy expenditure, including appetite and metabolism.
Aim: The aim of this study was to estimate thyroid hormones and Serum Leptin levels in patients with thyroid disorders and to find their correlation with each other.
Material and Methods: 50 diagnosed patients of thyroid disorders and 30 healthy controls were recruited in our study. Serum Leptin Levels, Serum T3, T4, TSH levels were estimated in both cases and controls using ELISA method.
Results: There was significant negative correlation between Serum Leptin and Serum T3. There was no significant but negative correlation between Serum Leptin and Serum T4. A very significant positive correlation was seen between Serum TSH and Serum Leptin levels.
Conclusion: Leptin problems are a driving force behind thyroid problems. Leptin triggers the decreased production of thyroid hormones. Improving leptin problems and losing weight will improve thyroid function.
EnglishLeptin, Thyroid, TSH- Thyroid Stimulating Hormone, T4- Thyroxine, T3- TriiodothyronineINTRODUCTION
Thyroid dysfunction is one of the most common endocrine disorders encountered in adults. The two most common thyroid diseases are inadequate thyroid function i.e. hypothyroidism and excessive thyroid function i.e. hyperthyroidism. [1] Thyroid hormones are essential for the regulation of important processes involved in thermogenesis, energy consumption and many other metabolic reactions. Leptin, the ob gene product is a peptide hormone, secreted by adipocytes. [2] It circulates at levels proportional to body fat. Leptin enters the central nervous system in proportion to plasma concentration. It controls food intake and energy expenditure by acting on receptors in mediobasal hypothalamus. [3] In human, leptin concentrations are elevated in the obese when compared with lean subjects, and their levels are positively correlated to the degree of obesity. In addition administration of leptin to rats deprived of food corrected many of the neuroendocrine changes (e.g. the decrease in the release of thyroid hormone) that occur as a result of food deprivation. [4] There are three general ways in which alterations of the leptin regulatory loop could lead to obesity. a) Failure to produce leptin as occur in ob/ob mice, would result in obesity b) inappropriately low leptin secretion for a given fat mass c) Obesity could result from relative or absolute insensitivity to leptin at its site of action. [5] Both thyroid hormones and leptin have effects on similar aspects of body homeostasis, but their potential interaction is controversial. [2]
Aims and Objectives
1. To study the serum leptin levels in various disorders of thyroid gland.
2. To evaluate thyroid hormone levels in various disorders of thyroid gland.
3. To study the correlation of serum leptin with thyroid hormones in various disorders of thyroid gland.
MATERIALS AND METHODS
The present study was conducted in Department of Biochemistry at Govt. Medical College, Patiala on 50 diagnosed cases of thyroid disorder referred by Department of Medicine, Rajindra Hospital, Patiala from October, 2011 to May, 2012. For comparison 30 age and gender matched healthy individuals constituted the control group. Patients with history of any drug intake, history of any infection/illness, pregnant females, diabetic patients, cancer including thyroid cancer were excluded from the study. Informed consent of all subjects and detailed history were taken at the beginning of the study. Fasting venous blood samples were collected under all aseptic conditions, and subsequently, Serum Leptin Levels, Serum T3 , T4 , TSH levels were estimated in both cases and controls. Serum Leptin, Serum T3 , T4 , TSH were estimated by ELISA method. ERBA-thyrokit was used for Serum.T3 , T4 and TSH whereas AviBion Human Leptin ELISA Kit [6] was used for Serum Leptin. Although the patients were known cases of thyroid disorders but when their hormonal status was assessed they were divided into 3 categories: euthyroid, hypothyroid and hyperthyroid. Out of the 50 cases, 20 cases were of euthyroidism, 20 cases were of hypothyroidism and 10 cases were of hyperthyroidism.
Statistical Analysis
Statistical analysis was performed using Statistical Package for Social Sciences (SPSS).Means and Standard Deviations (SD) were calculated for all parameters. The independent sample t-test was used to compare the means of different variables in the two groups. In addition, the Pearson correlation coefficient (r) was used for correlation analysis. P value Englishhttp://ijcrr.com/abstract.php?article_id=274http://ijcrr.com/article_html.php?did=2741. Constanti A, Bartke A, Khardori R. The Thyroid Gland. In: Taylor and Francis. Basic Endocrinology for Students of Pharmacy and Allied Health Sciences. Harwood Academic Publishers 4th edn.Singapore: 2005;59-61.
2. Baig M, Karira KA, Ahmed A, Zaidi P, Niaz K, Kamal S. Serum Leptin level in Hyperthyroid Female Patients. Journal of Pakistan Medical Association. 2003;53(5):176-81.
3. Williams KW, Scott MM, Elmquist JK. From observation to experimentation: leptin action in the mediobasal hypothalamus. Am. J. Clin. Nutr. 2009;89(3):985S–990S.
4. Al-Shoumer KA, Vasanthy BA, Makhlouf HA, Al-Zaid MM. Leptin levels in Arabs with primary hyperthyroidism. Ann Saudi Med. 2000;20(2):113-8.
5. Friedman JM and Halaas JL. Leptin and the regulation of body weight in mammals. Nature Macmillan Publishers Ltd 1998;395:766.
6. AviBion Human Leptin ELISA Kit, User Manual. Available at:http://www.anibiotech.fi/anibiotech/pdfs/Orgenium-Leptin_ User Manual Rev1.09.pdf
7. Janson A, Karlsson FA, Micha-Johansson G, Bolme P, Brönnegård M, Marcus C. Effects of stimulatory and inhibitory thyrotropin receptor antibodies on lipolysis in infant adipocytes. J Clin Endocrinol Metab. 1995;80(5):1712-1712.
8. Reinehr T. Obesity and thyroid function. Mol Cell Endocrinol 2010;316:165-171.
9. Zimmermann-Belsing T, Brabant G, Holst JJ, Feldt-Rasmussen U. Circulating leptin and thyroid dysfunction. Eur J Endocrinol. 2003;149(4):257-71.
10. Yoshida T, Momotani N, Hayashi M, Monkawa T, Ito K, Saruta T. Serum leptin concentrations in patients with thyroid disorders. Clin Endocrinol (Oxf). 1998;48(3):299-302.
11. Tene Pérez CE, Revilla-Monsalve MC, Amato D, Escobedo de la Peña J, Galván R, Millán-Guerrero RO. Correlation between serum leptin levels and insulin sensitivity in diffuse toxic goiter. Endocr Res. 2004;30(1):19-27.
12. Azza M. Abdu-Allah, Riham G. Mahfouz, Seham A. Khodeer, Walid A. Shehab-Eldin, Mostafa El Nagar. Study of Resistin and Leptin in patients with Thyroid Dysfunction. Journal of American Science, 2011;7(3):569-76.
13. Ozata M, Ozisik G, Bingol N, Corakci A, Gundogan MA. The effects of thyroid status on plasma leptin levels in women. J Endocrinol Invest. 1998;21(6):337-41.
14. Hsieh CJ, Wang PW, Wang ST, Liu RT, Tung SC, Chien WY et al. Serum leptin concentrations of patients with sequential thyroid function changes. Clin Endocrinol (Oxf) 2002;57(1):29-34.
15. Iacobellis G, Ribaudo MC, Zappaterreno A, Iannucci CV, Leonetti F. Relationship of thyroid function with body mass index, leptin, insulin sensitivity and adiponectin in euthyroid obese women. Clin Endocrinol (Oxf). 2005;62(4):487-91.
16. Siemi?ska L, Wojciechowska C, Kos-Kuda B, Marek B, Kajdaniuk D, Nowak M et al. Serum concentrations of leptin, adiponectin, and interleukin-6 in postmenopausal women with Hashimoto’s thyroiditis. Endokrynol Pol. 2010;61(1):112-6.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareHISTOGENESIS OF MUSCLE LAYERS OF HUMAN URINARY BLADDER
English5358Shinde Reshma B.English Laqeeue MohammadEnglish Ukey Rahul K.English Diwan Chaya V.EnglishBackground: Urinary bladder is an organ of considerable importance in mammals, being a site where urine is collected before micturition and without undergoing any significant exchange of water or ions with surrounding. Urinary epithelium (urothelium) is unique in being non-reabsorptive and non-secretory in nature. The earlier studies on the development of urinary bladder were mainly on its gross anatomical features.
Objectives: 1) To thankful to Dr. Mrs. Yelikar, Professor and Head, Department of Obstetrics and Gynecology, Aurangabad, for her support and co-operation. I am thankful to all the teachers, staff members and colleagues of department of anatomy, GMC, Aurangabad, Maharashtra for their help. Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.note structural differentiation and maturity of muscularis externa layer which it attains at different stages of development to show the adult picture. 2) To compare and contrast differences between different age groups and with previous studies and available literature.
Material and Method:
50 aborted human fetuses (29 females and 21 males) of different gestational age from 9th week onwards were collected, urinary bladder were taken out and fixed in a fixative. Blocks of tissues were made from bladder wall proper, trigone and bladder neck and processed to get sections which were stained with 1) Haematoxylin and Eosin 2) Masson’s trichrome stain.
Results: Beginning with 12th week, muscularis externa showed well developed circular muscle layer and a thin inner longitudinal layer in the form of thin, scattered bundles. Outer longitudinal layer appeared as discrete, nonuniform bundles of muscle fibres by 13th week. All three layers were seen well developed and thick by 16th week and found thickest by 32nd week with slight variations in their arrangement. Muscle layer thickness at bladder neck and trigone increased progressively from 18th wk onwards.
Conclusion: Muscular layer in bladder wall showed all three layers progressively increased in thickness and indistinctly well developed from 16th week onwards and found thickest at 32nd week. Thus Histogenesis of urinary bladder in this instance may represent a powerful tool to delineate structure – function relationship.
EnglishHistogenesis, Fetal urinary bladder, Muscularis externa, Trigone, Bladder neckINTRODUCTION
Understanding of the processes involved in the formation of various organs and systems of body has disclosed most cryptic secrets of nature. The earlier studies on the development of urinary bladder were mainly on its gross anatomical features. Not much work has been done on the development and differentiation of muscular layers of human fetal urinary bladder especially of Indian origin which differ largely from their western counterparts in the rate of growth, differentiation and maturity. Similar studies have been done in western countries by many researchers(1,2,3,4,5,6,7,8,9). Material and method:- Study design: Observational (Qualitative) study Statistical Analysis: No measurements have been taken as it is an Observational study, so statistical analysis is not applicable. Material and method Collection of materials: After approval from the institutional ethical committee, during period of 2 years, 50 aborted human fetuses (29 females and 21 males) of different gestational age from 9th week onwards were collected from the department of Obstetrics and Gynaecology, Aurangabad (Fig-1). Written consent from parents of aborted fetuses was taken. Inclusion criteria: Spontaneously aborted fetuses from 9th week onwards, stillborn fetuses, terminated fetuses under the Medical termination of Pregnancy Act of India 1971. Exclusion criteria: Fetuses less than 9 weeks, twins, presence of any congenital anomalies, post mortem decomposition. Fetuses were obtained within 1-2 hrs of abortion to avoid post-mortem decomposition changes and preserved immediately in 10% formalin. Gestational age was calculated from Body weight and Crown-rump length (CRL).They were dissected within 2 hrs of collection by taking a midline vertical incision extending from umbilicus to pubic symphysis (Fig 2 and3). Bladder was then carefully removed along with its neck (Fig 4). Subsequently bladders were passed through following procedures: (10) 1) Fixation of Bladder: in Bouin’s fluid for 4-5 days. Longitudinal and transverse sections of specimen were taken from bladder wall proper, trigone region and bladder neck region, each section being 3-4 mm thick. 2) Dehydration: The tissue was processed in ascending grades of 50%, 70% and 90% alcohol. 3) Clearing: done to remove alcohol from tissue. Tissue was placed in xylene for about 30 minutes. It also increases the refractive index of tissues. 4) Paraffin bath: It involves soaking of tissue in molten soft paraffin wax (melting point 45-500 C). Tissue was subjected to two changes of paraffin wax each for three hours. 5) Casting (block making): The blocks were prepared by pouring molten paraffin wax (melting point 55-600 C) into a mould. Using two ‘L’ moulds, suitable size bocks were prepared and wax impregnated tissue was placed eccentrically and oriented so that it could be sectioned in the right angle plane. 6) Microtomy (section cutting): The block was cut with the section thickness of 5-7 microns in the form of ribbon with the help of rotary microtome. 7) Fixing sections on the slide: The ribbon of sections was placed on the surface of warm water in the flotation bath. This removes all wrinkles from the tissue and wax (flattening). The glass slide was smeared with egg albumin and sections were mounted on it and slides were placed on the hot plate at 450 C - 500 C for 2 hours or more as per the requirement for drying. The sections were stained with the following stains:
A) Haematoxylin and Eosin staining:
(10) Technique:
1) Removal of paraffin wax from the sections was done by dipping the slide into two changes of xylene for one to two minutes each.
2) Removal of xylene done by dipping the slide into two changes of absolute alcohol for one to two minutes each and then treated with descending grades of alcohol- 90%, 80%, 70% for one minute each.
3) The slide was kept under running tap water for 2-3 minutes.
4) The slide was stained with Haematoxylin for about five to seven minutes followed by washing under running tap water for 2-3 minutes. This leads to bluing of the section.
5) Excess stain is removed (Differentiation) by dipping the slide in acid alcohol for few seconds. This changes blue color to red because of the acid.
6) The blue color was regained by washing in running tap water for 5 minutes and it was checked under the microscope, for nuclear staining.
7) The section was counterstained with 5% aqueous solution of eosin for about 5 minutes and dehydrated by dipping in ascending grades of alcohol as 70%, 90%, and absolute alcohol (100%) for one minute each.
8) Clearing was done in two changes of xylene for one minute each.
9) The slide was mounted in DPX (Distrene Plastsizer and Xylene) and coverslip was applied and the slide was kept at room temperature for some hours for firm adhesion of the coverslip to the section.
Result: Nuclei-blue, cytoplasm- pink, muscle cells- pink, collagen fibres- light pink.
B) Masson’s Trichome staining: (10)
Technique:
1) Wax was removed and section was brought to water.
2) Nuclei were stained with Weigert’s Iron Haematoxylin and then slide was washed well in water.
3) It was stained with diluted Ponceau Acid Fuschin for five minutes.
4) The slide was rinsed in distilled water.
5) Section was differentiated in 1% Phosphomolybdic acid until collagen was decolorized and again rinsed in distilled water.
6) Section was counterstained with light green or aniline blue for two minutes.
7) Light green was differentiated in water.
8) Slide was dehydrated and cleared.
9) Lastly the slide was mounted.
Result: Nuclei- blue to black. Muscle, red blood cells, fibrin and some cytoplasmic granules– red. Collagen, some reticulin, basement membrane, amyloid and mucin– green or blue according to counterstain used.
Observations and Results:- The slides were stained with Haematoxylin and Eosin and Masson’s Trichome stain, observed by uniocular light microscope under low (10X) and high (40X) magnifications for three indistinct anastomosing layers- inner and outer longitudinal muscle layers and intermediate circular muscle layer. At 12th week, all four layers of urinary bladder were clearly visible. Muscularis externa showed well developed circular muscle layer and inner longitudinal layer in the form of discrete, scattered bundles with absence of outer longitudinal layer (photomicrograph-1). At 13th week, all three muscular layers were seen with inner and outer longitudinal layers appeared as discrete, nonuniform bundles of muscle fibres (photomicrograph-2).. All three layers were well developed and thick from 16th week onwards (photomicrograph-3 and 4) and distinct and thickest by 32nd week (photomicrograph-5 and 6). At this stage muscle thickness was found comparative to adult picture in relation to the bladder size. With Masson’s Trichome, muscularis externa stained bright red 16th week onwards. Pattern of muscle layers in muscularis externa were different within same and different gestational age groups (Table 1). In the trigone region at 18th week, muscle layer showed intermingling of inner ureteral longitudinal and outer circular detrusor muscle fibres which became more pronounced from 20th week onwards (photomicrograph-7). In the bladder neck at 16th week, muscular layer showed indistinct internal longitudinal and outer circular layers (photomicrograph-8). Male fetus of 32nd week showed circular muscle layer more thicker than that in 34th week female fetus.
DISCUSSION
In the present study, at 12th week muscularis externa showed well developed circular muscle layer and a thin inner longitudinal layer in the form of discrete, scattered bundles. Outer longitudinal layer appeared as discrete, nonuniform bundles of muscle fibres by 13th week. All three layers were seen well developed and thick by 16th week and found thickest by 32nd week with slight variations in their arrangement. These findings were corroborative with the findings of others according to whom, musculature in the bladder begins to develop at 13th week and proceeded from apex of bladder towards the urethral orifice (1,2,3,4). It is said that muscle coat in bladder develops well when kidney starts producing urine, by the end of 2nd month (9 week) to 11 weeks of gestation(2). Mechanical distention of bladder stimulates myogenesis in the wall (2). By the 5th month (24 weeks) the cells had acquired most of adult picture in their arrangement and relationship with each other and co-ordinated activity (4). In the present study, considering trimester wise, at 12th week circular and inner longitudinal muscle layer were present while outer longitudinal layer of muscularis externa was absent. In the second trimester, out of total 44 cases 14 cases (32%) showed presence of circular and outer longitudinal muscle layer and absence of inner longitudinal layer, while 7 cases (16%) showed presence of circular and inner longitudinal muscle layer and absence of outer longitudinal muscle layer. 1 case (2%) showed presence of only circular muscle layer with absence of both inner and outer longitudinal muscle layer. Remaining 22 cases (50%) of second trimester showed presence of all three layers of muscularis externa. In the third trimester 1 out of total 5 cases showed absence of outer longitudinal layer. Other study also shows similar findings (5). In trigone region muscle layer showed intermingling of inner ureteral longitudinal and outer circular detrusor muscle fibres at 18th week and was more pronounced from 20th week onwards. Musculature of trigone developed between 11-20 cm CRL stage (13-18 weeks) and appeared continuous with the urethral smooth muscle (1,3). At bladder neck at 16th week muscle layer showed indistinct inner longitudinal and outer circular layer and this found similar with others (3). The male fetus of 32nd week showed circular muscle layer more thicker than that in 34th week female fetus. In male bladder at vesical orifice, circular muscle layer thickens and encircles proximal urethra completely to form ‘Trigonal ring’ (1,6). Urinary bladder is studied for Histogenesis upto Preprostatic part of urethra.
CONCLUSION
In Urinary bladder wall, muscularis externa shows all three layers indistinctly well developed and thick from 16th week onwards and found thickest at 32nd week. Trigone region shows intermingling of inner ureteral longitudinal and outer circular detrusor muscle fibres at 18th week with increase in thickness and intermingling from 20th week onwards. In the bladder neck, at 16th week the muscular layer shows indistinct internal longitudinal and outer circular muscle layer. Male fetus from 32nd week onwards shows circular muscle layer more thick than that in female fetus of comparative gestational age.
ACKNOWLEDGMENT
I am indebted to my post graduate teacher and guide, Dr. Mohammad Laeeque, and Dr. Mrs. C. V. Diwan. I am very thankful to Dr. Mrs. Yelikar, Professor and Head, Department of Obstetrics and Gynecology, Aurangabad, for her support and co-operation. I am thankful to all the teachers, staff members and colleagues of department of anatomy, GMC, Aurangabad, Maharashtra for their help. Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=275http://ijcrr.com/article_html.php?did=2751. Droes JT. Observations on the musculature of the urinary bladder and the urethra in the human fetus. . Br J Urol. 1974 Apr; 46(2):179-85.
2. Newman J, Antonakopoulos GN. The fine structure of the human fetal urinary bladder. Development and maturation. A light, transmission and scanning electron microscopic study. J Anat. 1989 Oct; 166:135-50.
3. Gilpin SA, Gosling JA. Smooth muscle in the wall of the developing human urinary bladder and urethra. J Anat. 1983 Oct; 137 (Pt 3):503-12.
4. Hoyes AD, Ramus NI, Martin BG. Differentiation of the muscle of the human fetal bladder: an ultrastructural study. Micron; 1972; 3 (4); 414–28.
5. Cankara N, Ozguner G, Koyuncu E, Kadir D, Sulak O. The development of muscular layers in the wall of fetal urinary bladder during the fetal period. S.D.U. Typ Fak. Derg. 2009:16(1); 16- 20.
6. Healy JC. Urogenital system in Standring S, editor. Gray’s anatomy: The Anatomical basis of Clinical Practice. 40th ed. London: Churchill Livingstone Elsevier; 2008. p. 1245-50.
7. Hicks RM. The mammalian urinary bladder: an accommodating organ. Biol Rev Camb Philos Soc. 1975 May; 50(2):215-246
8. Matsuno T, Tokunaka S, Koyanagi T. Muscular development in the urinary tract. J Urol. 1984 Jul; 132(1):148-52.
9. Oswald J, Schwentner C, Lunacek A, Fritsch H, Longato S, Sergi C et al. Reevaluation of the fetal muscle development of the vesical trigone. J Urol. 2006 Sep; 176(3):1166-70.
10. Drury RAB, Wallington EA. Carleton’s histological technique. 5th ed. Oxford, New York, Toronto: Oxford University Press; 1980.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareEVALUATION OF SYSTEMIC MARKERS RELATED TO ANEMIA IN PERIPHERAL BLOOD OF PATIENTS WITH CHRONIC GENERALISED SEVERE PERIODONTITIS A COMPARATIVE STUDY
English5963Chakravarthy MuppallaEnglish Ramakrishnan TheyagarajanEnglish Geetha AriEnglish Jaideep MahendraEnglishBackground: The purpose of this study was to evaluate systemic markers related to anemia in peripheral blood of patients with chronic generalized severe periodontitis and compare them with healthy controls.
Materials and Methods: A total of 60 systemically healthy males, aged 18 to 50 years were selected from the out patients department of periodontology, Meenakshi Ammal Dental College and Hospital. They were divided into two groups; Controls (group A) 30 male volunteers with healthy gingiva and Test Group (group B) 30 male patients with chronic generalized severe periodontitis. Periodontal clinical parameters and hematological parameters were recorded in both the groups.
Results: Blood parameters of patients with chronic generalized severe periodontitis especially Red Blood Cell (RBC) count, Haemoglobin (Hb) and Packed Cell Volume (PCV) values were reduced in group B indicating that chronic generalized severe periodontitis has a definite systemic effect.
Conclusion: RBC count, Haemoglobin (Hb) and PCV values of chronic generalized severe periodontitis patients were low compared to healthy individuals.
EnglishAnemia of chronic disease, Chronic generalized severe periodontitis, RBC Count, Packed cell volume, HaemogloblinINTRODUCTION
Periodontitis is an inflammatory disease of the periodontium which is characterized by a progressive destruction of the tissues supporting the tooth fundamentally initiated by chronic bacterial infection.(1,2) Its primary etiology is of microbial infections which may be composed of bacteria currently recognized in the oral cavity. Several reports have indicated that bacterial cells can be found in the pocket wall of periodontitis lesions. Substantial scientific data indicate that the localized infections characteristic of periodontitis can have a significant effect on the systemic health of humans.(3-6) This host response may offer illustrative mechanisms for the interactions between periodontal infection and a variety of systemic disorders,(7) infections, malignant cells, and autoimmune dysregulation all lead to the activation of the immune system and production of cytokines, most notably tumor necrosis factor- alpha and IL-1 and IL-6.(8) Such inflammatory cytokines can depress erythropoietin production leading to the development of anemia.(9-10) The anemia of chronic disease (ACD) can be defined as the anemia seen in chronic infections, inflammatory conditions, or neoplastic disorders that is not due to marrow deficiencies or other diseases and occurs despite the presence of adequate iron stores and vitamins. The aim of this study was to evaluate systemic markers related to anemia in peripheral blood of male patients with chronic generalized severe periodontitis and compare it with males having healthy periodontium.
MATERIALS AND METHODS
Materials A total of 60 systemically healthy males, aged 18 to 50 years were selected from the out patients Department of periodontology, Meenakshi Ammal Dental College and Hospital from June 2014 to July 2015. The “Institutional Ethics Committee” approved this study and written informed consent was obtained from all participants of the study. The study comprised of Group A which includes 30 male volunteers with healthy gingiva with no attachment loss and Group B which includes 30 male patients with chronic generalized severe periodontitis were recruited.
INCLUSION CRITERIA
Patients with a clinical attachment loss of ≥5 mm in >30% of sites classified as chronic generalized severe periodontitis were included.
EXCLUSION CRITERIA
patients, subjects with history of diabetes, kidney disease, cancer and infectious diseases, patients with a history of hospitalization or intake of medications in the last 6 months, patients with a current or past habit of tobacco smoking or chewing and with a previous history of periodontal therapy, and patients with iron deficiency were excluded. Methods Periodontal parameters such as bleeding on probing, probing depth, clinical attachment loss and plaque index and heamotological parameters like total no of erythrocytes (RBC), Haemoglobin concentration (Hb), Mean Corpuscular Haemoglobin (MCH), Mean Corpuscular Haemoglobin Concentration (MCHC), Mean Corpuscular Volume (MCV), Packed cell volume (PCV), Serum Ferritin were examined Blood parameters assessment Blood samples (5 ml) were collected by vene puncture of the cubital vein in the antecubital fossa by using a 5 ml disposable syringe. A component of the blood sample was then transferred to sterile vacuum tubes containing an anticoagulant ethylene diamine tetraaceticacid (EDTA), for whole blood analysis. The left over blood was collected in sterile vacuum tubes with no added anticoagulant this was designated for serum separation for serum ferritin The hematological parameters like RBC count, PCV, Hb, MCV, MCH and MCHC were estimated in an automated blood counting machine. Biochemical parameters like serum ferritin were analyzed by using an automated analyzer.
STATISTICAL ANALYSIS
Statistical analysis was performed with SPSS Software for means ± SD of all the parameters were calculated for both the groups. And to illustrate differences between groups, independent sample t test and mann whitney u test formula p value were used, and was considered statistically significant if p value was Englishhttp://ijcrr.com/abstract.php?article_id=276http://ijcrr.com/article_html.php?did=2761. Listgarten MA. Pathogenesis of periodontitis. J Clin Periodontol 1986;13:418-430.
2. Jotwani R, Cutler CW. Adult periodontitis Specific bacterial infection or chronic inflammation? J Med Microbiol 1998;47:187- 188.
3. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental disease and risk of coronary heart disease and mortality. Bio Med Journal 1993;306:688-691.
4. Kweider M, Lowe GD, Murray GD, Kinane DF, McGowan DA. Dental disease, fibrinogen and white cell count; Links with myocardial infarction? Scott Med J 1993; 38:73-74. 5. Syrjnen J, Peltola J, Valtonen V, Iivanainen M, Kaste M, Huttunen JK. Dental infections in association with cerebral infarction in young and middle-aged men. J Intern Med 1989;225:179- 184. 6. Collins JG, Smith MA, Arnold RR, Offenbacher S. Effects of Escherichia coli and Porphyromonas gingivalis lipopolysaccharide on pregnancy outcome in the golden hamster. Infect Immun journal 1994;62:4652-4655.
7. Mealey BL, Klokkevold PR. Periodontal medicine. In: Newman MG, Takei HH, Carranza FA, eds. Carranza’s Clinical Periodontology, 9th ed. Philadelphia: Saunders; 2002:229-244.
8. Weiss G, Goodnough LT. Anemia of chronic disease. Engl J Med 2005;352:1011-1023.
9. Faquin WC, Schneider TJ, Goldberg MA. Effect of inflammatory cytokines on hypoxia-induced erythropoietin production. Blood 1992;79:1987-1994.
10. Raja KB, O Latunde-Dada G, Peters TJ, McKie AT, Simpson RJ. Role of interleukin-6 in hypoxic regulation of intestinal iron absorption. Br J Haematol 2005; 131:656-662.
11. Cartwright GE. The anemia of chronic disorders. Semin Hematol 1966;3(4):351-75.
12. Hutter JW, Van der Velden U, Varoufaki A, Huffels RA, Hoek FJ, Loos BG. Lower numbers of erythrocytes and lower levels of hemoglobin in periodontitis patients compared to control subjects. J Clin Periodontol 2001;28:930-936.
13. Jongen-Lavrencic M, Peeters HR, Vreugdenhil G, Swaak AJ. Interaction of inflammatory cytokines and erythropoeitin in iron metabolism and erythropoiesis in anemia of chronic disease. Clin Rheumatol 1995;14:519-525.
14. Salvi GE, Lawrence HP, Offenbacher S, Beck JD. Influence of risk factors on the pathogenesis of periodontitis. Perio 2000 1997;14:173-201.
15. Pradeep AR, Sharma A, Arjun Raju P. Anemia of Chronic Disease and Chronic Periodontitis: Does Periodontal Therapy Have Effect on Anemic Status. J Periodontol 2011;82:388-394.
16. Agarwal N, Kumar VS, Gujjari SA. Effect of periodontal therapy on hemoglobin and erythrocyte levels in chronic generalized periodontitis patients: An interventional study. J Indian Soc Periodontol 2009;13:6-11.
17. Lu S-Yu, Eng HL. Dramatic recovery from severe anemia by resolution of severe periodontitis. J Dent Sci 2010;5:41−46
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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524189EnglishN2016May12HealthcareSQUAMOUS CELL CARCINOMA OF TONGUE - A CASE REPORT AND REVIEW OF LITERATURE
English6467L. KayalEnglish S. JayachandranEnglish Y. Hemavathy BhaskarEnglishOral Squamous cell carcinoma is the most common cancer of the Oral Cavity and it is usually seen in patients above the age of 50 years. It rarely occurs in patients who are less than 30 years old (0.4-5.5%). Diagnosis in advanced stage, misdiagnosis usually lead to inappropriate treatment and delayed definitive treatment. Studies show that nearly 30-40 % of all cancer-related mortality are due to human behaviors such as smoking, consumption of alcohol, poor diet quality and physical inactivity. The morbidity of this malignant neoplasm is low in young patientsonly about 2 % of patients was diagnosed with tongue cancer in patients under the age of 35 years. This case report describes a squamous cell carcinoma, involving anterolateral border of tongue in young adult.
EnglishMalignant, Neoplasm, Morbidity, Squamous cell carcinomaINTRODUCTION
Squamous cell carcinoma (SCC) constitute more than 90% of all head and neck cancers. It typically occurs in the elderly men during the fifth-eighth decade of life and rarely occurs in the young patients under the age of 401 . The recent literature has given increasing attention to SCC of tongue in young adults2 . Only approximately 2% of patients are diagnosed before the age of 35 and another 7% before the age of 45, despite the fact that there is an increasing prevalence of tongue SCC3 . Literary reports regarding the etiology, history, and management is limited due to the rarity of this tumor in young patients. Even though tobacco and alcohol abuse is said to be the main etiological factor, it was reported only for a small percentage of patients in some series.
The lack of significant habits in young patients have prompted many to postulate other factors like immune deficiency, genetic factors, and dietary factors in the etiology of cancer. Viruses like herpes simplex virus and human papilloma virus have also been reported as contributing factors.4 Patients in the younger age group were claimed to have a more aggressive disease with a higher incidence of local recurrence or regional lymph node involvement after treatment and a higher mortality rate compared with older patients5 In this paper a young adult male with a chronic non-healing ulcer which turned out to be a SCC is discussed. He had the habit of pan chewing and smoking and sharp teeth in relation to the affected site of the tongue. Case scenario A 29 year male patient reported to the department of oral medicine and radiology with the chief complaint of an ulcer in his tongue for past 6 months.
History revealed he was chronic smoker and pan chewer for past 10 years. Patient was well nourished with BMI 29.5 Kg/m2 .So patient was referred to tobacco cessation center for counselling regarding his habits . During our routine investigation he had a high blood pressure (160/100 mm Hg) and blood sugar level – FBS 111mg/dl, PBS- 181mg/dl. Patient then started taking medication tab, metformin 500mg 1-0-1 for diabetes and tab. Envas 2.5mg 1-0-1 for hypertension.
On extra-oral examination, no facial asymmetry was observed and level 2 lymph nodes palpable on left side. On intra-oral examination, an ulcero-proliferative growth was seen in left side of anterior two-third involving lateral border of tongue extending into ventral surface , which measures about 4.5 × 2cm, mixed white and red in colour, surface was granular, and margins were everted. On palpation, the growth bleeds on touch and soft in consistency, base is not indurated.
The presence of sharp cuspal edges in lingual cusp of 35,36 and buccal cusp of 24,25 was also noted in the region of the ulcer causing obvious trauma in the area. Provisional diagnosis of malignant ulcer with clinical staging of the tumour T3N1M0 was given and chair side investigation was carried away by applying toluidine blue stain which stained malignant cells and also helped in selecting biopsy site , laterincisional biopsy was performed under Local anaesthesia.
Histopathology revealed islands of malignant squamous epithelial cells with keratin differentiation in connective tissue stroma and result was well differentiated squamous cell carcinoma. CT scan revealed evidence of subtle soft tissue thickening of size 20.6 cm and minimal contrast enhancement on left lateral border of tongue and evidence of no lymph node enlargement Patient was then referred to department of surgical oncology, Royapettah govt. hospital for treatment, which consisted of modified unilateral radical neck dissection and wide local excision. After surgery, radiotherapy of 2Gy for 5 days/week for 5 weeks period. After RT patient has lost weight and his BMI is 20 kg/m2 . Despite radical neck dissection followed by radiotherapy , patient was comfortable for one month and again there was relapse, for which chemotherapy was advised. Patient had tab. Cisplastin 100mg once in 3week for 3 cycles of chemotherapy. Patient became thin and very ill, unable to walk. From the reports of the relatives of the patient we came to know that the patient died after 5months.
DISCUSSION SCC in young adults arerare. Tongue cancer has a male predominance and occurs in 6-8th decade of life after long term exposure to cigarette smoke and alcohol abuse. Tobacco use and alcohol consumption are not only risk factors for oral cancinoma but there also strong effects on patient morbidity, recurrence and second primary tumour and mortality6 . Chronic mechanical trauma due to sharp teeth, under fillings, badly fitting dentures in the etiology of oral squamous cell carcinoma has been reported in literature In the present case, patient was chronic smoker and pan chewer which has a significant adverse effect on survival7 Though environmental exposure to tobacco and other carcinogens are important factors for cancer, it is now well documented that other factors such as diet have play an important role in the carcinogenesis process. Several dietary factors act as risk modifiers. In general, dietary deficiencies have not been shown to initiate events, but epidemiological and experimental studies provided strong evidence for dietary substance, in promotion, progression and inhibition of cancer8 .In the present report also due to dietary deficiencies patient become immaciated which might be a factors for his death.
Dental health care workers are a largely untapped resource for providing advice, educate and brief counseling to tobacco-using patients, and there are good reasons to believe that they can be effective in this role. Here in this case report , our patient underwent tobacco cessation counselling9 . Friedlander et al , in a study of younger and older (6oyrs) patients with tongue cancer matched for alcohol and tobacco usage and other factors, found no difference in survival, although younger group of patients had a higher incidence of local regional recurrence1 . Kuriakose et al found that in young patients the cancer was more aggressive with an invasive pattern and prognosis was poor in early stage of disease compared to older patients10. In diabetic patients, alterations occur in the oxidative equilibrium of free radicals.
Increased consumption of saturated fats increases the risk of diabetes mellitus, but recently it has been suggested that it also increases the risk of oral cancer11 Treatment of squamous cell carcinoma of tongue remains mainly surgery, with adjuvant radiotherapy added for advanced stage disease or in patients at risk of local regional failure. The achievement of clear resection margin is important because survival is closely related to resection regardless of any subsequent therapy the patients may receive12. In the present case, tumour removed with 1cm clearance followed by adjuvant radiotherapy.
Metastatic spread of squamous cell carcinoma of tongue is facilitated by the tongue’s rich lymphatic network, which tends to increase with the size of the primary tumour. Approximately 50% of tongue cancers present with lymph node involvement. Lymph node metastasis is a well known negative prognostic factor for squamous cell carcinoma of tongue, and it decreases the survival rate by 50%12. Studies have shown that survival rates in men are lower than women with tongue cancer13.It is well documented that the incidence of local recurrence is higher with positive histological resection margin compared with negative histological resection margin in head and neck cancer14.The reported incidence of local recurrence rates in the margin ranged from 29% - 70% and were 4%-38% for negative resection margins15.
CONCLUSION Oral cancer occurring in young adult is uncommon but nevertheless should always considered such patients present with sharp tooth will produce ulceration particularly in the high-risk sites of the tongue. Several studies suggested that oral cancer in younger patients is inherently more aggressive with a worse prognosis than the disease in older individual. By prompt diagnosis and treatment stratergies the life span of these patients may be prolonged further.
Englishhttp://ijcrr.com/abstract.php?article_id=277http://ijcrr.com/article_html.php?did=2771. Friedlander PL, Schantz SP, Shaha AR, Yu G, Shah JP : Squamous cell carcinoma of the tongue in young patients: A matchedpair analysis. Head Neck 1998;20:363-368.
2. Myers JN, Elkins T, Roberts D, Byers RM. Squamous cell carcinoma of the tongue in young adults: Increasing incidence and factors that predict treatment outcomes :Head Neck Surg 2000; 122: 44-51.
3. Aleksandra Crede, Michael Locher and Marius Bredell : Tongue cancer in young patients: case report of a 26-year-old patient. Head and Neck Oncology 2012, 4:20.
4. Elizabeth Mathew Iype, Manoj Pandey, AleyammaMathewy, Gigi Thomasz, Paul Sebastian and Madhavan Krishnan Nair : Squamous Cell Carcinoma of the Tongue Among Young Indian Adults: Neoplasia . Vol. 3, No. 4, 2001, pp. 273–277
5. Sarkaria J N, Harari P M. Oral tongue cancer in young adults less than 40 years of age: rationale for aggressive therapy. Head And Neck 1994; 16: 107-111.
6. G. Bachar, R. Hod, D.P. Goldstein, J.C. Irish, P.J. Gullane, D. Brown, R.W.Gilbert, T.Hadar, R. Feinmesser, T. Shpitzer: outcome of oral tongue squamous cell carcinoma in patients with and without known risk factors. Oral oncology 47(2011) 45-50.
7. Orbak R, Bayraktar C, Kavrut F, Gundogdu C. Poor oral hygiene and dental trauma as the precipitating factors of squamous cell carcinoma. Oral Oncol 2005;41:109–13.
8. MPR. Prasad, TP Krishna, S Pasricha, MA Quereshi, K Krishnaswamy:Diet and oral cancer - a case control study:Asia pacific j clinnutr(1995) 4: 259-264.
9. PavanUdayPatil , S Vivek , Thatimatla Chandrasekhar, NaliniParimi , B H Praveen , Sunil Lingaraj: Patient Receptivity to Tobacco Cessation Counseling and Services in a Dental Teaching Institute: A Patient Review: Journal of International Oral Health 2015; 7(1):1-4).
10. Kuriakose M, Sankara Narayanan M, Nair MK et al.: comparison of oral squamous cell carcinoma in younger and older patients in India. Eur J cancer B Oral Oncol 1992: 288: 113-20.:
11. AjitAuluck : Diabetes Mellitus: An Emerging Risk Factor for Oral Cancer?: JCDA: July/August 2007, Vol. 73, No. 6.
12. Mildasuslu MD, Ali sefikHosal MD, TugbaAslan MD, BulentSozeri MD, and Anil Dolgunphd : carcinoma of the oral tongue : a case series analysis of prognostic factors and surgical outcomes: J Oral maxillofacsurg 71: 1283-1290, 2013.
13. BerrinoF ,Gatta G: variation in survival of patients with head and neck cancer in Europe by the site of origin of tumours. Eurocare Working Group. Eur J cancer 34:2154, 1998.
14. Po Wing Yuen, FRCS, FACS, King Yin Lam, FRCPA, Alexander Chak Lam Chan, FRCPA, William Ignace Wei, FRCS, FACS, Lai Kun Lam, FRCS, Hong Kong: Clinicopathological Analysis of Local Spread of Carcinoma of the Tongue: Am J Surg. 1998;175:242–244. © 1998.
15. Zieske LA, Johnson JT, Myers EN, Theale PB. Squamous cell carcinoma with positive margins. Arch Otolaryngol Head Neck Surg. 1986;112:863–866.