Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcareCONCENTRATED GROWTH FACTOR MEMBRANE - A NOVEL BARRIER FOR ACCELERATED REPAIR OF GINGIVAL DEFECT ALONG WITH SLIDING FLAP TECHNIQUE
English0105Ramakrishnan T.English Shobana P.English VidyaSekharEnglish Nirmala J.I.English EbenezerEnglish Sivaranjani K.EnglishAim: Periodontal regenerative procedures like root coverage procedures are still a valid treatment option for exposed root surfaces caused by gingival recession. So far, many alloplastic as well as autologous materials were used for regeneration; of which platelet was found to be having greater regenerative potentiality and several platelet aggregates were developed recently in the field of regeneration. The concentrated growth factor (CGF) is the new generation platelet aggregate; this CGF may be a valuable aid in the field of regeneration to speed up the process of healing.
Case Report: This case report elaborates the use of CGF as a barrier membrane, along with laterally displaced procedure to accelerate soft tissue healing, in lower anterior tooth (31) with class II gingival recession in a 20 years old female patient.
Discussion: Many studies about concentrated growth factor showed a great regenerative properties and versatility. Its use has been proposed in various procedures like filling the extraction socket, sinus lift procedures, moreover it can also be combined with bone grafts to accelerate bone formation.
Conclusion: The result of this case report suggested that the CGF barrier membrane has the potential to accelerate the soft tissue healing which when combined with the root coverage procedures like sliding flap technique, thus results in achieving the expected gain in the width of the attached gingival in class II Gingival recession defects.
EnglishConcentrated Growth Factor, Gingival recession, Laterally Displaced flapINTRODUCTION:
Location of the gingival margin apical to cemento-enamel junction is called Gingival recession.1 The most common cause of such mucogingival deformity is abrasive and traumatic tooth brushing habit. The recession may also be associated with high frenal attachment, minimal width or absence of attached gingiva, persistent inflammation, or root hypersensitivity which might require some form of mucogingival surgery.2 Periodontal inflammation and the resultant loss of attachment results in reduced attached gingiva, the problem is more common on the facial surfaces, but it may also occur on the lingual surface. There are various periodontal plastic surgical techniques available till date to treat these defects in order to increase the width of the attached gingiva and to improve the aesthetics. Generally treating these defects and associated mucogingival problems, by means of surgery may be best accomplished by the reestablishment of a functional zone of attached gingiva.2 Healing studies have confirmed that plastic repair of denuded root surfaces is possible when the laterally positioned flap is used, where the “bridging” phenomenon is effected by new connective tissue and epithelial attachment to the previously exposed cementum.3 The displaced pedicle flap technique was originally described by Grupe and Warren in 1956.4 This can be used to cover isolated, denuded root surfaces that have adequate donor tissue laterally. Prini Prato et al. 1992 described a technique where pedicle soft tissue graft procedures can be combined with a barrier membrane, in order to create space for tissue formation between the facial root surface and the membrane. The main objective of our procedure is to evaluate the accelerated healing efficacy of CGF membrane when combined with laterally displaced flap operation in treating a single tooth with denuded gingiva in the facial aspect. Growth factors are proteins which regulate in the complex processes of wound healing. Growth factors play a main role on cell migration, cell proliferation and angiogenesis in tissue regeneration therapy. Concentrated growth factor (CGF) was first developed by Sacco (2006). According to Professor Rodella at University of Brescia, Department of Biomedical Sciences and Biotechnologies, CGF shows higher tensile strength, more growth factors, higher viscosity and higher adhesive strength than early generation platelet concentrates like PRF (platelet rich fibrin).5
CASE REPORT:
A patient named Ms. Ranjitha 20 years old female came to our college with a chief complaint of irregularly placed front teeth and wants to align it. Patient was referred to the Department of Periodontics for oral prophylaxis. On intra oral examination 31 was found with Miller’s class II gingival recession. Coronoplasty and intentional RCT was done, Root coverage procedure in 31 was planned. The treatment plan for gingival recession was Lateral Sliding flap operation combined with CGF as the barrier membrane a novel approach.
PREPARATION OF CGF:
An autologous CGF material can be prepared by obtaining the patient’s venous blood samples without any anticoagulant and immediately centrifuged in a special centrifuge device (“MEDIFUGE”), at variable rpm from 2400-2700 for 12 minutes to separate the cells in the blood which results in fibrin rich blocks that are much larger, denser and richer in Growth Factor. CGF can be used as barrier membrane to accelerate soft tissue healing or can be mixed with bone graft to accelerate new bone formation.5
OPERATIVE PROCEDURE:
Patient’s venous blood of 9 ml was collected without anticoagulant [fig.1] and kept for centrifugation; [fig.2]. Later patient was immediately taken for surgery. 12 minutes after centrifugation CGF was obtained [fig.4] and it was separated from the RBC layer and kept in between the compressing disc [fig.3, 5] to get as a membrane [fig.6]. Meanwhile Patient’s recipient site preparation was done [fig.7]. The de-epithelialisation was done around the root surface. With #15 blade a vertical incision was given from the distal gingival margin of 32 including the interdental papilla extending beyond mucogingival junction and a full thickness flap was raised. The flap has to be sufficiently wider than the recipient site. A releasing incision may be needed to avoid tension on the base of the flap. Now the flap is ready to slide laterally onto the adjacent root [fig.8]. The prepared CGF membrane was placed first on the denuded root surface as a barrier membrane; [fig.9] above which the lateral pedicle flap was positioned [fig.10] and suturing done covering the CGF membrane. Aluminium foil and periodontal dressing was placed finally.
RESULT:
Three days after patient was recalled, [fig.11] no sign of infection was seen. One week post operatively suture removal was done [fig.12]. There was significant increase in the width of the attached gingiva. Evidence of Healing was good and root coverage was satisfactory at one month post operative period [fig.13].
DISCUSSION:
The advantage of sliding flap technique is that the flap has enough blood supply which paves way for better healing. With respect to the use of CGF membrane the dual coverage was provided to the exposed root surface. Concentrated growth factor was first developed by Sacco (2006).6 Platelet’s regenerative potentiality was introduced in the year 1974. Rose et al were first to describe that platelet has growth factors.7 Periodontal surgical procedures using biomaterial like platelet concentrates is a new way to accelerate and enhance the natural wound healing mechanism.8 There are some clinical and anatomic factors limiting the treatment outcome for gingival recession, so even when there is no loss of interproximal attachment and bone complete root coverage is not always achievable.9 In this case CGF membrane was exposed in certain areas which might be the reason for not achieving 100% root coverage.But healing was accelerated without any complication in unexposed areas and increase in the width of attached gingival was also achieved.
CONCLUSION
Within the limits of this present case report, the utilisation of CGF barrier membrane can be best accomplished along with lateral sliding flap technique in managing the gingival defects. This novel barrier membrane accelerates the soft tissue healing and better results can be achieved if used properly. Further studies with sufficient sample size are necessary to support this result.
ACKNOWLEDGEMENT
The 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=168http://ijcrr.com/article_html.php?did=168
American Academy of Periodontology. Glossary of Periodontal Terms. Chicago: American Academy of Periodontology; 2001;(4):47.
Guinard A E, Caffesse G R. Treatment of localized gingival recessions. J Periodontol1978; 49(9):457-61.
Smuckler H. Laterally positioned Mucoperiosteal pedicle grafts in the treatment of denuded roots. J Periodontol 1976; 47(10):590-5.
Carranza F, Newman M, Takei H, Klokevold P. Periodontal plastic and esthetic surgery. Clinical periodontology.2015; 11:919-23.
Sohn DS. The effect of concentrated growth factors on ridge augmentation. Implant Journal. 2009; 34-40.
Sacco L. Lecture. International academy of Implant prosthesis and osteoconnection. 2006.12.4
Naik B, Karunakar P, Jayadev M, Marshal RV. Role of platelet rich fibrin in wound healing: A critical review. Journal of Conservative Dentistry 2013; 16(4): 284-93.
Khiste SV, Naik R. Platelet- Rich fibrin as a Biofuel for Tissue regeneration. ISRN Biomaterials. 2013:1-6.
Zuchelli G, Testori T, Sanctis De M. Clinical and anatomical factors limiting treatment outcomes of gingival recession: A new method to predetermine the line of root coverage. J Periodontol2006;77(4): 714-21.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcareHOSPITAL BASED STUDY OF THYROID DISORDERS IN RURAL POPULATION OF GURGAON, HARYANA
English0611Poonam AroraEnglish Smita PrasadEnglish Busi KarunanandEnglishIntroduction: Endocrine disorders pose a major threat to public health. Current research shows that 300 million people are suffering from thyroid disorders globally and 42 million among them reside in India.
Objective: Our objective is to find the prevalence of thyroid disorders in rural population of Gurgaon, Haryana.
Materials and Methods: This study was conducted in SGT Medical College and Hospital, Budhera, Gurgaon, Haryana from January, 2015 to July, 2016. 3940 patients were screened for thyroid function. Thyroid function was assessed by quantitative estimation of T3 (Triiodothyronine), T4 (Thyroxine) and TSH (Thyroid Stimulating Hormone) in serum by chemiluminscent immuno assay.
Results: The prevalence of thyroid disorder was found to be 25.17% (992) in the study population. 74.82% (2948) patients were euthyroid. Among the thyroid dysfunction patients 16.85% (665) belonged to hypothyroidism group (11.70% primary, 3.20% sub clinical and 3.24% clinically euthyroid) and 8.29% (327) to hyperthyroidism group (2.66% primary, 0.15% T3 thyrotoxicosis, 0.58% sub clinical and 4.89% central)
Conclusion: The study findings call for a review of current practices in the management of thyroid disorders because of high prevalence of thyroid disorder in the reproductive age group (21-40). Thyroid disorders must be actively screened and monitored and to be effectively treated in diagnosed patients.
EnglishHypothyroidism, hyperthyroidism, thyroid dysfunctionIntroduction:
Endocrine disorders pose a major threat to public health. Thyroid dysfunction due to abnormal production of thyroid gland hormones (T3-Triiodothyronine and T4-Thyroxine) forms a major proportion of endocrine disorders after diabetes1. Thyroid hormones are metabolic hormones and are regulated by Thyroid Stimulating Hormone (TSH) secreted by pituitary gland.
Current research shows that 300 million people are suffering from thyroid disorders globally and 42 million among them reside in India2. Genetic and various environmental factors including geographical location, nutrition and diet especially iodine intake affect the prevalence of thyroid disorders. The utility of symptoms for screening of patients with thyroid disorders has become limited considering the recent trend of asymptomatic patients. Thyroid disorders are usually associated with additional morbidities: hypercholesterolemia, hypertension, infertility, adverse pregnancy outcomes and neuropsychiatry diseases, causing its under diagnosis. Even though there is no permanent cure, the patient can lead a normal life after diagnosis and treatment3.
Despite the optimal iodine nutrition status of India classified by WHO in 2004, many parts of India are still iodine deficient4,5.
Paucity of data and the fact that Budhera and its surrounding region has iodine deficient status even in post iodization phase of India warrants for thyroid status surveillance of this region.
Materials and methods:
This study was conducted in the SGT Medical College, Budhera, Gurgaon, Haryana from January, 2015 to July, 2016. The study proposal was reviewed and approved by hospital ethical committee. A Total of 3940 outpatient department patients suspected of thyroid disorders were screened for thyroid function after obtaining consent from all the patients.
4 ml of fasting blood sample was collected and centrifuged for serum separation. Thyroid function was assessed by quantitative estimation of T3, T4 and TSH levels in serum performed using SEIMENS-Centaur CP analyzer based on chemiluminescent immuno assay (CLIA).
The subjects were categorized as euthyroid (normal TSH), hypothyroid (high TSH) and hyperthyroid (low TSH) based on serum thyroid hormone levels.
Normal thyroid hormone levels:
Triiodothyronine (T3) (ng/ml) : 0.45-2.0
Thyroxine(T4) (µg/ml) : 4.4-11.6
Thyroid Stimulating Hormone (TSH) (µIU/ml): 0.39-5.0
Further classification of hypothyroid and hyperthyroid patients was done using following definitions6:
S.No.
Type of thyroid disorder
Definition
A.
Hypothyroidism
High TSH (>5.0)
I.
Primary
Low T3 and/or low T4 with high TSH
II.
Sub-clinical
Normal T3, T4 with high TSH
III.
Clinically euthyroid
Normal/high T3, high T4 with high TSH
B.
Hyperthyroidism
Low TSH (Englishhttp://ijcrr.com/abstract.php?article_id=169http://ijcrr.com/article_html.php?did=169
Bose A, Sharma N, Hemvani N, Chitais DS. 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.
Nimmy NJ, Aneesh PM, Narmadha MP, Udupi RH, Binu KM. A Survey on Prevalence of Thyroid Disorders Induced by Demography and Food Habits in South Indian population. Ind J Pharm Prac 2012;5:49-52.
Abraham R, Murugan VS, Pukazhvanthen P, Sen SK. Ind J Clin Biochem 2009;24(1):52-59.
Iodine status worldwide, WHO global database on iodine deficiency, Department of nutrition for health and development. Department of nutrition for health and development. Geneva:WHO 2004.
Andersson M, Pakkouche B, Egli I, Allen HE, Benoist B. Current global iodine status and progress over the last decade towards the elimination of iodine deficiency. Bull World Health Organisation 2005;83:518-525.
Burtis CA and Bruns DE. Tietz fundamentals of Clinical Chemistry and Molecular Diagnostics. 7th ed. Saunders;2015.p.819.
Laurberg P, Pederson KM, Hreidarsson A, Sigfussen N, Iversen F et al. Iodine intake and the pattern of thyroid disorders: a comparative epidemiological study of thyroid abnormalities in the elderly in Icelend and in Jutland. Denmark J Clin Endocrinol Metab 1998;83:765-769.
Sheila C. Current Status of Iodine Deficiency Diseases and Strategy for its control in India. Indian J of Pediatr 2002;69: 589-96.
Chandra AK, Tripathy S, Lahari D, Mukhopadhyay S. Iodine nutritional status of school children in a rural area of Howrah district in the Gangetic West Bengal. Indian L Physiol Pharmacol 2004;48:219-24.
Chandra AK, Mukhopadhyay S, Lahari D, Tripathy S. Goitrogenic content of Indian cyanogenoc plant foods and their in vitro anti thyroidal activity. Indian J Med Res. 2004;119:180-5.
Dhok AJ, Adole PS, Puppalwar PV, Agrawal U. Status of Thyroid disorders at Acharya Vinobha Bhave Rural Hospital, Sawangi(Meghe), Wardha, India. Thyroid Research and Practice 2105;12(2):62-66.
Skaria LK, Sarkar PD, Agnihotram G, Thakur AS, Pamidamarri G. Thyroid Dysfunction in Tribal Women of the Bastar Region of Chattisgarh, India. Thyroid Science 2011;6(6):5.
Bhutia SC, Bhutia KL, Singh TA. Thyroid Dysfunction in Central Referral Hospital, Sikkim. Asian J Biomed Pharmaceu Sci 2016;6(56):17-19.
Kalra S, Unnikrishnan AG, Sahay R. Thyroidology and public health: The challenges ahead. Indian J Endocrinol Metab. 2011;15:S73-5.
Siddhanti SR, King MW, Tove SB. Influence of dietary fat on factors in serum that regulate thyroid cell metabolism. J Nutr. 1990;120(11):1297-304.
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 Clin Endocrinol Metab 2002;87:489-99.
Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado Thyroid Disease Prevalence Study. Arch of Intern Med 2000;160:526-34.
Mahto RV, Jha B, Singh KP, Yadav BK, Shah SK, Lamsal M. Status of Thyroid disorders in Central Nepal: A Tertiary care Hospital based study. Int J App Sci Biotechnol. 2015;3(1):199-222.
Freidman MN. Screening for thyroid disease. Ann Med. 1999;130:161-162
Rama J, Shivashankara AR, Vidya SP, Sameena. A hospital based study of prevalence study of thyroid dysfunction in Srinagar. Int J Med Sci Public Health 2015;4(2):151-154.
Mayo Foundation for Medical Education and Research (MFMER)
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcareOBJECTIVE ASSESSMENT OF PHYSIOLOGIC AGEING CHANGES BY PATTERN REVERSAL VISUAL EVOKED POTENTIALS
English1218Sangeeta GuptaEnglish Gaurav GuptaEnglishBackground: Impairment of visual information processing is one of the profound physiologic effects of ageing. Visual evoked potentials can record electrophysiological alterations in the visual pathways that can occur due to ageing and the nature of the impact in the older adults can be evaluated. Rapidly increasing size of the older population further emphasizes the acquisition of the data for this proportion of population optimizing the clinical evaluation in this group.
Methods: Pattern-reversal visual evoked potentials (PRVEP) were recorded in 120 healthy subjects in the age-group of 20-80 years (60 males and 60 females). Mean P100 latencies and N75-P100 amplitudes were compared in different age-groups by one way ANOVA. Correlations of latencies and amplitudes with age were performed using Pearson correlation coefficient. Gender differences were studied by unpaired t test. P valueEnglishVisual evoked potentials, Ageing, P100 latency, N 75-P100 amplitudeIntroduction
Physiologic ageing, a universal and natural phenomenon of gradual deterioration of physiologic functions with age has been of particular interest to the researchers studying the mechanism of ageing and age-related diseases.The effects of ageing are widespread in the body with brain as no exception. Slowing in visual processing speed is a common characteristic of ageing and has been a well-established phenomenon.1Visual abilities decline during normal (non-pathological) ageing. Many physiologic changes in the vision during ageing often represent same continuum as those due to disease. More objective criteria in defining normal ageing should be used by the investigators. Changes in the optical factors such as senile miosis and opacification of the ocular media cannot entirely account for the age-related declines in the visual abilities and there might be involvement of retina or central visual pathways in the older subjects.
Visual evoked potentials (VEPs) can be a productive research methodology for studying such age-related visual declines owing to its objective and sensitive nature.Theyprovide a measure of normal functioning of the visual system and also for assessing the changes during different stages of life.2 Each sensory system has its own time of maturation and senescence.Visual evoked potentials can serve as a window into the central nature of neural processing and the pattern of age-related signal transmission delays in the visual system can be measured. Visual evoked potentials represent electrophysiologic responses to visual stimulation. Patterned visual stimuli are the preferred stimuli in various clinical settings. PVEP (pattern visual evoked potential) testing detects minor visual pathway abnormality with much greater sensitivity and accuracy than unpatterned stimuli.3 Of the various VEP components described in normal subjects- the N75, P100, and N145, P100 is the most consistent and least variable peak and the most clinically useful measurements on the responses to monocular full-field stimulation are (1) the P100 latency and (2) amplitude (N75-P100) of the P100 component. Additional latency, duration, and amplitude are highly variable measures and generally add little to clinical interpretation. 3
Determining the standards of normality for the visual evoked potentials is necessary, owing to the profound ageing effects on the visual evoked potential values during clinical interpretation of the tests.Assessment of various neurological diseases by the test becomes more reliable if the ageing effects have been taken into account. The clinical utility is required to be considered in the light of these physiologic effects.Moreover, it has been suggested that visual evoked potential (VEP) results are difficult to transfer even if stimulating and recording conditions are similar, due to the poorly understood effects of variation in stimulus conditions, as compared to the somatosensory and auditory evoked potential values.4Furthermore, the recent trends in the increase in the older population emphasizes the importance of acquisition of the data for this proportion of population for better clinical evaluations of this group of subjects. The maturation and senescence of different sensory system reflects different patterns. Glimore R (1995) who studied the process of senescence in sensory system found that the latencies of visual evoked potentials prolong by 2-4 ms/decade after age 40 years. 5In a study by Allison T et al (1983),VEP P100 latency did not change between 20 and 59 years.4 Also, there are strong evidences for the fact that the gender differences in young adults characteristically reveal increased P100 latency in males while increased N75-P100 amplitude in females. 6, 7 The characteristic variations have also to be investigated and ascertained in the older groups. The present study hence, is an attempt to contribute to the researches and share our investigations and findings by performing an objective evaluation of the visual functions in the subjects with the older age-group by way of pattern reversal visual evoked potentials (PRVEPs).
Materials and methods
The study was conducted on 120 healthy adults in the age group of 20-80 years(60 males and 60 females) with normal or corrected visual acuity. It was a cross-sectional analytical study. PRVEP was recorded in Electrophysiology laboratory in the department of Physiology, Maharishi Markandeshwar Institute of Medical Sciences and Research, Mullana, Ambala. Approval from the institutional ethical committee was acquired to carry out the research work. A written informed consent was obtained. Subjects underwent complete neuro-ophthalmological examination after taking a detailed clinical history.
Inclusion criteria for the study were adult healthy subjects in the age group of 20-80 years with normal or corrected visual acuity, normal fundus and visual field examinations while exclusion criteria were subjects with metabolic, endocrine or demyelinating pathologies; glaucoma, optic neuropathies, inherited or acquired neurological disorders, compressive lesions of anterior visual pathways, HIV infections and history of cerebro-vascular accidents.
VEP testing was optimized byinstructing the subjects to come without the application of hair-oil or any hair chemical to the scalp and asked to wear their usual glasses or corrective lens. To prevent the effects of drowsiness on the VEP responses, they wereadvised to have an adequate sleep, the previous night. Before starting the procedure, they were explained about the test to ensure optimum cooperation. It was also ensured that no mydriatic or miotic drug 12 hours before the test was given to them. Application of electrodes was done after proper cleaning of the scalp skin.
VEP (visual evoked potential) was performed onAllengers Scorpio EMG, EP, NCS system in a specially equipped electro-diagnostic procedure room with dark and sound attenuated environment for the test. Subjects were seated comfortably about 95 cm away from a video-monitor with a 30 cm screen. The video-monitor presented a black and white checker-board pattern with a fixation spot in the center of the screen (mean luminance 50 candela/m2 and contrast 70%). The checks reversed alternately at the rate of 2 cycles/sec. The visual angles subtended by the checksand the screen were 54.6 min and 19 degrees respectively. The signals were amplified (gain 20,000) and filtered with a system band pass filter of 2-100 Hz. Number of epochs were 100. Standard disc surface electrodes were placed and the electrode placement was according to the International 10/20 system with active electrode placed at Oz, reference electrode at Fz and ground electrode at Fpz.3 Volunteers were instructed to focus on a small red square at the center of the screen of video-monitor. Monocular stimulation was performed. To validate the reproducibility of the waveform, two responses were recorded and superimposed. P100 latencydifference within 2.5 ms and N75-P100 amplitudewithin 15% difference in replicated responses was accepted.3Parameters for the study were P100 latency and N75-P100 amplitude. The data was expressed as mean ± S.D.
The subjects were classified into six different age-groups: Group I (20-30 years), Group II (31-40 years), Group III (41-50 years), Group IV (51-60 years), Group V (61-70 years) and Group VI (71-80 years). The effect of age in different age groups onPRVEP P100 latency and N75-P100 amplitude inboth the eyes (total 120 subjects/240 eyes) was compared and analyzed using one way ANOVA and post hoc tests (Tukey multiple comparison tests). Correlations of age with PRVEP latency and N75-P100 amplitudewas obtained using Pearson correlation coefficient. The effect of gender was obtained by unpaired t test. Statistical analysis was done by using SPSS (Statistical package for social science) version 20.0 statistical software. The analysis was done at 5 % level of significance.
Results
Mean age of the study group (with 60 males and 60 females) was 50.14±17.23 years. Demographic and anthropometric data for males and females revealed no statistically significant differences in mean ages for males (50.5± 17.1 years)and females (49.83 ± 17.5 years), while height (males: 170.4±6 cms, females: 158.5±7.01 cms), weight (males: 65.1±11.2 kgs, females: 55.8±8 kgs) and head sizes (measured from nasion to inion) (males: 34.29±0.8 and females: 32.63 ±1.1 cms) were statistically significantly different (PEnglishhttp://ijcrr.com/abstract.php?article_id=170http://ijcrr.com/article_html.php?did=1701. Walsh DA. Age differences in central perceptual processing: A dichoptic backward masking investigation. Journal of Gerontology 1976; 31: 178-85.
2. Onofrj M, Thomas A, Iacono D, D'Andreamatteo G, Paci C. Age-related changes of evoked potentials. ClinNeurophysiol2001; 31:83-103.
3. American Clinical Neurophysiology society Guideline 9 B: Guidelines on Visual evoked potentials. J ClinNeurophysiol. 2006; 23(2):138-56.
4. Allison T, Wood CC, Goff WR. Brain stem auditory, pattern-reversal visual, and short-latency somatosensory evoked potentials: latencies in relation to age, sex, and brain and body size. ElectroencephalogrClinNeurophysiol. 1983 Jun;55(6):619-36.
5. Gilmore R. Evoked potentials in the elderly. J ClinNeurophysiol. 1995 Mar;12(2):132-8.
6. Gregori B, Pro S, Bombelli F, La Riccia M, Accornero N Vep latency: sex and head size. ClinNeurophysiol 2006; 117:1154-1157.
7. Kaneda Y, Nakayama H, Kagawa K, Furuta N, Ikuta T: Sex differences in visual evoked potential and electroencephalogram of healthy adults. Tokushima J Exp Med 1996; 43:143-157.
8. Stockard JJ, Hughes JR, SharVough FW. Visually evoked potentials to electronic pattern reversal: latency variations with gender, age and technical factors. Am J EEG Technol, 1979; 19(4):171-204.
9. Mitchell K W, Howe J W and Spencer S R. Visual evoked potentials in the older population: age and gender effects. Clin. Phys. Physiol. Meas., 1987; 8(4): 317-24.
10. Tobimatsu S, Kurita-Tashima S, Nakayama-Hiromatsu M, Akazawa K, Kato M. Age- related changes in pattern visual evoked potentials: differential effects of luminance, contrast and check size. ElectroencephalogrClinNeurophysiol. 1993 Jan-Feb; 88(1):12-19.
11. Allison T, Hume AL, Wood CC, Goff WR. Developmental and aging changes in somatosensory, auditory and visual evoked potentials.ElectroencephalogrClin Neurophysiol. 1984 Jul;58(1):14-24.
12. Kuba M, Kremlá?ek J, Langrová J, Kubová Z, Szanyi J, Vít F. Aging effect in pattern, motion and cognitive visual evoked potentials. Vision Res. 2012 Jun 1;62:9-16.
13.Wright CE, Williams DE, Drasdo N, Harding GF. The influence of age on the electroretinogram and visual evoked potential. Doc Ophthalmol. 1985 Jun 30; 59(4):365-84.
14. Emmerson-Hanover R, Shearer DE, Creel DJ, Dustman RE. Pattern reversal evoked potentials: Gender differences and age-related changes in amplitude and latency. ElectroencephalogrClinNeurophysiol 1994; 92:93-101.
15. WealeRA . Retinal illumination and age. Transactions of the Illuminating Engineering Society 1961; 26: 95-100.
16. Marshall J, Grindell J, Ansell PL and Borwein B. Convolution in human rods: An aging process. British Journal of Ophthalmology 1980; 63: 181-87.
17. Kuwabara T. Age related changes in the eye. In: Han SS and Coons DH, eds. Special senses in aging. Ann Arbor, Institute of Gerontology: University of Michigan, 1979: 47-78.
18. Devaney KO and Johnson HA 1980 Neuron loss in the aging visual cortex of man Journal of Gerontology 1980; 35: 836-841.
19. Fenwick PB, Brown D, Hennesey J. The visual evoked response to pattern reversal in 'normal' 6-11-year-old children. ElectroencephalogrClinNeurophysiol. 1981Jan; 51(1):49-62.
20. Guthkelch AN, Bursick D, Sclabassi RJ: The relationship of the latency of the visual P100 wave to gender and head size. ElectroencephalogrClinNeurophysiol 1987; 68: 219-222.
21. Gupta S, Gupta G, Deshpande VK. Visual evoked potentials: Impact of age, gender, head size and BMI. International Journal of Biomedical and Advance Research 2016;7(1): 22- 26.
22.Celesia GG, Kauufman D, Cone S. Simultaneous recording of pattern electroretinography and visual evoked potentials. ElectroencephalogrClinNeurophysiol,1987; 68 (3):161-71.
23. Fein G, Brown FF. Gender differences in pattern reversal evoked potentials in normal elderly. Psychophysiology. 1987 Nov; 24(6):683-90.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcareCLINICAL STUDY OF CONTEMPORARY PATTERN AND OUTCOME OF HYPERTENSION IN PREGNANCY AMONG PRIMIPAROUS AND MULTIPAROUS WOMEN IN A TERTIARY CARE CENTRE
English1924Renukadevi B.English Kavitha G.English Rathna RamamurthyEnglish Raja rajeshwariEnglishIntroduction: Hypertension complicates 10% of all pregnancies. Various adverse outcomes of hypertension in pregnancy include antepartum hemorrhage, postpartum hemorrhage, acute renal and hepatic failure, maternal death, preterm birth, intrauterine growth retardation, and neonatal death. Despite various screening tools, there is high prevalence of hypertension in pregnancy and its related complications. Periodical analysis such cases are of utmost importance as it may help in early identification of the problem and measures to prevent its complications.
Objectives: The objectives of this study is to identify the difference in pattern of hypertension in primiparous and multiparous women and its maternal and fetal outcomes and differences in lab parametersin both groups.
Methodology: This was a retrospective study conducted among 88 women with hypertension and /or proteinuria complicating pregnancy who were admitted for delivery in the department of obstetrics and gynaecology, Velammal Medical College over a period of 1 year (Aug 2015 – July 2016). The data were collected from the patients’ records. The patients were divided into two groups, primiparous and multiparous. The data were collected in terms of age, parity, gestational age, mode of delivery, birth weight of baby and complications. The results were statistically analysed with IBM SPSS statistics software 23.0 version.
Results: The frequency of hypertensive disorders of pregnancy was 11.6 % in our study. The prevalance of eclampsia was 0.7%. The mean gestational age of babies was 39 weeks and 36 weeks in mild and severe preeclampsia in primiparous women and 37.5 and 34.2 weeks in multiparous women. The mean platelet count in mild and severe cases were 2.5 and 1.8 lakhs/cu mm in primiparous and 2.4 and 1.9 lakhs/cu mm in multiparous women.
Conclusion: Though the prevalence of hypertension in primiparous women is more, the prevalence of severe preeclampsia in more common in multiparous women. Almost all cases of eclampsia occurred in primiparous women. A different pathophysiology could be a cause of hypertension in pregnancy in primiparous and multiparous women, as implied by significant differences in both groups.
EnglishEclampsia, Gestational hypertension, Hypertension, IUGR, PreeclampsiaINTRODUCTION
Hypertensive disorders in pregnancy is one of the most commonly encountered medical problem which causes significant maternal and fetal morbidity and mortality. The classification of hypertension disorders in pregnancy as recommended by the National high blood pressure education program working group includes 1) Gestational hypertension 2) Preeclampsia –Eclampsia 3) chronic hypertension 4) preeclampsia superimposed on chronic hypertension.Gestational hypertension is defined as blood pressure of >140/90 on two separate occasions atleast 6 hrs apart without proteinuria after 20 weeks of gestation. Mild Preeclampsia is defined as BP of 140/90 mmHg or more on two separate occasions atleast 4 hours apart with urinary protein excretion of > 300mg/ 24 hrs . Because of its wide spectrum of prevalence, edema is no longer included in the diagnostic criteria. Severe preeclampsia is defined as BP ≥ 160/110 mmHg and significant proteinuria of ≥3 + or > 5gm/day with evidence of other organ dysfunction.
MATERIALS AND METHODS
This was a retrospective study done among 88 women with hypertension and /or proteinuria admitted for delivery in the department of obstetrics and gynaecology in velammal medical college. This study was conducted over a period of 12 months from august 2015 – July 2016.
METHODS OF COLLECTION OF DATA
The data of the patients were obtained from patients’case records.Demographic details of the patient ,obstetric history, gestational age, blood pressure recordings, mode of delivery, fetal weight, lab investigations were collected and entered in excel sheet.They were divided into groups of primiparous and multiparous women and data analysed.
INCLUSION CRITERIA
All pregnant women admitted for delivery with hypertension with or without proteinuria in pregnancy were included in the study.
EXCLUSION CRITERIA
All pregnant women with secondary hypertension were excluded from the study.
DATA ANALYSIS
The collected data were analysed with IBM.SPSS statistics software 23.0 Version.To describe about the data descriptive statistics frequency analysis, percentage analysis were used for categorical variables and the mean and S.D were used for continuous variables. To find the significant difference between the bivariate samples in Independent groups the Unpaired sample t-test was used. For the multivariate analysis the one way ANOVA with Tukey's Post-Hoc test was used.To find the significance in categorical data Chi-Square test was used. In all the above statistical tools the probability value .05 is considered as significant level.
RESULTS
The frequency of hypertensive disorders of pregnancy was 11.6 % in our study .There was a total of 757 deliveries during the study period. Eighty eight (88) women were diagnosed as hypertensives during pregnancy and thus the prevlance of hypertension in pregnancy was 11.6%. The prevalace of eclampsia was 0.7%(n=6) .Among 88 patients, mild GHT was 29%, mild Preeclampsia was 32%, severe preeclampsia was 32% and eclampsia was7%.(FIG 1)
The prevalence of mild preeclampsia was 27.6% in primiparous and 29.4% in multiparous women whereas the prevalence of severe preeclampsia was 25.9% and 41.2% in both groups with significant increase in multiparous women. P value (0.410). In our study eclampsia was present in 11.1% of primiparous women whereas none of multiparous women had eclampsia. (FIG 3)
Mean uric acid level in mild and severe preeclampsia in primiparous women was 4.74 mg% and 6.23 mg% respectively and 4.6 mg% and 5.2 mg% in mild and severe preeclampsia in multiparous (p value 0.001) (FIG 9).
The mean platelet count in mild and severe cases were 2.5 and 1.8 lakhs/cu mm in primiparous and 2.4 and 1.9 lakhs/cu mm in multiparous women. P value 0.001. (FIG 10) Among 88 patients, 2 (2.2%) had abruption, 2(2.2%) developed HELLP, 1 (1.1%) pt had PPH and 1(1.1%) patient had massive ascites. The prevalence of eclampsia was 0.7% in our study. Mean age of patients was 24.1±2.5SD yrs. Mean gestational age was 38±1.7SD weeks and Mean birth weight 2.6 ±0.8kg.
DISCUSSION
The frequency of hypertensive disorders of pregnancy was 11.6 % in our study.It is a leading cause of maternal and fetal morbidity and mortality in both developed and developing countries and contributes significantly to economy of health care.3,4The incidence of preeclampsia in India is reported to be 7-10% of the pregnancies.2We also observed preeclampsia in 6.7% of our study population.It is the second largest cause of maternal mortality in India and is responsible for 14% of maternal deaths.Racial differences, socioeconomic status and other parameters like parity and age attribute to the variations in incidence .1 The prevalence of Eclampsia in our study was found to be 0.7 % of pregnancies. The reported incidence of eclampsia from India is 0.71 % which is comparable with our study.
Age and Parity has an important influence on the incidence of hypertensive disorders of pregnancy. A study done in Saudi Arabia showed that women at extremes of maternal age, the nulliparous women, and high-parity women are at an increased risk of developing pre-eclampsia. Young primigravidae under 20 years and all patients over 30 years have an increased chance of hypertension.5 In our study highest incidence of the hypertensive disorders occurred among those aged 19 to 27 years. This could be because the majority of conceptions take place in this age group in our country. The age distribution of eclampsia patients in our study is similar to other reports and suggests that eclampsia is, probably, a disease of young women6.Eclampsia exclusively occurred in primigravida in our study.
The incidence of PIH increases with advancing gestation and early-onset PIH is often associated with severe preeclampsia.7This correlates with our study in which the mean gestational age was 34 weeks in cases of severe preeclampsia and 38 weeks in mild cases.
In our study the incidence of caesarean section was 77.5%. (FIG 7) According to Miguil M et al 8 and Dissanayake VH et al9, caesarean section rates hypertension complicating pregnancy was 71% and 78% respectively.
Complications of fetus parallels the severity of disease in preeclampsia .With increasing severity of hypertension and proteinuria, there is an increased incidence of IUGR and preterm labour.According to Eskenazi et al, increased incidence of SGA fetus occurred in multiparous women with severe preeclampsia.10This correlates with our study which shows that incidence of IUGR in multiparous women was 24.2 % compared to13.2 % in primiparous with severe preeclampsia.Another study by Gleicher et al showed that with different parity in hypertension there was no difference in fetal birth weight.11
According to Al-Mulhim A.A et al, placental abruption was the leading maternal complication (12.6%) in women with preeclampsia, followed by oliguria (7.9%), coagulopathy (6.0%), and renal failure (4.1%).7 In our study, abruption occurred in 3.4%, 2.2% had HELLP syndrome and 1.1% had severe ascites complicating preeclampsia.
Thrombocytopenia is the most common hematological abnormality seen to occur in 11% to 29% of patients with preeclampsia.12,13.They are also associated with qualitative changes suggesting increased platelet production and destruction.
S. Joshi et al (2004) reported platelet count of 2.2 lakh/cumm in control group, 2.0 lakh/cumm in mild preeclampsia, 1.40 lakh/cumm in severe preeclampsia and 1.30 lakh/cumm in eclampsia. In our study the values correlate well with 2.48lakhs/cu mm in mild cases and 1.88lakhs/cu mm in severe cases.
Increase in uric acid is associated with 8–9 fold risk for preeclampsia and a 1.6–1.7-fold risk for SGA infants. An ROC analysis suggests that a uric acid of 5.2 mg/dl provides excellent sensitivity, specificity and likelihood ratios for diagnosis and prognosis. Hence measurement of serum uric acid is clinically useful and should be a part of evaluation of the pregnant patient with preeclampsia. An elevated serum uric acid in pregnancy may is a valuable biomarker for preeclampsia and also has a contributory role in the pathogenesis of the maternal and fetal manifestations as suggested by evidence.14,15It is a potent inhibitor of endothelial function, induces systemic and glomerular hypertension in animals, and passes freely into the fetal circulation and has a direct role in blocking fetal angiogenesis resulting in SGA infants.16This correlates with our study in which patients with severe preeclampsia had a mean uric acid level of 6.2 and 5.2 mg/dl in primiparous and multiparous women.
Currently there are no well established measures for prevention of preeclampsiaand there is no single reliable test for screening.17Moderate reduction in blood pressure has been observed with calcium supplementation in women at high risk for hypertension in pregnancy. In women with abnormal uterine artery doppler in second trimester ultrasound, low dose aspirin has been shown to reduce the incidence of preeclampsia.
Patients with risk factors and rapid increase in weight gain and facial edema are closely monitored for onset of hypertension and proteinuria.For patients with established diagnosis of preeclampsia a series of lab tests should be conducted and repeated frequently if required.Fetal growth is tested with a baseline sonogram at 25-28 weeks.Biweekly non stress test and biophysical profile is indicated in the presence of IUGR and oligoamnios and delivery is contemplated in the presence of fetal compromise. Regional anaesthesia with minimal risks is preferred during caesarean delivery and contraindicated in the presence of coagulopathy.
The management goals during labour includes control of hypertension and prevention of seizures. Antihypertensive agents that are used in severe preeclampsia includes labetalol and hydralazine. Magnesium sulphate is the drug of choice to prevent seizures though it does not prevent the progression of disorder.19
CONCLUSION
According to our study though preeclampsia is more in primiparous women , severity was increased in multiparous women which could be attributed to varying pathophysiology in both groups.In our study eclampsia solely occured in primiparous women.Though preeclampsia is not preventable, maternal deaths due to this condition can be avoided. Quality antenatal care, early detection of the condition ,close monitoring with maternal and fetal surveillance and effective management will be crucial in reducing morbidity and mortality associated with this condition.
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.
Ethics committee approval: Obtained
Source of funding: None
Conflicts of interest: None
Englishhttp://ijcrr.com/abstract.php?article_id=171http://ijcrr.com/article_html.php?did=1711. Al-Ghamdi Saeed MG, Al-Harbi AS, Khalil A, El-yahya AR. Hypertensive disorders of pregnancy: prevalence, classification and adverse outcomes in northwestern Saudi Arabia. Annals of Saudi Medicine Journal 1999; 19:557-560.
2. MoodleyJ.South Africa Med.j.CME-1991;9:72.
3. World Health Organization. Global Program to Conquer Preeclampsia/Eclampsia.2002.
4. Dolcea C. AbouZahr C. Global burden of hypertensive disorders of pregnancy in year 2002. In: Global Burden of Diseases;2000; World Health Organisation..
5. Zibaeenazhad MJ, M Ghodsi P Arab, Gholzom N. the prevalence of hypertensive disorders of pregnancy in Shiraz, Southern Iran; Iranian Cardiovascular Research Journal 2010; 4:169-172
6. J.Nadkarni, J. Bahl, P. Parekh. Perinatal outcome in pregnancy associated hypertension, Indian pediatrics 2001,38:174-178
7. Al-Mulhim AA, Abu-Heija A, AlJamma F, El-Harith el-HA. Preeclampsia: maternal risk factors and perinatal outcome. Fetal Diagn Ther. 2003; 18 (4): 275-80.
8. Miguil M, Chekairi A. Eclampsia, Study of 342 cases. Hypertension in Pregnancy. 2008; 27 (2): 103-11.
9. Dissanayake VH, Samarasinghe HD, Morgan L, Jayasekara RW, Seneviratne HR, Pipkin FB. Morbidity and mortality associated with preeclampsia at two tertiary care hospitals in Sri Lanka. J Obstet Gynaecol Res. 2007; 33 (1): 56-62.
10. Eskenazi B, Fenster L, Sidney S, Elkin EP. Fetal growth retardation in infants of multiparous and nulliparous women with preeclampsia. Am J Obstet Gynecol 1993; 169: II 12-8.
11. Gleicher N, Boler LR, Norusis M, Del Granado A Hypertensive diseases of pregnancy and parity. Am J Obstet Gynecol 1986; 154: I 044-9.
12. Gibson G, Hunter D, Neame PB, Kelton JG. Thrombocytopenia in pre-eclampsia and eclampsia. Semin Thromb Hemost. 1982;8:234-247.
13. Pritchard JA, Cunningham FG, Mason RA. Coagulation changes in eclampsia: their frequency and pathogenesis. Am J Obstet Gynecol. 1976;8:855-864.
14. Kang DH, Finch J, Nakagawa T, Karumanchi SA, Kanellsi J, Granger J, Johnson RJ. Uric acid, endothelial dysfunction and pre-eclampsia: searching for a pathogenetic link. Journal of hypertension. 2004; 22:229–235. [PubMed: 15076175]
15. Bainbridge SA, Roberts JM. Uric Acid as a Pathogenic Factor in Preeclampsia. Placenta. 2008 29S: 67–72.
16. Feig DI, Nakagawa T, Karumanchi SA, Oliver WJ, Kang DH, Finch J, Johnson RJ. Hypothesis: Uric acid, nephron number, and the pathogenesis of essential hypertension. Kidney international. 2004; 66:281–287. [PubMed: 15200435]
17. ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. No. 33, January 2002.
18.American College of Obstetricians and Gynecologists. Obstet Gynecol 2002;99:159-67Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol 2000;183:S1-22.
19. Livingston JC, Livingston LW, Ramsey R, Mabie BC, Sibai BM. Magnesium sulfate in women with mild preeclampsia: a randomized controlled trial. Obstet Gynecol 2003;101:217-20.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcareTREND IN EXTRAPULMONARY TUBERCULOSIS WITH SPECIAL REFERENCE TO LYMPH NODES-A FIVE YEARS STUDY
English2528Pammy SinhaEnglish K. SivakamiEnglish R. ThamilselviEnglishIntroduction: Tuberculosis is still one of the most frequently occurring infectious diseases worldwide. The term extrapulmonary tuberculosis has been used to describe the isolated occurrence of TB at body sites other than the Lung. In India extrapulmonary tuberculosis comprises 20% of all cases of tuberculosis. Aim and Objective: To study the clinicomorphological pattern of lymphnode pathology.
Material and Methods: Our study is a retrospective analysis of all lymphnode excision cases received in the Department of Pathology for a period of 5 years (January 2007 to December 2011).
Result: We received a total of 98 cases, of which 36 were tubercular lymphadenitis. Maximum number of cases was in the age group of 22-31 years and females outnumbered males.
Conclusion: Cervical group of lymphnodes were most commonly involved and cases w ere at peak in 2011 after which it reduced.
EnglishTuberculosis, Extrpulmonary, Lymphadenitis, CervicalIntroduction
Tuberculosis (TB) is still one of the most frequently occurring infectious diseases worldwide. According to the World Health Organization, approximately one third of the world's population is infected with tubercle bacilli. Eight million new cases of the active disease develop each year and three million people die from it [1].
India has the highest TB burden accounting for one fifth of the global incidence. According to a report issued by the government of India, nearly 40% of the Indian population is infected with the TB bacillus [2].
The term “extrapulmonary TB” has been used to describe the isolated occurrence of TB at body sites other than the Lung. [3]. An increasing incidence of extrapulmonary TB has been noted both in developing and developed countries since the mid-1980s. Almost one-fifth of TB cases in the United States are extrapulmonary [4].
In India, extrapulmonary TB comprises 20% of all TB cases. Extrapulmonary TB has become more common since the advent of human immunodeficiency virus (HIV) infection. [5].
Mycobacterial lymphadenitis comprises about 2% to 5% of all cases of TB and is more common among children, women and minorities, as well as in immunosuppressed patients, especially those with HIV [1].
Tuberculous lymphadenitis in the cervical region is known as scrofula, a term derived from the Latin for “glandular swelling.” [6]. The cervical lymph nodes are most frequently involved, followed by the mediastinal lymph nodes and the axillary lymph nodes. [7].
The M. tuberculosis granuloma, classically characterized by the presence of central caseous necrosis, is referred to as a tubercle. Typically, there is a central area of amorphous caseating granular debris and loss of cellular detail, and presence of acid-fast bacilli, the area is encircled by epithelioid cells, lymphocytes, histiocytes, fibroblasts, and occasionally Langhans' giant cells. These histologic features of the granuloma are sufficiently characteristic to allow reasonably accurate diagnosis of tuberculosis [8].
While caseating granuloma is the classic finding in cases of tuberculosis, Immunosuppression may alter the classic histopathologic features of tuberculosis. A spectrum of histopathologic granulomatous tissue reactions are seen in patients infected with HIV [9]. Classic well-formed granulomas have been observed in individuals with early HIV disease whose CD4 cell counts have remained adequate. In patients with advanced HIV disease, the granulomas are less well formed and more necrotic [8]..
Extrapulmonary TB is more common in HIV-infected patients compared to patients without HIV infection [10, 11]
Material and Methods
This retrospective study was conducted in the Department of Pathology, Vinayaka Mission’s Kirupananda Variyar Medical College, Salem. A total of ninety eight consecutive cases of lymphadenitis, from January 2007 to December 2011 (5years), diagnosed on histopathology were reviewed for clinicomorphological studies. All the slides were stained by Haematoxylin and eosin (H and E) stain. Special stains were used wherever necessary.
Results
We studied a total of 98 sample retrieved from the files of Department of Pathology, Vinayaka Mission’s Kirupananda Variyar Medical College , Salem , from January 2007 to December 2011.
The age range was from 2.5 years to 72 years with the mean age being 35 years.
Most of the samples were fallen in the age group of 22 to 31 years. The least incidence of disease is seen in the age group of 72 to 81 years. (Table – 1)
In this study , females were predominantly affected compared to males, the ratio being 9:7. (Female :Male) (Table – 2)
The pathology in lymphnodes ranged from caseating tuberculous granuloma to reactive lymphadenitis to nonspecific lymphadenitis to primary tumours and secondary tumours. (Table – 3)
However the commonest disease was Tuberculosis with Extensive caseating necrosis and the least disease was Suppurative lymphadenitis.
In our study , the commonest extra pulmonary site of tubercular involvement was cervical lymphnode (45) and the least involved lymphnodes were supraclavicular and anterior chest wall one each case. (Table – 4)
Our study revealed that incidence of caseating granuloma, s/o tuberculosis show decreasing trend from year2007 (10.2%),2008 (8.1%), 2009( 6.1%) 2010 (4.0%) and again increased upto 8.1 % in 2011. (Table – 3)
Discussion
Tuberculosis is a major health problem in the developing countries. Its incidence is also increasing due to increased incidence of AIDS.
Microscopically the disease progresses through early exudative to caseous to late fibrocalcific lesions. [12].
The World Health Organization reported 1.1 million new cases of TB among HIV-infected persons in 2009 . High HIV prevalence regions have experienced a greater burden of extrapulmonary TB . Extrapulmonary TB is more
common in HIV-infected patients compared with patients without HIV infection , and its incidence has doubled since the beginning of the HIV pandemic . Furthermore, the most common form of extra-pulmonary TB is in peripheral lymph nodes in HIV-infected patients [13].
In our study the more common age group for extrapulmonary tuberculosis was younger age group and more common in females in contrast to pulmonary tuberculosis which is more common in males and in the older age group as seen in literature and the commonest lymph nodes were in cervical region as in literature [5].
In this study, the extra pulmonary tuberculosis was diagnosed mainly by the presence of granuloma with extensive caseous necrosis. It is apparent that granulomatous conditions of diverse etiologies share common histologic features, although the etiologic agent is not always identifiable. Although the histopathologic patterns in various infectious granulomas may be sufficiently
different to prevent an accurate diagnosis, atypical presentations may necessitate identification of the specific etiologic agent by direct microscopic examination, culture, serology, or molecular detection. [8].
The differential diagnosis of isolated peripheral tuberculous lymphadenitis includes adenitis due to other mycobacteria, bacterial adenitis, fungal disease, toxoplasmosis, sarcoidosis, cat-scratch disease, cystic hygroma, nonspecific hyperplasia, and primary or metastatic neoplasms [7].The literature has classically supported excisional biopsy as the definitive diagnostic procedure for diagnosis of nodal TB [7,30]. Identification of caseating granulomatous inflammation with Langhans and foreign body giant cells supports a diagnosis of TB. [5].
Tuberculosis is now the most common co-infection that occurs with HIV disease and is a major factor responsible for the increased morbidity and
mortality rates in HIV-infected individuals (Toosi et al., 2004).
In our study ,the incidence of extrapulmonary tuberculosis in early years started declining and in the year 2011 again the incidence of extrapulmonary
tuberculosis with extensive caseous necrosis started rising probably because of rising HIV incidence in the later years.
HIV alters the course of TB. The non-cyto- pathic nature of HIV in phagocytic cells enables these cells to produce a prolonged milieu of cytokine factors, including IFN-gamma and IL-6, which are conducive to both disease pathologies (Bal et al., 2004). Co-infection with HIV inhibits cell-mediated responses to MTB through interruption of IL-2 signaling (Lawn et al., 2001). Under these conditions the risk of acquiring MTB infections from the environment, progression to disease, or re-activation of a latent TB infection may occur rapidly (Glassroth, 2005; Swaminathan, 2004). Co-infection with HIV and TB presents various diagnostic challenges (Kassu et al., 2007). An atypical presentation may be observed due to HIV-induced immunodeficiency, mycobacterial dissemi- nation and the lack of self-limiting tissue damage in the host (Lawn, 2005). [14].
Conclusion
In this study, the incidence of extrapulmonary tuberculosis is more common in younger age group and in females. Its incidence started rising after year 2011 possibly due to a rise in immunosuppression like HIV. The worldwide incidence of TB is increasing currently, as HIV-infected patients are at extremely high risk
for progression from latent TB to active disease. The unusual clinical manifestations of TB should not be ignored in high-risk group. We should distinguish between tuberculous lymphadenitis and Non – tuberculous lymphadenitis as the treatment modalities are different.
Englishhttp://ijcrr.com/abstract.php?article_id=172http://ijcrr.com/article_html.php?did=172Gerogianni I, Papala M, Kostikas K, Ioannou M,
Karadonta A.V. and Gourgoulianis K.; Tuberculous disseminated lymphadenopathy in an immunocompetent non-HIV patient: a case report; Journal of Medical Case Reports 2009, 3:9316
2. Ministry of Health and Family Welfare. TB India 2009: RNTCP status report. New Delhi: Central TB Division, Directorate General of Health Services, Ministry of Health and Family Welfare; 2009.
3. Backer AID, Mortele KJ, Keulenaer BLD, Parizel PM (2006) Tuberculosis: epidemiology, manifestations, and the value of medical imaging in diagnosis. JBR-BTR 89: 243-250.
4. Peto HM, Pratt RH, Harrington TA, LoBue PA, Armstrong LR (2009) Epidemiology of extrapulmonary tuberculosis in the United States, 1993–2006. Clin Infect Dis 49: 1350-1357.
5. HandaU , Mundi I, Mohan S ;Nodal tuberculosis revisited: a review .J Infect Dev Ctries 2012; 6(1):6-12.
6. Artenstein AW, Kim JH, Williams WJ, Chung RCY (1995) Isolated peripheral tuberculous lymphadenitis in adults: current clinical and diagnostic issues. Clin Infect Dis 20: 876-882.
7.Geldmacher H, Taube C, Kroeger C, Magnussen H, Kirsten D:Assessment of lymph node tuberculosis in northern Ger-many. Chest 2002, 121:1177-1182.
8. Zumla A and James D. G ; Granulomatous Infections: Etiology and Classification. Clinical Infectious Diseases 1996;23:146-58
9 Zumla A, James DG. Lung immunology in the tropics. In: Sharma OP,
ed. Lung disease in the tropics. New York: Marcel-Dekker, 1991:1- 64
10. M. D. Frye, C. J. Pozsik, and S. A. Sahn, “Tuberculous pleurisy
Is more common in AIDS than in non-AIDS patients with tuberculosis,” Chest, vol. 112, no. 2, pp. 393–397, 1997.
11 J. M. FitzGerald, S. Grzybowski, and E. A. Allen, “The impact of human immunode?ciency virus infection on tuberculosis and its control,” Chest, vol. 100, no. 1, pp. 191–200, 1991
12.Ayesha Sarwar, Anwar Ul Haque, *Sara Aftab, Mahera Mustafa,
Ambreen Moatasim, Saadia Siddique and Aaliya Sani Spectrum of Morphological Changes in Tuberculous Lymphadenitis . International Journal of Pathology; 2004; 2(2):85-89
13. A . Aljohaney, 1, 2 K. Amjadi, 2 andG.G.Alvarez2 A Systematic Review of the Epidemiology, Immunopathogenesis, Diagnosis, and Treatment of Pleural TB in HIV- Infected Patients Clinical and Developmental Immunology .Volume 2012, Article ID 842045, 9
14. Yoshan Moodley .The interaction of HIV and tuberculosis. Scientific Research and Essay Vol. 3 (12), pp. 565-566,
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcareRELATIONSHIP OF GRIP AND PINCH STRENGTH TO BODY MASS INDEX AMONG DENTAL PROFESSIONALS-CROSS SECTIONAL STUDY
English2934Fazin Abdul SalamEnglish Thangadurai ChinnakalaiEnglishAim: To determine the relationship of grip and pinch strength to body mass index among dental professionals.
Methodology: In this cross sectional study total number of 150 dental professionals, aged 22 to 40 years, who fulfilled selection criteria, were recruited through Purposive sampling. Participant’s height, weight, body mass index, grip strength, lateral pinch strength, Pad to Pad pinch strength and Tip to Tip pinch strength were then assessed. All measurements were taken by using standardized procedures. The data collected was analyzed by using Pearson’s correlation test.
Results: The inferential statistics had shown that there was a significant positive correlation between body mass index and grip strength with correlation coefficient (r) value of 0.233 (p = 0.004), body mass index and lateral pinch strength with of r value 0.259 (p value = 0.01), body mass index and pad to pad pinch strength with r value of 0.209 (p value = 0.05), body mass index and tip to tip pinch strength with r value of 0.169(p value = 0.05).
Conclusion: The study shows that there is a significant weak positive correlation between body mass index and Grip strength, body mass index and lateral pinch strength, body mass index and pad to pad pinch strength and body mass index and tip to tip pinch strength.
EnglishBody Mass Index, Grip strength, Lateral pinch strength, Pad to Pad pinch strength, Tip to Tip pinch strengthINTRODUCTION
Grip and pinch strength of dental professionals have been focused in numerous studies worldwide. The prevalence of work-related upper extremity Musculo-Skeletal Disorders are increased among dentists and dental hygienists than other professionals.1 As the work area of dentists is narrow, dental treatment is performed in a very inflexible work posture, 2so they are more prone for Musculo-Skeletal Disorders even from early stage of their career.3 One of the factors associated with the high prevalence of upper extremity Musculo-Skeletal Disorders among dental practitioners is the repeated high pinch force applied during periodontal scaling4. Overuse and extreme range of motion of certain muscle groups and joints are caused by repeated identical or similar motions, which are performed over a period of time can eventually lead to muscular fatigue which in turn affects the grip and pinch strength.5
Hand strength evaluation has been identified as an important factor in predicting Musculo-Skeletal Disorders, the grip strength and pinch strength are considered to be an objective outcome measures.6 Grip and pinch are measures of the hand muscles strength 7, 8 Pinch grip strength has been used as indices of strength in hand therapy assessments.9 The grip strength and pinch strength was reported to be higher in dominant hand.10
Body mass in adults can be classified using body mass index, which is a simple index of weight-for-height, With the increase in body mass index grading, the health risk may be differ among different population.11,12 Research has shown that individuals fall into overweight or obese categories has higher chances of experiencing health problems.13body mass indexis one of the key factors in the development of musculoskeletal dysfunction, that may vary among different professionals.
Singh A, Prohit B reported that Obesity was observed in third-year (22.4%), final-year (16.3%) students, interns (20.4%) and faculty members (40.8%).14Ibegbu Augustine Oseloka et.al stated that body mass index have positive correlation with grip strength among Nigerian students.15T Kamarul, TS Ahmad stated thathand grip strength was positively correlated with hand dominance, gender, occupation, height, and weight, but not with body mass index.16Also, Angelica Soares et.al concluded that there was no association between grip strength and body mass index in general population.17
Disparity exists in the literature over the relationship between hand grip strength and body mass index in different professionals, some researchers claiming a positive relationship between grip strength and body mass index in all age groups, while other researchers found no relationship18-21. Especially in dental profession there are lacks of studies in finding the relationship between body mass index with grip and pinch strength. Hence, this study aims to find the correlation between grip and pinch strength with body mass index among dental professionals.
MATERIALS AND METHODS
This study was conducted among dental professionals aged 22 to 40 years with a sample size of 150. Purposive sampling method was used. The participants who fulfilled the selection criteria were included in the study. Prior to the participation, the study was explained and written informed consent was obtained from each of them. Ethical clearance was obtained from University ethics committee. The inclusion criteria: healthy dental professionals who are practicing at least for 1 year, males and females between 22 to 40 years of age with full functional range of motions of upper limb and neck. Exclusion criteria were participants with MSD, a history of recent surgery, any neurological disorder and any systemic illness.
A standardized weighing machine was used to measure the weight of each Participant. The height was measured by using a stadiometer. Body Mass Index was calculated for each participant by using the formulaBody Mass Index =Weight(Kg)/Height(m)2
METHODS
Grip strength was measured by using a Jamar Dynamometer (figure 1), lateral pinch (figure 2), pad to pad(figure 3) and tip to tip (figure 4) pinch strengths were measured by using a pinch gauge. The standardized functional positions were used.22-25 Participants were asked to Grip/pinch with his/her dominant hand; other end of the pinch gauge was hold by the investigator. Explanation was given to squeeze the dynamometer and press the pinch gauge. Then, they were allowed to familiarize themselves with the instrument by a sub-maximal practice trial. Finally, they were asked to squeeze/pinch the handle of dynamometer/pinch gauge as strong as possible and measurement was taken (in Kg). The same was repeated for 3 times, allowing a 10 seconds rest between the measurements.23Average of 3 measurements was calculated and documented.
STATISTICAL ANALYSIS
The collected data was analyzed using SPSS version 22. Descriptive Statistics was produced for Age, Gender, Hand dominance, body mass index, grip strength, lateral pinch, pad to pad and tip to tip pinch strength distribution. The Pearson’s Correlation test was used to check the relationship between body mass index and grip strength, lateral pinch, pad to pad and tip to tip, PEnglishhttp://ijcrr.com/abstract.php?article_id=173http://ijcrr.com/article_html.php?did=173
Milerad E, Ekenvall L. Symptoms of the neck and upper extremities in dentists. Scandinavian journal of work environment and health. 1990 Apr 1:129-34.
Bramson JB, Smith S, Romagnoli G. Evaluating dental office ergonomic risk factors and hazards. The Journal of the American Dental Association. 1998 Feb 28;129(2):174-83.
Yi J, Hu X, Yan B, Zheng W, Li Y, Zhao Z. High and specialty-related musculoskeletal disorders afflict dental professionals even since early training years. Journal of Applied Oral Science. 2013 Aug;21(4):376-82.
Villanueva A, Dong H, Rempel D. A biomechanical analysis of applied pinch force during periodontal scaling. Journal of biomechanics. 2007 Dec 31;40(9):1910-5.
An introduction to ergonomics: Risk Factors, msds, Approaches and Interventions. American dental association. 2004
Angst F, Drerup S, Werle S, Herren DB, Simmen BR, Goldhahn J. Prediction of grip and key pinch strength in 978 healthy subjects. BMC musculoskeletal disorders. 2010 May 19;11(1):94.
John Brookfield (1995). Mastery of Hand Strength.
John Brookfield (2002). The Grip Master's Manual.
Nayak US, Queiroga JM. Pinch grip, power grip and wrist twisting strengths of healthy older adults. Gerontechnology. 2004 Jan 4;3(2):77-88.
Incel NA, Ceceli E, Durukan PB, Erdem HR, Yorgancioglu ZR. Grip strength: effect of hand dominance. Singapore medical journal. 2002 May;43(5):234-7.
World Health Organization. BMI classification. Global database on body mass index.available fromhttp://apps.who.int/bmi/index.jsp?introPage=intro_3.html[homepage on the Internet] c2016[updated 2016 January 17, 12.30a.m]
Body Mass Index: Considerations for Practitioners. Department of health and human service center for disease control and prevention. CDC; [homepage on the Internet] updated 2015; available from:http://www.cdc.gov/healthyweight/assessing/bmi
National Heart foundation in association with the faculty of Public Health and department of Health, 2007. Lightening the load. Tackling overweight and obesity. a toolkit for developing local strategies to tackle overweight and obesity in children and adults. [Online] London: department of Health. Available at: http://www.dh.gov.uk/en/Publicationsandstatistics/ Publications/Publications Policy and Guidance/dH_073936 [accessed May 2009]. ?
Singh A, Purohit B. Evaluation of Global Physical activity Questionnaire (GPAQ) among healthy and obese health professionals in central India. Baltic Journal of Health and Physical Activity. 2011 Jan 1;3(1):34-43.
Oseloka IA, Bello BM, Oliver HW. Association Of Handgrip Strength With Body Mass Index Among Nigerian Students. IOSR Journal of Pharmacy and Biological Sciences (IOSR-JPBS). 2014; PP 01-07
Kamarul T, Ahmad TS, Loh WY. Normal hand grip strength in the adult Malaysian population. Journal of Orthopaedic Surgery. 2006;14(2):172-71.
Nascimento AS, Pinto IR, Abreu MM, Almeida SP, Fernandes B, Tomás M. Association between grip strength, anthropometric data and functional capacity. 2 health ipleiria.congresso internacional de saúde do ipleiria.
Madaan V, Chaudhari A. Prevalence and Risk Factor associated with Musculoskeletal Pain among Students of MGM Dental College: A cross sectional survey. Journal of Contemporary Dentistry. 2012 May;2(2):22-7.
Apovian CM, Frey CM, Wood GC, Rogers JZ, Still CD, Jensen GL. Body mass index and physical function in older women. Obesity Research. 2002 Aug 1;10(8):740-7.
Koley S, Kaur N, Sandhu JS. A study on hand grip strength in female labourers of Jalandhar, Punjab, India. J. Life Sci. 2009;1(1):57-62.
Sucharita S, Bharathi AV, Vaz MA. Effect of age and nutritional status on heart rate responses to cough and maximum handgrip. Indian journal of physiology and pharmacology. 2004 Jan 24;48(1):106-10.
Sirajudeen MS, Shah UN, Pillai PS, Mohasin N, Shantaram M. Correlation between grip strength and physical factors in men. International Journal of Health and Rehabilitation Sciences (IJHRS). 2012;1(2):58-63.
Hand Grip Strength protocol. Tufts university nutrition collaborative. Center for drug abuse and AIDS research. TNC-CDAAR.1986; Revised 09/03
Shin H, Moon SW, Kim GS, Park JD, Kim JH, Jung MJ, Yoon CH, Lee ES, Oh MK. Reliability of the pinch strength with digitalized pinch dynamometer. Annals of rehabilitation medicine. 2012 Jun 1;36(3):394-9.
Jansen CW, Simper VK, Stuart HG, Pinkerton HM. Measurement of maximum voluntary pinch strength:: Effects of forearm position and outcome score. Journal of Hand Therapy. 2003 Dec 31;16(4):326-36.
Liao KH. Systematic exploring the relationship between hand-grip strength and body mass index (BMI). InThe 11th Asia Pacific Engineering and Management Systems Conference. Taiwan 2010.
Tajika T, Kobayashi T, Yamamoto A, Shitara H, Ichinose T, Shimoyama D, Okura C, Kanazawa S, Nagai A, Takagishi K. Relationship Between Grip, Pinch Strengths and Anthropometric Variables, Types of Pitch Throwing Among Japanese High School Baseball Pitchers. Asian journal of sports medicine. 2015 Mar;6(1).
Habibi E, Kazemi M, Dehghan H, Mahaki B, Hassanzadeh A. Hand grip and pinch strength: Effects of workload, hand dominance, age, and body mass index. Pak J Med Sci. 2013; Vol. 29 No. 1
Thong-Ngam D. Body mass index and percentage of body fat determined physical performance in healthy personnel. Asian Biomedicine (Research Reviews and News). 2012 Apr 2;6(02):313.
Thong-Ngam D. Body mass index and percentage of body fat determined physical performance in healthy personnel. Asian Biomedicine (Research Reviews and News). 2012 Apr 2;6(02):313.
Abbas SU. Pinch Force and Workrelated Musculoskeletal Disorders in Dental Professionals. UCHC Graduate School Masters Theses. 2004 Jun 1:12
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcarePOSTPARTUM ACUTE KIDNEY INJURY: FALLING TREND IN DEVELOPING WORLD
English3537Nikunj NavadiyaEnglish Hina V. OzaEnglish Pallavi NinamaEnglish Hafsa VohraEnglishAims and Objectives: To study epidemiological factors, risk factors, morbidity and mortality among patients in postpartum period having acute kidney injury at a tertiary care centre. Materials and Methods: This is a Retrospective Study based on obstetric patients with oliguria/anuria or referred for high s.creatinine to Civil Hospital, Ahmadabad, Gujarat, India from July 2014 to January 2015. Details of these patients like history, examination and investigation findings were recorded and final data analysis done. Results: All of the patients with postpartum AKI had oliguria/anuria and /or high serum creatinine. Most of the patients were anaemic. Most of the AKI occurred in early (EnglishAKI-acute kidney injuryINTRODUCTION
Post-partum acute kidney injury (AKI) is a challenging health problem in pregnant women, especially in the developing countries. The incidence of AKI requiring dialysis in pregnancy is approximately one in 20,000 births in developed countries. But pregnancy is still responsible for 9–25% of total AKI cases in developing countries[1-3].The marked decline in this complication over the past 50 years is a result of improved antenatal care, advancements in obstetric practice and legalization of abortion. Acute kidney injury associated with late obstetrical complications is well described in literature in developed countries but the data on postpartum AKI from India is limited[4-6]. Therefore, this study was designed to study the incidence and clinical spectrum of maternal outcomes of AKI in postpartum period. Hypertensive disorders during pregnancy, Antepartum hemorrhage, Post-partum hemorrhage, HELLP syndrome and puerperal sepsis are considered to be the major causes of post-partum AKI. Although the incidence of AKI has declined sharply in the past 40 years in developed countries, its prevalence is still significant in the developing countries.
MATERIALS AND METHODS
Study type: Retrospective study
No. of patients: n=36
Institute: B. J. Medical College, Civil Hospital, Ahmedabad, Gujarat, India.
Exclusion criteria: -Obstetric patients having chronic renal failure,
-AKI associated with non-obstetric conditions.
The obstetrical outcomes studied:
- Postpartum maternal morbidity and mortality.
Study period: Between July 2014 to January 2015.
AKI was defined based on changes in serum creatinine or changes in urine output or both.
Obstetric records including age, parity data, pregnancy-related disorders and delivery information were recorded. The post-partum course was also reviewed, with specific attention to post-partum complications and timing of recovery of kidney function. RESULTS
Incidence of postpartum acute kidney injury was 3.89 % in our study.
Mean age was 25.7years. Majority of the patients belonged to the peak reproductive age ranged between 20 and 30 years. Primipara and multipara constituted 52.77% and 47.22 % of the patients, respectively.
Most of the patients were anemic and mean hemoglobin concentration was 6.79±2.06 g/dl.
The mean peak serum creatinine and blood urea concentration were 3.49 ± 2.88 mg/dl and 96.24 ± 37.21 respectively.
Mode of delivery was vaginal delivery in 30 (83.33%) patients and caesarean section in 6 patients (16.66%). Most of the patients developed AKI in early (Englishhttp://ijcrr.com/abstract.php?article_id=174http://ijcrr.com/article_html.php?did=174
Chugh KS, Singhal PC, Sharma BK, et al. Acute renal failure of obstetric origin. ObstetGynecol 1976;48:642-6.
Prakash J, Singh RG, Tripathi K, et al. Acute renal failure in pregnancy. J ObstetGynaecol India 1985;35:233-8.
Naqvi R, Akhtar F, Ahmed E, et al. Acute renal failure of obstetrical origin during 1994 at one centre. Ren Fail 1996;18:681-
Grunfeld JP, Ganeval D, Bourneris F. Acute renal failure in pregnancy. Kidney Int.1980;18:179–191
SelcukNY, Tonbul HZ, San A, Odabas AR. Changes in frequency of acute renal failure in pregnancy (1980-1997)Ren Fail 1998;20:513-7.
Prakash J, Niwas SS, Parekh A, et al. Acute kidney injury in late pregnancy in developing countries. Ren Fail 2010;32:309-13
Stratta P, Besso L, Canavese C, et al. Is pregnancy-related acute renal failure a disappearing clinical entity? Ren Fail.1996;18:575–584
Brady HR, Clarkson MR, Lieberthal W. Acute renal failure.In: Brenner BM, ed. The Kidney. 7th ed. Philadelphia, PA:Saunders; 2000:1215–1270.
Chugh KS. Etiopathogenesis of acute renal failure in the tropics.AnnNatlAcad Med Sci (India) l987;23: 88-99
Chugh S, Sakhuja V, Malhotra HS et al. Changing trends in acute renal failure in third world countries—Chandigarh study. Q J Med 1989; 272: 1117–23.
Goplani KR, Shah PR, Gera DN, et al. Pregnancy related acute renal failure: a single centre experience. Indian J Nephrol 2008;18:7–21.
Ansari MR, Laghari MS, Solangi KB, et al. Acute renal failure in pregnancy: One year observational study at Liaquat University Hospital, Hyderabad. J Pak Med Assoc.2008;58:61–64.
Kumar SK, Krishna CR, Kumar VS. Pregnancy related acute renal failure. J ObstetGynecol India.2006;56:308–310.
Hachim K, Badahi K, Benghanem M, et al. Obstetrical acute renal failure. Experience of the nephrology department, Central University Hospital ibnRochd, Casablanca. Nephrologie. 2001;22:29–31.
Alexopoulos E, Tambakoudis P, Bili H, et al. Acute renal failure in pregnancy. Ren Fail.1993;15:609–613.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30General SciencesINVESTIGATION ON THE SOLAR CYCLE SIGNATURE ON THE HADLEY CIRCULATION BASED ON THE INTENSITY AND DURATION OF THE SOLAR CYCLE
English3846C. VedavathiEnglish M. Venkat RatnamEnglish V.V.M. Jagannadha RaoEnglish N. Venkwateswara RaoEnglish and S. VijayaBhaskara RaoEnglishIt is well known that there are profound effects of solar cycle (SC) on the tropical deep convection and hence the atmospheric circulations. However, it is unknown how the intensity and duration of SC is going to affect the circulation patterns. In the present study, the effect of SC on the Hadley circulation (HC) is investigated based on intensity and duration of the SC using ERA-Interim dataset obtained during 1979-2012. Maximum and minimum SC is differentiated based on sunspot number (SSN) with cut-off at >=100 and EnglishSolar cycle, Convection, Hadley circulationIntroduction
Tropical latitudes are the prime regions for atmospheric general circulations due to the existence of active convective centres[1]. Among these, prominent are Hadley (meridional or N-S) and Walker (zonal or E-W) circulations. Interestingly, both these circulations have common source region in the tropical latitudes. While the Hadley Circulation (HC) is mainly due to pressure gradient between the land and ocean, the Walker Circulation (WC) is due to the temperature difference between the east and western Pacific oceans[2,3]. The characteristics of these circulations vary (upward and downward branches) from season to season. The HC is dominated by a strong winter hemisphere cell and a very weak summer hemisphere cell [4]. The direction of the HC will be reversed from summer to winter season, and is dominant in the winter hemisphere[4,5]. From December to March, the HC extends roughly between 10oS and 30oN dominant by intense Northern Hemisphere (NH) Hadley cell, whereas during June to September it extends between 10oN and 35oS in Southern Hemisphere (SH) Hadley cell[6].Over the Indian region, the direction of HC during monsoon season is opposite to that in winter[6,7].
Apart from seasons, other phenomena like El Niño–Southern Oscillation (ENSO) and solar cycle (SC) strongly modulate the strength and direction of the circulations[8,9]. Thus, strong inter-annual variability is expected in these circulations. It is well known that SC affects these circulations both directly and indirectly [10,11]. Several studies are carried out using different data sets to examine the role of SC on these circulations. When sun is more active, stronger Hadley cell was observed [12],using vertical velocities from NCEP re-analysis dataset [12]. Similar dependence of the Hadley cell strength on the solar activity was observed [13,14]. During solar maximum condition, suppression of near equatorial convective activity and enhanced off equatorial convection in the Indian monsoon region was noted [15]. Using NCEP zonal mean temperature and zonal wind data a weakened and broadened Hadley cell under solar maximum conditionswas noted [16,17].Again using vertical velocities, poleward expansion of the HC during solar maximum with stronger ascending motions at the edge of the rising branch was observed [18]. [14]and[19]found a strengthened WC during higher solar activityand[20] also found strengthening of the WC during solar maximum in SC 21 and SC 22. The associated sea surface temperature response during solar maximum is to cool anomaly in the equatorial eastern pacific and pole ward shift of Inter Tropical Convergence Zone (ITCZ) and South Pacific Convergence Zone (SPCZ)[14,19]. A clear modulation of the ENSO which is manifested mainly in the western extent of the Walker cell and links to the behaviour of the Indian monsoon is also clearly found [9].
Simplified global circulation models(GCM) provide some indications of the variation in HC and WC by the solar activity on how these responses arise[2,8,21,22].All model runs in which thermal perturbations were applied only in the lower stratosphere show effects throughout the troposphere, with the vertically banded anomalies in the temperature and zonal wind, and changes in the tropospheric mean circulation[10], which is typical of the results of data analysis. Heating the lower stratosphere increases the static stability in this region, lowers the tropopause, and reduces the wave fluxes[17]. Experiment with simplified GCM suggests that the transfer of solar signal to lower levels from stratosphere is due to secondary temperature maximum in the equatorial lower stratosphere [10].
Several previous studies observed the strengthening of tropical circulations during solar maximum [12,13,14,18]while some studies indicate that HC was weakened and broadened to the pole ward region[15,16,17,23]. In general, during high solar activity, larger convective activity is expected which results in to active circulation[24]. Whether this is true for all the solar cycles is not known. Further, how intensity and duration of solar cycle affects the circulation is not understood to the best of our knowledge. Thus, in the present communication, SC effects on the HC are investigated by considering the duration and intensity of the SC using the data covering three SCs (SC21 to SC 23).
Database and methodology
ERA-Interim data products
ERA-Interim is a re-analysis of the global atmospheric data archived at ECMWF (European Center for Medium Range Weather Forecasts). This data is available since 1979 at 0.125o x 0.125o latitude-longitude grids with more (37) pressure levels than the ERA-40 and 15-yr ECMWF Re-analysis (ERA-15) data sets. More details of model development can be obtained from[25]. For the present study, the meridional and vertical wind data from 1979 to 2012 available at 6 h intervals for 37 pressure levels between 1000 hPa and 1 hPa is used.
Sunspot number (SSN)
To represent the solar activity, several types of indicators are available which includes sunspot number (SSN), solar diameter, solar radio flux at 10.7 cm and geomagnetic activity index. The SSNis one of the best known indicators of the solar activity, which has been recorded since the early 17th century. In the present study, we use the monthly mean SSN during 1979-2012 obtained from http://www.ngdc.noaa.gov.
Outgoing Long-wave Radiation (OLR)
We also make use of OLR, which is considered as proxy for tropical deep convection. Monthly mean gridded OLR available during 1979 to 2012 at 2.5o x 2.5o latitude-longitude grids from NOAA climate diagnostics center web site (http://www.cdc.noaa.gov) is used in the present study. Since the main aim is to investigate the SC influence, we made use of the monthly mean OLR data.
El Niño–Southern Oscillation (ENSO) Index
The Oceanic Niño Index (ONI) is one measure of the ENSO and other indices can confirm whether features consistent with a coupled ocean-atmosphere phenomenon accompanied these periods[26].Periods of ENSO Index was based on a threshold of +/- 0.5oC for the ONI (3 month running mean of ERSST.v4 SST anomalies in the Nino 3.4 region (5oN-5oS, 120-170oW)), based on centred 30-year base periods updated every 5 years. ENSO index used in the present study is downloaded from the web site http://www.cpc.ncep.noaa.gov/products/analysis_monitoring/ensostuff/ensoyears.shtml.
Methodology
To estimate the HC,we calculate the mass stream function (MSF). In general MSF is commonly known as meridional overturning circulation (further known as Hadley, Ferrel, Polar cells depending on the latitudes) with unit 109 Kg/s. The meridional over turning velocities are related to MSF (ψ) by υ(meridional wind) and w(vertical wind). MSF ψis computed using pressure coordinates from the ERA-Interim dataset. It is determined by normalization of the inverse gravity and latitudinal belt using the equation
By defining MSF (ψ) as a vertically integrated northward mass flux at latitude θ from pressure level p to the top of the atmosphere, the analytical solution for v can be obtained as .
Results
Solar cycle intensity and duration
As the present study mainly depends on the intensity of the SC, the classification of the maximum and minimum periods of SC is discussed first. The monthly mean SSN observed during the period of 1976–2012 along with annual mean is shown in Figure 1. There are three SCs (SC 21, SC 22 and SC 23) in the periodconsidered here. Though period and amplitude of SC varies from one cycle to another, it is well known that the average period is 11years. After careful analysis in our earlier publication[27], we considered time period during which the magnitude of SSN exceeding 100 as solar maximum periods and less than 20 as solar minimum periods as shown with green lines in Figure1. Note that thisis an arbitrary choice of a threshold to identify solar maximum and minimum, and main results will not be affected by changing the threshold of 80 (maximum) and 40 (minimum) used by [28], except change in the duration of maximum and minimum periods.This classification is quite different from that of[28], where they removed the climatological mean from the solar maximum which was defined with SSN>80. In comparison, the cut-offs used in this study are more robust to identify the solar maximum and minimum periods as already discussed in[27]. With these cut-offs, the time periods that fall under solar maximum (minimum) for the SC 21, SC 22 and SC 23 are September 1978 to October 1982 (June 1985 to October 1986), August 1988 to June1992 (April 1995 to March 1997), and August 1999 to April 2002 (April2006toJune2010), respectively.
Table 1 shows the duration, intensity and number of months that fall in solar maximum and minimum periods. From the table it is clear that there are 10.9 years, 9.7 years and 12.6 years in SC 21, SC 22 and SC 23, respectively. Interestingly, SC 23 duration is more than average SC period and this is the longest (extended minimum) SC that occurred in this century. The maximum (peak) SSN is observed to be 164.1, 158 and 120.8 in SC 21, SC 22 and SC 23, respectively, which shows a gradual decrease. The number of months that fall under solar maximum (minimum) periods are 50 (17), 47 (24) and 33 (51) months, respectively. Thus, it is clear that duration of solar maximum (minimum) is decreasing (increasing) from SC 21 to SC 23 and the intensity decreases from SC 21 to SC 23. It will be interesting to see the changes in the HC with respect to the SC intensity and duration. Since the HC depends on the deep convection, first we show how tropical convection is organised during different SC conditions.
Solar cycle effect on the tropical convection
To investigate the SC dependency on the tropical deep convection, we considered OLR as a proxy for convection. Figure 2a shows the global distribution of climatological mean OLR observed during 1979 to 2012. Low OLR indicates deep convection. In general, deep convection centres prevail along the equator over African, Indonesian and South American regions near equator. In order to understand the role of SC on the convective activity, difference in the OLR between solar maximum and minimum periods of SC 21 to SC 23 is shown in Figure 2b. Negative (positive) OLR indicates deep (shallow/no) convection. During solar maximum, convection shifts southward over South American and African (10oS) sectors and no convection over Indian and adjoining sectors. Interestingly, heating centre at equator shifted towards west pacific (150o to 180o longitude). If we clearly observe the Indonesian deep convection in figure 2a, it is puzzling to see that it is divided into two parts in difference of maximum and minimum periods of solar cycles. one shifted towards southward to Australia and another towards east i.e., to western Pacific regions. That means these two heating centres might be shifted to above locations by two different circulations, one due to HC (southward) and another due to WC (eastward –west pacific). It is possible that the ITCZ and SPCZ reinforce and lead for strong heating over those areas. The associated SST response during solar maximum is the existence of cool anomaly in the equatorial eastern pacific and pole ward shift of ITCZ and SPCZ[14,19].
Interestingly, the shift in the convective activity is not same and varies significantly from cycle to cycle which is shown in Figure 3. Figure 3 shows the difference in OLR between solar maximum and minimum in each of SC 21, SC 22 and SC 23. Again, negative (positive) OLR indicates deep (no) convection. In SC 21 and SC 22, no convection is observed over Indian and Indonesian sectors and deep convection exists over the pacific region, whereas, in SC 23(extended minimum) quite contrasting features are noticed i.e., deep convection over southern Indian Ocean, Indonesian region and less convection over the pacific region. Precipitation data set also supports the contrasting feature observed (figure not shown) in SC 23. During SC 21, high convection appeared over Pacific region, Australian continent, South America and South Africa sectors and less convection appeared from equator to north Indian Ocean and North West pacific region. This shift in the convection pattern will strongly influence the HC, as the upward branch of HC will be located over deep convection centres.
During SC 21, southward shift deep convection towards northward and eastward shift of Walker means towards western pacific is observed similar to the climatological picture shown in Figure 2a. In SC 22, only shift in WC towards western Pacific is seen and no southward shift of HC is observed. During SC 23, there is only southward shift of HC and no shift in the WC. An additional feature noted is that besides this shift to Australian region, another deep convection persists over the Indonesian region. Note that ENSO will strongly influence these convection patterns and hence HC and WC.
If we correlate the SC intensity and duration with the convection, it is clear that during SC 21, when the intensity (164.1) is more with longer maximum SSN months (50) with average duration of 10.9 years, both zonal and meridional shift in convection is noticed. Whereas during SC 22, intensity (158) is more with longer maximum SSN months (47) with average duration of 9.7 years, only zonal shift in convection centres is noticed. During SC 23, intensity (120.8) is small with smaller maximum SSN and with average duration of 12.6 years, only meridional shift is seen. Thus, it is clear that SC with larger intensity cause the convection centres shift to Pacific i.e. zonally and longer duration in SC cause shift to SH i.e. meridionally. Earlier it is reported that the longer duration SC with lesser number of SSN causes low heating of earth[29].
In order to quantify the SC effects on the HC, we estimated the MSF for each cycle separately after removing the ENSO contribution i.e., without ENSO affected months. MSF estimated during SC 21, SC 22 and SC 23 maximum and minimum conditions is shown in Figure 4. The contours are (± 0.05, 0.1, 0.15, 0.2, 0.4, 0.8, 1.0) × 109kg s−1 with red (blue) colour indicating positive (negative) values. Following the definition of MSF, the red (or positive contours) denote clockwise flow, while the blue (or negative contours) denote counter clock-wise flow. During SC 21 minimum, there are two Hadley cells one in NH and another in SH with rising motion slightly shifting to north of 5oin NH which peaks at 500 hPa. NH HC is strong compared to the SH one but its width is less compared to SH counterpart.
During SC 21 maximum, the NH HC is intensified and its width increased significantly. The upward branch is shifted to slightly to SH around 2oS. The SH HC is shifted to further south but weakened both in intensity and width. This SH HC shift with rising branch seems to coincide with deep convection centre shown in Figure 3 over South Africa (15oS), Australia (15oS) and South America (15oS).
During SC 22 maximum, the HC is strengthened and not much shift in the circulation is observed. This exactly coincides with the OLR difference shown in Figure 3. The deep convection shifted towards western Pacific and no southward shift is observed.The increased rising motion near equator might be due to coincidence of Walker and Hadley upward branches (or collocation of rising branches).
During SC 23,a similar feature of SC 21 is observed. If we compare the circulations during solar maximum of three cycles, it is clear that the NH HC is relatively weak during SC 21 and SC 23 compared to SC 22. There is no SH HC in SC 22. This is interesting when compared the same with the circulations during solar maximum, i.e., the NH circulations during SC 21 and SC 23 intensified in strength and width and also shift to SH as compared to the SC 22 and also vertical extension of HC upto 200 hPa is noticed.
To understand the exact difference in the HC between solar maximum and minimum conditions, difference in the MSF observed during SC 21, SC 22 and SC 23 is shown in Figure 5. The contours are (± 0.05, 0.1, 0.15, 0.2, 0.4, 0.8, 1.0) × 109kg s−1 with red (blue) colour indicating positive (negative) values. From the difference in the MSF, it is clear that during the SC 21 and SC 23, there is an enhancement in the upper level HC whereas no such feature exists in SC 22. Careful observation prompts us to follow that the strong SH HC present during solar minimum in SC 21 and SC 23 is absent during solar maximum whose rising branch contributes to upper level HC. Since the SH HC during SC 22 is weak there by no contribution to HC.
Comparing the shift in the HC and the deep convection centres,we can conclude that the southward shift of NH HC and weakening of SH HC interact in such a way to strengthen the NH Hadley circulation at upper level and shifting to SH i.e., meridional shift. During SC 22, there is only zonal shift in the deep convection to the western pacific andwe see corresponding absence of enhancement in MSF. It is to be noted that the solar influence on the HC is only prominent at upper levels which can be seen from MSF difference.
As the MSF is estimated over zonal means, there may be chance that the signals get cancelled or enhanced due to large spatial variation. In order to bring out the spatial variability, we select a few regions (Indian, Indonesian and Pacific) that are shown with open circles in Figure 3. All the above mentioned analysis is repeated for each of these sectors. MSF observed during SC 21, SC 22 and SC 23 maximum and minimum conditions over Pacific region (174-186oE) is shown in Figure6. Note that ENSO months are not considered in this analysis. Observing each panel indicates that the NH HC is intensified during SC 21 and SC 22 maximum. In SC 23 minimum, both SH and NH HC intensified but NH HC width has increased.
Indonesia region is the common point to HC and WC.Note that these circulations will be quite different during NH winter and summer months. In order to see the SC influence more clearly on the HC, meridional and vertical wind profiles observed over Indonesian region (0oN,120oE) during solar maximum and minimum conditions in the month of July are shown in Figure 7. Note that ENSO affected months are not considered in this analysis. In order to find the effect of ENSO on these circulations, the difference in the profiles of meridional and vertical wind between ENSO and without ENSO months (July) is also superimposed in the same panels of Figure 7. In only SC 23 maximum and SC 22 minimum no ENSO affected July months are there.
During July month, winds become weak northward in the lower level and southward in the upper level over Indonesia. In this region, always upward wind is observed with northward wind and southward wind in the lower and higher altitudes, respectively. This is mainly due to ITCZ shift towards NH and part of SPCZ[14]. Meridional winds are northward in the lower level and southward in the upper levels. In SC 21, peak southward wind was observed at 200 hPaand differences between with and without ENSO affected profiles show very less magnitudes. Vertical windsare high during SC 23 minimum compared to the SC 21 and SC 22 maximum and minimum conditions. The difference with and without ENSO affected profiles indicate the high magnitudesin SC 21 and SC 22.
Summary and Discussion
In the present study, role of solar cycle (SC) on the Hadley circulation (HC) is explained based on intensity and duration of the solar activity using ERA-Interim reanalysis data sets obtained from 1979 to 2012. In the last three SCs (21, 22 and 23), the duration of solar maximum (minimum) months is found decreasing (increasing) while the intensity decreases from SC 21 to SC 23. Role of SC on the tropical deep convection is investigated first using the NOAA interpolated outgoing longwave radiation (OLR) as a proxy during above mentioned period. During solar maximum, convection shifts southward over South American and African (10oS) sectors and no convection over Indian and adjoining sectors. Over Indonesian region, it is puzzling to see that convection centre is divided into two parts one shifted towards southward to Australia and another towards right i.e., to western Pacific regions. This shift is attributed to the shifting of two heating centres by two circulations namely HC (downward) and Walker circulation (WC) (right side –west pacific). However, this variability is found to differ from cycle to cycle.
Similar variability is also seen in the HC which is represented by estimating the mass stream function (MSF) using ERA-Interim meridional and vertical winds. One striking difference noticed between the SC 21 and SC 22 is decrease in HC during solar maximum in SC 22 against SC 21. Theoretical studies and observations suggest a reduction in HC during solar maximum near equatorial regions[15,16,17]. The above mentioned features during SC 22 support this whereas SC 21 differs. This might be due to occurrence of solar maximum and minimum in two different seasons. During SC 21, peak solar activity occurred around Dec. 1979 whereas solar maximum occurred around Jul. 1989 in SC 22. Moreover during SC 22, there is a consistent peak solar activity for the longer period. Effect of ENSO is found to be strong on the HC similar to that reported earlier where reduced HC during ElNino year 1998 is being observed[30, 31].
The reduction of HC during solar maximum is expected. But this is seen only during SC 22. Overall observations show that during SC 22, the HC decreased compared to SC 21 and SC 23 against increase or no change in HC around pacific region. This might be due to persistence in the high sunspot activity for a larger period with large sunspot number. Moreover the peak activity happened during summer months for SC 22. Northward wind (southerly) during SC 23 increased during solar maximum and minimum compared to SC 21 around pacific region i.e., HC is relatively strong compared to SC 21 which means the effect of solar influence is relatively more in SC 21 compared to SC 23. These can be explained based on intensity and duration of SC. Peak SSN during SC 23 is 120.8 (during Mar. 2000) with duration of 12.6 years. Peak SSN during SC 21 is 164.1 (during Dec. 1979) with duration of 10.9 years. Thus, even though the duration of SC 23 is more (12.6 years), the SSN is less (120.8) compared to SC 21 (10.9 years with peak SSN 164). This strong and less period of solar activity might be the reason for relatively strong influence of solar activity on SC 21 compared to SC 23. In addition, the spotless days are very less during SC 21 (273 days) compared to SC 23 (821 days). The above hypothesis is further strengthened if we see circulation during SC 22. During SC 22 (9.7 years duration with SSN 158) the HC is decreased i.e. influence of solar activity is predominant. Further the spotless days are less (309 days).
SC 23 is long with less intensity and more number of spotless days cause less heating over equatorial regions. Observations of convection centres show that heating is more over land regions in SH compared to the oceanic regions. This indicates that during solar maximum the convection is relatively more over SH land regions. Observations of HC show the broadening of cell and extension towards SH and SH HC present in solar minimum is totally weakened.SC 22 is short and intensified causing strong heating over equatorial regions especially over western pacific. HC which is present in solar minimum in NH is little bit strengthened with no change in the SH Hadley cell exactly coinciding with deep convection over equator. SC 21 which has on average duration of 10.9 years with high intensity (164.1) is a mixed phenomenon of SC22 and SC23 with weak NH HC shifted to southward with weakened SH HC.It is evident that the longer or average duration of SC 21 (10.9 years) and SC23 (12.6 years) show weakening of SH HC whereas short duration of SC22 (9.7 year) doesn’t exhibit such feature indicating that the duration of SC influence circulation and convection.
Conclusion
From the above discussion, it is concluded that, HC is strongly influenced (reduced) during solar maximum which depends further on duration and intensity of SC. Less duration causes more influence on the HC.
Acknowledgements
This work is carried out as a part of CAWSES India Phase-II fully sponsored by ISRO. One of authors (CV) wishes to thank UGC-SVU centre for MST radar application for support. Authors
acknowledge the immense help received from the scholars whose articlesare cited and included in references of this manuscript.The authors arealso grateful to authors / editors / publishers of all those articles, journalsand books from where the literature for this article has been reviewed anddiscussed.
Englishhttp://ijcrr.com/abstract.php?article_id=175http://ijcrr.com/article_html.php?did=175
Annes, V.H, Mohan Kumar, K., Joseph, P.V., 2001. Winter and summer Hadley circulations over Peninsular India as monitored by MST radar at Gadanki (13.47oN, 79.18oE). Inter. J.Climat. 21, 593-601.
Lau, K-M., Yang, S., 2002. Walker circulation. Elsevier Sciences, doi:10.1006/rwas.2002.0450.
Tapio Schneider., 2006. General circulation of the Atmosphere, Annu. Rev. Earth Planet. Sci. 2006. 34:655–88.
Cook. K., 2004. Hadley circulation Dynamics: Seasonality and the Role of Continents. Adv. Global Clim. Cha. Res.,
Roja Raman. M.,Jagannadha Rao, V.V.M., VenkatRatnam, M., Kishore Kumar, G., Narendra Babu, A., VijayaBhaskara Rao, S., Prabhakara Rao, N., Narayana Rao, D., 2008. Atmospheric circulation during active and break phases of Indian summer monsoon: A study using MST radar at Gadanki (13.5 N, 79.2E). J. Geophys. Res, 113, D20124, doi:10,1029/2008jD010341.
Oort, A. H., Rasmusson, E.M., 1970. On the annual variation of the monthly mean meridional circulation. Mon. Weather Rev., 98, 423–442, doi:10.1175/1520-0493(1970)0982.3.CO;2
Sikka, D.R., 1980. Some aspects of the largescale fluctuations of summer monsoon rainfall over India in relation to fluctuations in the planetary and regional scale circulation parameters. Proc. Indian Acad. Sci. Earth Planet. Sci. 89:179–95.
Foley, A., Jonathan, Aure ´lie Botta, and Michael T. Coe., 2002. El Nin ˜o–Southern oscillation and the climate, ecosystems and rivers of Amazonia. Global Biogeo. Cycles, 16, 4, 1132, doi:10.1029/2002GB001872.
Kodera, K., Coughlin, K., Arakawa, O., 2007. Possible modulation of the connection between the Pacific and Indian Ocean variability by the solar cycle. Geophys. Res. Lett., 34, L03710, doi:10.1029/2006GL027827.
Gray, L.J., 2010. Solar influences on climate. Rev. Geophys. 48, RG4001, http://dx.doi.org/10.1029/2009RG000282.
Dubey, S.C., 2005. Solar variability and climate change.Indian J. of Geo-Marine Sci., 43(5), 871-875.
Labitzke, K., Van Loon, H., 1995. Connections between the troposphere and stratosphere on a decadal scale. Tellus, Ser. A, 47, 275–286, doi:10.1034/j.1600-0870.1995.t01-1-00008.x.
Van Loon, H., Meehl, G.A., Arblaster, J.M., 2004. A decadal solar effect in the tropics in July–August. J. Atmos. Sol. Terr. Phys., 66, 1767–1778, doi:10.1016/j.jastp.2004.06.003.
Van Loon, H., Meehl, G.A., Shea, D., 2007. The effect of the decadal solar oscillation in the Pacific troposphere in northern winter. J. Geophys. Res., 112, D02108, doi:10.1029/ 2006JD007378.
Kodera, K., 2004. Solar influence on the Indian Ocean Monsoon through dynamical processes. Geophy. Res. Lett., 31, L24209, doi:10.1029/2004GL020928.
Haigh, J. D., 2003. The effects of solar variability on the Earth’s climate, Philos. Trans. R. Soc. London, Ser. A, 361,95–111, doi:10.1098/rsta.2002.1111
Haigh, J. D., Blackburn, M., Day, R., 2005. The response of tropospheric circulation to perturbations in lower?stratospheric temperature. J. Clim., 18, 3672–3685, doi:10.1175/JCLI3472.1.
Gleisner, H., Thejll, P., 2003. Patterns of tropospheric response to solar variability. Geophys. Res. Lett., 30(13), 1711, doi:10.1029/2003GL017129.
Meehl, G. A., Arblaster, J.M., Branstator, G., Van Loon, H., 2008. A coupled air?sea response mechanism to solar forcing in the Pacific region. J. Clim., 21, 2883–2897, doi:10.1175/ 2007JCLI1776.1.
Lee, J. N., Shindell, D.T., Hameed, S., 2009. The influence of solar forcing on tropical circulation. J. Clim., 22, 5870–5885, doi:10.1175/2009JCLI2670.1.
Chunzai Wang., 2002. ENSO and Atmospheric circulation cells. CLIVAR Exchanges. 7, 2, 9-11.
Gastineau, Guillaume., Li, Laurent., Le Treut, Hervé., 2009. The Hadley and Walker circulation changes in global warming conditions described by idealized atmospheric simulations. J. Clim., 22, 14, 3993-4013.
Bronnimann, S., Ewen, T., Griesser, T., Jenne, R., 2006. Multidecadal signal of solar variability in the upper troposphere during the 20th century. Space Sci. Rev., 125, 305-317.
Fleagle, Rabert, G., Joost, A. Businger., 1980. An Introduction to atmospheric physics. Second edition, Acadamic Press.
Simmons, A.J., Willett, K.M., Jones, P.D., Thorne, P.W., Dee, D.P., 2010. Low-frequency variations in surface atmospheric humidity, temperature, and precipitation inferences from re-analyses and monthly grided observational data. J. Geophys.Res. 115, D01110, http://dx.doi.org/10.1029/2009JD012442.
Trenberth, Kevin E., 1997. The Definition of El Niño. Bull. Amer. Meteor. Soc. 78, 12, 2771-2777., 10.1175/1520-0477(1997)0782.0.CO;2
VenkatRatnam M., Venkateswara Rao. N., Vedavathi, C., Krishna Murthy. B.V., VijayaBhaskara Rao, S., 2014. Diurnal tide in the low-latitude troposphere and stratosphere: Long-term trends and role of the extended solar minimum. J. Atmos. Sol. Terr. Phy., http://dx.doi.org/10.1016/j.jastp.2014.06.0.04.
Roy.I, Haigh, J., 2012. Solar Cycle Signals in the Pacific and the Issue of Timings, J. Atmos. Sci., 69, 1446-1451, doi: 10.1175/JAS-D-11-0277.1.
Bhattacharya., 2011. Longer duration solar cycle with lesser number of SSN causes low heating of earth. Inter. J. Eng. Sci. and Tech. 3, 8012-8017.
Jagannadha Rao, V. V. M., Narendra Babu, A., VijayaBhaskara Rao, S., Narayana Rao, D., 2007. Anomalous wind circulation observed during 1997/98 ElNino using Indian MST Radar. J. Appl. Meteorol. Clima., 46, 112-119.
Jagannadha Rao, V.V.M., Narayana Rao, D., VenkatRatnam, M., Mohan, K., VijayaBhaskar Rao, S., 2003. Mean Vertical Velocities Measured by Indian MST Radar and Comparison with Indirectly Computed Values. J. App. Meteo., 42 (4), 541-552.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241821EnglishN-0001November30HealthcarePROGRESSIVE MASSIVE FIBROSIS IN A CASE OF SILICOSIS- A CASE REPORT
English4750Vishnukanth GovindarajEnglish Ravindrachary MulkojuEnglish BallaNagamalli KumarEnglish Vishal Kumar ChitkeshiEnglish Adimulam Ganga RavindraEnglishAim: Silicosis also known as potters rot is the most common occupational lung disease. People employed in occupations like sandblasting, surface drilling, tunneling, silica flour milling, ceramic making are predisposed to developing silicosis. We report a case of progressive massive fibrosis secondary to silicosis in a stone quarry worker.
Case Report: A forty five year old stone quarry worker presented with chronic dry cough and breathlessness. His chest CT showed presence of multiple calcified mediastinal lymphnodes with irregular mass like areas. Based on the occupational exposure and radiographic images, a diagnosis of progressive massive fibrosis due to silicosis was made.
Discussion: Pneumoconiosis is group of lung diseases related to occupational exposure to inhaled dust. The most common among pneumoconiosis is silicosis. Based on the amount and duration of exposure the clinical and radiological features of silicosis vary. Progressive massive fibrosis is a potentially fatal stage in complicated silicosis. In a majority of cases, a positive occupational history and radiological features are sufficient to make a diagnosis.
Conclusion: There is no specific treatment for silicosis. Avoidance of further exposure, using personal protective measures, periodic medical checkup and strict legislations to protect employees and a system to check compliance should be ensued.
EnglishProgressive massive fibrosis, Silica dustINTRODUCTION:
Progressive Massive Fibrosis(PMF) is a potentially fatal and debilitating occupational hazard occurring in persons working in respirable dust industries1. This condition most commonly occurs in association with occupational lung diseases like coal workers pneumoconiosis and silicosis. We report a patient with progressive massive fibrosis secondary to silicosis. The diagnosis was established by occupational history and radiological features.
CASE DESCRIPTION:
A forty five year old man presented with symptoms of dry cough and breathlessness on exertion of six months duration. He was not a smoker and had no previous history of tuberculosis. He had worked in a stone quarry for twenty years and had no co morbid illness. On examination his vitals were stable. On Respiratory examination there were bilateral scattered crepts . His chest x ray(fig 1)showed diffuse reticulonodular opacities and multiple mass-like symmetrical lesions with irregular margins in the hilar region bilaterally. High resolution computed tomography (HRCT) of chest revealed presence of multiple calcified mediastinal lymphnodes with irregular mass likes areas in the bilateral upper and left lower lobe predominately in the hilar and peri hilar region . Few specks of calcification were noted within the lesion. There were also multiple nodules of varying sizes with centrilobular and perilymphatic distribution.(fig2,3) Imaging, supported by occupational history was suggestive of progressive massive fibrosis (PMF) due to silicosis. The patient is currently on symptomatic management and has not worsened till the last contact.
DISCUSSION:
Silicosis also known as “potters rot” is an important occupational lung disease caused by inhalation of crystalline silica. Silicon is abundant in nature as free silica in combination with oxygen(quartz) or as silicates in combination with oxygen and other elements. Silicon contributes to about 28% of the earth's crust and a major part exists in quartz form2 . The sand stone industry, stone quarrying and dressing, granite industry, grinding of metals, sand blasting, iron and steel foundries, silica milling, flint crushing and manufacture of abrasive soaps are some of the occupations related to silica exposure. Slate pencil industry and agate grinding industry which are peculiar to India carry a high risk of silicosis2-4. Crystallinesilica is classified as a group 1 substance by the InternationalAgency for Research on cancer5.
Silicosis has affected humans since ages. In 1705, Ramazzini cited Diembrock's description of the lungs of stonecutters who possibly had silicosis6. The term silicosis was coined by Visconti in 18707. Though occurring since ages, due to industrialization and mechanized mining, the prevalence of silicosis has increased alarmingly in the twentieth century. In 2007, the U.S. Occupational Safety and Health Administration (OSHA) estimated that more than two million employees are exposed to silica in general industry, construction, and maritime industry8. Epidemiological studies on silicosis in India has shown varied prevalence ranging from 3.5% in ordnance factory to 54.6% in slate pencil industry.4
The primary pathology in silicosis is the formation of silicotic nodules. The inhaled silica particle are engulfed by the alveolar macrophages. However they are unable to digest the material. The silica particle in the macrophages damages the lysosomal membranes of the alveoli which triggers the release of proteolytic enzymes into the cytoplasm leading to death of the macrophage. Continued exposure results in an alteration of the macrophage function. Release of inflammatory cytokines like interleukin 1, free radicals and growth factors follows which stimulates collagen synthesis and production of antibodies against collagen. These anticollagen antibodies stimulate fibroblasts to then produce more collagen which eventually leads to silicotic nodule formation3,9.
Based on the amount, duration of exposure and onset of symptoms, silicosis can be classified as acute silicosis , chronic silicosis and accelerated silicosis. "Chronic simple silicosis", the commonest form, develops after long term exposure usually 10-30 years to smaller amounts of silica dust. "Accelerated silicosis" develops 5-10 years after exposure and progresses rapidly with a higher risk of complicated disease. "Acute silicosis" also called Silicoproteinosis develops a few weeks to 5 years after exposure to high concentration of silica dust.Acute silicosis progresses rapidly to respiratory failure and death. Whensevere scarring leads to confluence of small nodulesinto a larger lesion with more severe symptoms andrespiratory impairment, it is termed as "Complicatedsilicosis". It is more common in accelerated type thanwith the chronic variety10.
Majority of the patients present in chronic silicotic stage. Even in the presence of advanced radiological lesions, patients are asymptomatic.The most common symptom is dyspnoea on exertion .The severity of dyspnoea increases with progress of the disease. Cough is associated with minimal expectoration in the initial stages and the productivity increases as the disease advances. Chest pain and haemoptysis indicate the possibility of complication like tuberculosis. In late stages corpulmonale results. Silicosis may be complicated with other lung diseases including lung cancer and autoimmune diseases. Patients with silicosis are more susceptible to developing pulmonary tuberculosis, "silicotuberculosis"6. Patients with silicosis are also prone to develop repeated Infections, chronic obstructive pulmonary disease and tracheobronchial compression by enlarged mediastinal lymphnodes. Pleural involvement in silicosis is rare. Few instances of bilateral pneumothorax has been reported3.
Radiological lesions vary in different types of silicosis. On HRCT thorax, multiple bilateral centrilobular opacities, multifocal patchy ground-glass opacities, and consolidation with occasional crazy paving characterize acute silicosis. Chest x ray of patients with chronic simple silicosis shows the presence of multiple small nodules, 2-5 mm in diameter with associated calcifications. These nodules have a upper lobe predominance. HRCT in chronic simple silicosis shows perilymphatic distribution of nodules in centrilobular, paraseptal, and subpleural regions. Hilar and mediastinal lymphadenopathy may precede the parenchymal lesions. Eggshell pattern calcification of lymph nodes is common. Complicated silicosis, also known as progressive massive fibrosis, develops with confluence of individual silicotic nodules. On CT scan , PMF appears as focal soft-tissue masses, usually measuring more than 1 cm in diameter, with irregular margins, calcification, and involving apical and posterior segments of the upper lobes, surrounded by areas of emphysematous changes. With advancing fibrosis, these opacitiesmigrate towards hila with resultant paracicatricial emphysema. In silicosis associated with tuberculosis(silicotuberculosis) the radiological picture incudes asymmetric nodules or consolidation, cavitation and a rapid disease progression11,12.
Silicosis is usually diagnosed by eliciting a positive occupational exposure history. A positive occupational history with radiological features of silicosis is sufficient to make a diagnosis of silicosis. Lung biopsy is rarely required. Lung biopsy may show the presence of silicotic nodules. A typical silicotic nodule has the following characteristics; a central zone with whorls of dense, hyalinized fibrous tissue, a midzone with concentrically arranged collagen fibers and an outer zone with randomly orientated collagen fibers mixed with dust-loaded macrophages and lymphoid cells9. Patients of silicosis should be screened for tuberculosis6.
There is no specific treatment for silicosis. Avoidance of further exposure is the first step in treatment. Only a few treatment options are available and they are mostly for symptomatic management. Bronchodilators and corticosteroid therapy may be useful13,14. N-Acetyl cysteine has shown reduction in lung fibrosis in silica exposed rats15.Lung transplant has been an option for end-stage disease treatment. However, logistic reasons prevent advising lung transplant for all patients. It should be remembered that silicosis is a completely preventable disease. Education to workers , use of personal protective equipment and periodic medical screening should be made compulsorily. If PMF is diagnosed the person should immediately cease work in the industry. Strict legislations to protect employees and a system to check compliance should be ensued.
CONCLUSION:
Silicosis is a common occupational disease which can present even after cessation of exposure. Majority of the patients can be diagnosed by eliciting a proper occupational exposure history. There is no specific treatment. Strict legislations with regard to using personal protective equipment in the occupational area and a periodic health check up for the employees is the need of the hour. In countries with high incidence of Tuberculosis, possibility of silico tuberculosis should always be considered.
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.
SOURCE OF FUNDING: NONE
CONFLICT OF INTEREST: NONE
Englishhttp://ijcrr.com/abstract.php?article_id=176http://ijcrr.com/article_html.php?did=176
Progressive massive fibrosis. www2.isu.edu/radsci/papers14/05_2014. Accessed on 01/05/2016 at 23:00 hrs.
G.K.Kulkarni. Prevention and control of silicosis- a national challenge.Indian J Occup Environ Med. 2007 11(3): 95–96.
Mishra P, Jacob SE, Basu D, Panigrahi MK, Govindaraj V. Bilateral spontaneous pneumothorax in chronic silicosis: a case report. Case Reports in Pathology. 2014;2014:561861-561861.
Silicosis - An Uncommonly Diagnosed Common Occupational Disease.icmr bulletin 1999;29(9).
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, Silica, Some Silicates, Coal Dust and Para-Aramid Fibrils, vol. 68, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Lyon, France, 1997.
MY Ali, SA Alam, F Fattah, MT Ahmed, SS Parveen, M Royesuddin, MN Ahmed, SY Ali. Silicosis - A Case Report. Faridpur Med. Coll. J. 2010;5(2):69-71.
Basil Varkey.http://emedicine.medscape.com/article/302027-overview.Published dec 2015. Date accessed 01/05/2016.
Carson R. Thomas and Timothy R. Kelley. A Brief Review of Silicosis in the United States. Environmental Health Insights 2010:4 21–26
Brooke T. Moosman, Andrew Churg. Mechanisms in the Pathogenesis ofAsbestosis and Silicosis.Am J Respir Crit Care Med1998; 157(5) 1666-1680.
Vincent Castranova, Val Vallyathan. Silicosis and Coal Workers' Pneumoconiosis. Environmental Health Perspectives; Vol 108, Supplement2000 Aug;pg.675-684.
Satija B, Kumar S, Ojha UC, Gothi D. Spectrum of high resolution computed tomography imaging in occupational lung disease. Indian J Radiol Imaging 2013;23:287-96.
Angela santos Ferreira, Valeria barbosa Moreira. Progressive massive fibrosis in silica-exposed workers.High-resolution computed tomography findings. J Bras Pneumol. 2006;32(6):523-8
Goodman GB, Kaplan PD, Stachura I, Castranova V, Pailes WH, Lapp NL. Acute silicosis responding to corticosteroid therapy. Chest. 1992; 101(2):366-70.
Sharma SK, Pande JN, Verma K. Effect of prednisolone in treatment in chronic silicosis. Am Rev Respir Dis 1991; 143:814-21.
Zhang L, He YL.N-acetylcysteine alleviated silica-induced lung fibrosis in rats by down-regulation of ROS and mitochondrial apoptosis signaling. Toxicol Mech Methods.2014 Mar;24(3):212-9.