Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30General SciencesFUNCTIONAL PERFORMANCE OF STATE COMMISSIONS - A COMPARATIVE ANALYSIS
English0106M. ManoharanEnglish M. Anto AuxcelianEnglishBackround: In India consumer protection has gained momentum especially after independence and the enactments of many acts benefited to the consumers from exploitation from unfair trade practices. Consumer protection can also be asserted by many ways like government and non government organizations. Technological advancement throughout the globe especially after the institution of multi national companies had widened the gap between the manufacturers and consumers in all disciplines.
Need of Study: To evaluate the products and services he needs expert knowledge, which is usually beyond his capability. As per current scenario, there is no reliable agency to provide true and fair information. The Government of India realizing the need of consumer protection and eliminating consumer exploitation enacted many acts and the most important one for the consumers is the Consumer Protection Act 1986 which was exclusively designed to redress the grievances of the consumers by establishing three tier quasi judicial redressal machineries at the central, state and district level.
Analysis: In this paper the researcher has made an attempt to analyze the working performance of Tamil Nadu, Andhra Pradesh and Puducherry UT consumer disputes redressal commissions The performance of these commissions are analyzed in terms
of disposal of original complaints, rate of pendency, and filing of cases with some meaningful suggestions for qualitative and quantitative enhancement in its performance. Conclusion: From the analysis under study, it is observed that the overall disposal rate of Andra Pradesh state commission is much better when compared to the other two commissions
EnglishConsumer protection, Consumer disputes redressal commissions, Consumer exploitationINTRODUCTION
The Consumer Protection Act 1986 was a milestone in the consumer protection movement in the country. It has been enacted with a view to provide simple, speedy and inexpensive remedy to consumers and save them from unscrupulous traders and service providers. Accordingly three tier quasi judicial redressal machineries have been set up at the District, State and National levels to defend the legitimate rights of consumers provided under the act. They are adjudicatory bodies formed exclusively for the consumers where disputes are heard and decisions are made legally. If any consumer having grievances can file a complaint in the District forum for the value up to Rs twenty lakhs, State commission for the value more than Rs twenty lakhs to one crore and National commission for the value above Rs one crore in respects of deficiency in services and defects in goods. This study is all about two state commissions and one Union Territory consumer disputes redressal commission. Structure of State consumer disputes redressal machinery The Consumer Protection Act 1986 prescribes the establishment of three tier Consumer Disputes Redressal Adjudicatory Bodies. It provides that the state government shall establish a District Consumer Disputes Redressal Forum (DCDRF) for each district and State Consumer Disputes Redressal Commission (SCDRC) for the state. A National Consumer Disputes Redressal Commission (NCDRC) shall also be established by the central government. The State Commission is the second in the hierarchy of the three tier quasi judicial system. The state commission will consist of a president, who shall be a sitting or retired judge of High court and shall consist of two members one of whom shall be a woman. The state commission can entertain the complaints where the total claim exceeds 20 lakhs but does not exceed 1 crore and it adjudicates original, appeal and revision petitions. The order of any State Commission can be appealed to the National Commission within one month. Any appeal against the order of the District forum can be filed to state commission within thirty days of the order of the District forum. The complaints should be filed in the above forums within two years from the date of occurrence of event. The complainant can file and conduct the case directly himself in the forums without the need of legal experts. The cases should be decided within 90 days or 150 days if testing of goods of dubious quality is essential from the date of receipt of notice by the respondent. Principle of natural justice is followed in adjudication and the order of the forums should be of the majority of members. Need for the study: The Consumer Protection Act merely provides separate enforcement machinery with the aim of giving consumers a simple and expeditious solution to consumer problems. State commissions being the middle in the hierarchy, instituted almost all the states. This study was undertaken to analyze at what extent the state commissions disposed the original cases speedily to protect the interests of aggrieved consumers. Further the analysis of the performance of the state commissions would help us to find out the problems which are affecting their progress and we can suggest some appropriate measures to improve its performance. Hence the present study has been undertaken. The present paper aims at achieving the following objectives 1. To analyze the working performance of selected state consumer disputes redressal commissions. 2. To analyze the trend growth and magnitude of variability of number of cases filed,disposed and pending in the state commissions during the period under study and 3. To find out the gap between cases filed and disposed and suggest suitable measures for their betterment
METHODOLOGY OF THE STUDY
The present study is made only with the secondary data sources. The secondary data has been collected from three commissions for a period of 10 years that is from 2001 to 2010. Besides various articles published in different books, journals and websites are also referred for the study.
STATISTICAL METHODS
The secondary data was analyzed by using appropriate statistical techniques such as mean, simple percentages and regression analysis. Mean and simple percentages are used to find out the tendency of cases filed, disposed and pending during the study period. To study the growth rate with regard to number of cases pending, cases filed cases for disposal and cases disposed compound growth rate has been calculated using semi log or exponential function. Co-efficient of variation is used to find out the magnitude of variability in number of cases filed, disposed and pending during the study period.
ANALYSIS AND INTERPRETATION
The working performance of State Consumer Disputes Redressal Commissions of Tamilnadu, Andra Pradesh and Puducherry Union Territory are analyzed and presented hereunder
I. Case Disposal History of Tamil Nadu SCDR
It is revealed that averages of 663 cases were there in the SCDRC of Tamil Nadu and out of which 124 cases were disposed constituting 18 per cent. The pending cases which were 847 in 2001 got reduced to 359 in 2010. However, the filing of the cases had a fluctuating trend and the rate of disposal of cases also is not encouraging. In general the performance of SCDRC of Tamil Nadu has to improve its performance in terms of disposal of cases. The trend of cases pending in the beginning in Tamil Nadu SCDRC is negative and statistically significant at one per cent level. It implies that there is a significant decrease in the cases pending at the rate of 14.29 per cent per annum. The cases filed are negative and significant at five per cent level. It indicates that the cases filed had declined at the rate of 15.08 per cent per annum. The cases for disposal are negative and statistically significant at one per cent level that indicates a significant decrease at the rate of 14.29 per cent per annum. The trend of cases disposed is negative and significant at five per cent level. It shows that there is a significant decrease in cases disposed and it had declined at the rate of 25.31 per cent per annum during the study period. The analysis shows that there is 74.55 per cent variation in cases disposed of which shows a high degree of inconsistency. The trend of cases pending at the end is negative and significant at five per cent level. It indicates that there is a significant decrease in the cases pending at the end of the year at the rate of 12.72 per cent per annum. The pendency level decreases due to decrease in cases filed and not due to more cases disposed. This does not mean there was no consumer rights violations, but consumers were not forthcoming to approach the commissions fearing a long legal wrangle. The non attendance and frequent boycott of advocates during hearings and having untrained assistants are the other reasons for the slow disposal of cases.
II. Case Disposal History of Andra Pradesh SCDRC
It is revealed that the performance of the SCDRC of Andra Pradesh is encouraging. It is inferred that an average of 403 cases were there in the SCDRC of Andra Pradesh and of which 139 cases constituting 34 per cent were disposed. The rate of disposal of cases was consistent throughout the period of study. The pending cases which were 625 in 2001 cleared gradually and the same was 152 in the year 2010.In general the performance of Andra Pradesh state commission is moderate. It is found that that the cases pending in the beginning is negative and statistically significant at one per cent level. It indicates that there is a significant decrease in the pending cases at the rate of 19.12 per cent per annum. It had the highest co-efficient variation of 53.73 per cent which indicates a high degree of volatility in pending cases at the beginning. The cases filed in Andra Pradesh SCDRC are negative but not significant. It shows that there is no significant decrease in cases filed during the study period. The trend of cases for disposal is negative and statistically significant at one percent level. It indicates that the cases for disposal had declined at the rate of 13.76 per cent per annum. The magnitude of variability in cases for disposal is 47.72 per cent. The trend of cases disposed is negative and significant at five per cent level which discloses that there is a significant decrease in cases disposed at the rate of 12.46 per cent per annum. The cases pending at the end is also negative and significant at one per cent level. The analysis reveals that there is a significant decrease in cases pending at the end at the rate of 14.29 per cent per annum. Even though there is a significant slackness in the number of cases disposed, the pendency level is not at increasing rate. The pendency goes down significantly due to the cases filed is at decreasing trend. The slackness in filing cases may be due to unawareness, less enthusiasm and delayed justice exhibited by the state commission. III. Case Disposal History of Puducherry UT CDRC It is revealed that that an average of 19 cases were there in the CDRC of Puducherry for disposal and out of this only 5 cases were disposed of. The pendency and disposal of cases in the CDRC of Puducherry is not much impressive. Being comparatively smaller in area, lesser in population and less number in pendency and also cases filed, the Union Territory of Puducherry CDRC could perform still better in the interests of the consumers. The pending cases in the beginning are negative but not significant. The trend of cases filed is positive but not significant. It indicates there is no significant increase in cases filed and it had increased at the rate of 0.93 per cent per annum. The cases for disposal are also negative but not significant. The trend of cases disposed is negative but not significant. It indicates that there is no significant decrease in cases disposed in Puducherry CDRC. It had the highest variation of 120.68 per cent which indicates the high degree of volatility in cases disposed. The cases pending at the end of the year is also negative but not significant. The pendency level is at decreasing rate since the cases filed is not encouraging and not due to much number of cases disposed. Absence of president and members and lengthy legal arguments may be the reasons for slow disposal.
RESULTS
1. In Tamil Nadu State Commission, on an average, 663 cases were there for disposal every year during the study period of which 124 cases were disposed of constituting 18 per cent of the filed cases settled annually and the remaining 82 percent were at pendency.
2. In Andra Pradesh State Commission, on an average, 403 cases were there for disposal every year during the study period of which 139 cases were disposed of constituting 34 per cent of the filed cases settled annually and the remaining 66 percent were at pendency.
3. In Puducherry Union Territory Redressal Commission, on an average, 19 cases were there for disposal every year during the study period of which 5 cases were disposed of constituting 23 per cent of the filed cases settled annually and the remaining 77 percent were at pendency.
DISCUSSION
On the basis of the above analysis, the following suggestions are recommended in order to strengthen the functioning of state commissions
1. The most important aspects in consumerism are speedy disposal of cases, minimizing the number of pendency of cases and creating awareness about filing of cases among the people and thereby effective steps to be taken up by the government to improve the performance in these aspects.
2. Efforts should be taken by the government to inspire awareness in the minds of consumers and to regularize these commissions by fixing at least minimum target of cases to be disposed each month in order to reduce pendency. The national commission should monitor this aspect more closely and ensure strict adherence.
3. Additional benches would be set up in state commission to reduce the pendency level
4. The time limitation to dispose the cases at each stages (numbering the case, serving summon, filing counter affidavit, arguments, pronouncement of judgment) to be well defined to the consumers to avoid unnecessary adjournment and dragging of the case.
5. The existing vacancies of appointment may be filled in time. Successors to the staff members or presidents or members of commissions who retire on definite date should be identified well in ad-vance to avoid delay in the appointment of president or members or staff members of these commissions. The Government may prepare a standby list in order to appoint them from the said list, immediately when vacancy arises.
CONCLUSION
From the analysis under study, it is observed that the overall disposal rate of Andra Pradesh state commission is much better when compared to the other two commissions. On the overall performance basis, the Andra Pradesh state commission may be assigned first rank in respect of disposal (34 per cent). It is followed by Puducherry UT Redressal Commission (23 per cent) and Tamil nadu state commission (18 per cent) respectively. In general, the working performance of these three commissions is not impressive. In case the suggestions given by the researcher if implemented, these commissions will strengthen further in redressal.
ACKNOWLEDGEMENT
Authors acknowledge the great help received from the scholars whose articles 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. Authors are grateful to IJCRR editorial board members and IJCRR team of reviewers who have helped to bring quality to this manuscript.
Englishhttp://ijcrr.com/abstract.php?article_id=595http://ijcrr.com/article_html.php?did=5951. Chahar.S.S,Consumer protection movement in India Problems and Prospects, Kanishka Publishers, New Delhi 2007
2. Sivaprakasam.P and Rajamohan.S,ConsumerEmpowerment-Rights and Responsibilities Kanishka Publishers, New Delhi 2001 3. Sundaram I.S Consumer Protection in India, Delhi, B.R Publishing Corporation 1985
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30HealthcareMINIMAL ADENOCARCINOMA IN PROSTATE NEEDLE BIOPSY TISSUE: IMMUNOHISTOCHEMICAL STUDY
English0714Hayam E. RashedEnglish Abdelmonem A. HegazyEnglish Ragab A. AhmedEnglishBackground: Diagnosis of small foci of prostate cancer in a core biopsy is one of the major diagnostic challenges. Immunohistochemistry plays an important role in the diagnosis of minimal prostate cancer and to exclude the benign lesions. The α-methylacyl CoA racemase (AMACR) and p63 have been used for such purpose.
Aim of work: To investigate which basal cell marker; 34βE12 or p63 should be the first choice used with AMACR to increase diagnostic accuracy of minimal prostate cancer in core biopsy, in a trial to reduce the errors in diagnosis and to decrease the need for repeated biopsies.
Methods: Sections from formalin-fixed paraffin-embedded tissues of 60 prostate needle biopsy specimens were stained immunohistochemically with 34βE12, p63, Ki-67 and AMACR.
Results: AMACR was expressed in 90% of minimal prostatic carcinoma. Nuclei of basal cells in 90% of normal glands were stained for p63. Regarding 34βE12, all benign subjects showed linear cytoplasmic basal staining. 34βE12 had very high sensitivity and specificity values (96.3% and 100%, respectively), followed by p63 (97.9% and 85.3%). There were significant differences in cytoplasmic p63 expression between benign tissue and prostate cancer, and between low and high grade carcinoma (P EnglishProstate, Minimal adenocarcinoma, AMACR, p63, 34?E12, ImmunohistochemistryINTRODUCTION
There is an increase in use of prostate needle biopsies, due to increased awareness and the widespread use of serum prostate specific antigen (PSA) as a mass screening test along with imaging studies for prostate cancer. The histopathologic interpretation of such biopsies remains the single most important tool for establishing a diagnosis of prostate cancer (1). The accurate diagnosis is of great importance for early detection of malignancy. This directs the line of management of patients towards a lesser invasive procedure instead of more radical one associated with significant morbidity and mortality (2). Thus the pathologist is faced with an increasing number of prostate needle biopsies with a limited number of well-differentiated or limited numbers of malignant glands which has been problematic with increased false negative results. Also a typical small acinar proliferation that are suspicious for carcinoma may be found in up to 9.0% of all prostate biopsies, in which up to 59% are found to be malignant after using immunohistochemical markers (3,4). The diagnosis of prostatic adenocarcinoma, especially in needle biopsy samples may be difficult either due to presence of small foci (limited ≤1mm carcinoma in needle tissue), or the difficulty in distinguishing prostatic carcinoma from benign mimickers (5).INTRODUCTION There is an increase in use of prostate needle biopsies, due to increased awareness and the widespread use of serum prostate specific antigen (PSA) as a mass screening test along with imaging studies for prostate cancer. The histopathologic interpretation of such biopsies remains the single most important tool for establishing a diagnosis of prostate cancer (1). The accurate diagnosis is of great importance for early detection of malignancy. This directs the line of management of patients towards a lesser invasive procedure instead of more radical one associated with significant morbidity and mortality (2). Thus the pathologist is faced with an increasing number of prostate needle biopsies with a limited number of well-differentiated or limited numbers of malignant glands which has been problematic with increased false negative results. Also a typical small acinar proliferation that are suspicious for carcinoma may be found in up to 9.0% of all prostate biopsies, in which up to 59% are found to be malignant after using immunohistochemical markers (3,4). The diagnosis of prostatic adenocarcinoma, especially in needle biopsy samples may be difficult either due to presence of small foci (limited ≤1mm carcinoma in needle tissue), or the difficulty in distinguishing prostatic carcinoma from benign mimickers (5).
Considering the fact that the loss of basal cell layer is a hallmark of prostate adenocarcinoma, the basal cell markers can help to differentiate prostate adenocarcinoma from cancer mimickers (6). In this respect, there are several basal cell markers, such as high-molecular weight cytokeratin 34βE12 and p63 which belong to the family of transcription factors that also includes p53. Prostate requires p63 expression for its development. It is expressed in myoepithelial cells surrounding normal acinar glands. Therefore, p63 is used to evaluate the presence of normal basal cells thus distinguishing between benign and malignant glands (7). AMACR also known as P504S, has been reported as a new potential prostatic adenocarcinoma specific marker. It is a mitochondrial and peroxisomal enzyme involved in the beta-oxidation of branched fatty acids and bile acid intermediates (4). A previous study showed that AMACR and p63 were used to confirm or rule out diagnosis of small focal prostatic carcinoma in limited biopsy materials (8). In this study, we aimed to investigate which basal cell marker; 34βE12 or p63 may be used with AMACR to increase diagnostic accuracy; and to emphasize the importance of cytoplasmic p63 expression in prostate cancer progression. This was a trial to reduce the errors in diagnosis and to decrease the need for repeated biopsies.
PATIENTS AND METHODS
Patients and tissue Specimens
A total of 60 prostate needle biopsy specimens including 30 cases of prostate needle biopsy with small foci (≤ 1 mm or less than 5% of needle core tissue) of prostatic adenocarcinoma and 30 benign prostates’ tissues as a control were obtained and diagnosed at Urology and Pathology departments, Faculty of Medicine, Zagazig University, Egypt, during the period from February 2012 to July 2014. Informed consent was obtained from each patient and the study was approved by the local ethics committee. Tissue specimens were fixed in 10% buffered formalin and embedded in paraffin. Consecutive 4 µm sections were prepared and stained with hematoxylin and eosin (H and E) for histopathological examination, the diagnosis of prostate cancer was established from examination of H and E-stained sections and was confirmed by absence of basal cell staining and/or positivity for AMACR (P504S) (4). The Gleason histopathologic grading was done based on the histologic pattern of arrangement of carcinoma cells in H and E-stained prostatic tissue sections. The study complied with the guidelines of the local ethics committee.
Immunohistochemistry
Immunohistochemical staining was carried out using streptoavidin-biotin immunoperoxidase technique. 3–5 µm thick sections were cut from formalin-fixed, paraffin-embedded blocks and mounted on positive charged slides. They were deparaffinized in xylene and rehydrated in graded alcohol. The mounted sections were immersed and boiled in a ready to use Dako target retrieval solution (PH 6.0) for 20 min, and then washed in phosphate buffer saline (PBS). Thereafter, blocking of endogenous peroxidase activity with 6% H2O2 in methanol was carried out. The slides were then incubated over night using a polyclonal anti-AMACR antibody (1:200 dilution; Dako, Glostrup, Denmark), a mouse monoclonal antibody (34βE12, 1:100 Dako, Glostrup, Denmark), Ki-67 antibody (clone MIB-1, 1:50 dilution; Dako, Glostrup, Denmark) and incubated with a 1:50 dilution of the 4A4 mouse monoclonal antibody (IgG2a, kappa, Dako, Glostrup, Denmark), which binds to all isoforms of p63. Incubation with a secondary antibody and product visualization were performed (Dako, Glostrup, Denmark) with diaminobenzidine substrate as the chromogen. The slides were finally counterstained with Mayer’s haematoxylin, and washed with distilled water and PBS. Squamous cell carcinoma was used as positive control for 34βE12 and P63. Human tonsillar tissue and prostate cancer were used as positive controls for KI67 and AMACR respectively. Staining procedure included negative controls. They were obtained by substitution of primary antibodies with blocking buffer.
Immunohistochemical Evaluation
The percentage of glands (extensiveness) that stained for the immunohistochemical markers (AMACR, 34βE12 and nuclear P63) was evaluated as follows: negative, 90% (9). The intensity of the 34βE12 and P63 was classified as negative, weak, moderate, and strong (10). AMACR staining intensity was graded as negative, weak (weak nongranular cytoplasmic staining), moderate (granular staining with weak or moderate intensity), and strong (granular staining with strong intensity) (11). For p63 cytoplasmic expression, percent of positively stained cells is scored from 0% to 100% in 5 fields of views. Low p63 expression was considered Englishhttp://ijcrr.com/abstract.php?article_id=596http://ijcrr.com/article_html.php?did=5961. Herawi M, Parwani AV, Irie J, Epstein JI. Small Glandular Proliferations on Needle Biopsies, Most Common Benign Mimickers of Prostatic Adenocarcinoma Sent in for Expert Second Opinion. Am J Surg Pathol 2005;29(7):874-880.
2. Singh V, Manu V, Malik A, Dutta V, Mani NS, Patrikar S,. Diagnostic utility of p63 and α-methyl acyl Co A racemase in resolving suspicious foci in prostatic needle biopsy and transurethral resection of prostate specimens. J Cancer Res Ther 2014;10(3):686-692.
3. Iczkowski KA, Chen HM, Yang XJ, Beach RA. Prostate cancer diagnosed after initial biopsy with atypical small acinar proliferation suspicious for malignancy is similar to cancer found on initial biopsy. Urology 2002;60(5):851-854.
4. Molinié V, Hervé JM, Lugagne PM, Lebret T, Botto H. Diagnostic utility of a p63/α-methyl coenzyme A racemase (p504s) cocktail in ambiguous lesions of the prostate upon needle biopsy. BJU Int 2006;97(5):1109-1115.
5. Hameed O, Humphrey PA. Immunohistochemistry in the diagnosis of minimal prostate cancer. Diagnostic Histopathology 2006;12(4):279-291.
6. Kalantari MR, Anvari K, Jabbari H, Tabrizi FV. p63 is more sensitive and specific than 34βE12 to differentiate adenocarcinoma of prostate from cancer mimickers. Iran J Basic Med Sci. 2014;17(7):497-501.
7. Hameed O, Sublett J, Humphrey PA. Immunohistochemical stains for p63 and alpha-methylacyl-CoA racemase, versus a cocktail comprising both, in the diagnosis of prostatic carcinoma: a comparison of the immunohistochemical staining of 430 foci in radical prostatectomy and needle biopsy tissues, Am J Surg Pathol 2005;29(5):579-587.
8. Rashed EH, Kateb MI, Ragab AA, Shaker SS. Evaluation of minimal prostate cancer in needle biopsy specimens using AMACR (P504S), P63 and KI67. Life Sci J 2012;9(4):12-21
9. Abrahams NA, Ormsby AH, Brainard J. Validation of cytokeratin 5/6 as an effective substitute for keratin 903 in the differentiation of benign from malignant glands in prostate needle biopsies. Histopathology 2002;41(1):35- 41.
10. Shah RB, Zhou M, LeBlanc M, Snyder M, Rubin MA. Comparison of the basal cell-specific markers, 34βE12, and p63, in the diagnosis of prostate. Am J Surg Pathol 2002;26(9):1161-1168.
11. Zhou M, Aydin H, Kanane H, Epstein JI. How often does α-methylacyl-CoA-racemase contribute to resolving an atypical diagnosis on prostate needle biopsy beyond that provided by basal cell markers? Am J Surg Pathol 2004;28(2):239-243.
12. Dhillon PK, Barry M, Stampfer MJ, Perner S, Fiorentino M, Fornari A, et al. Aberrant cytoplasmic expression of p63 and prostate cancer mortality. Cancer Epidemiol Biomarkers Prev 2009;18(2):595-600.
13. Jiang Z, Woda BA, Rock KL, Xu Y, Savas L, Khan A, et al. P504S: a new molecular marker for the detection of prostate carcinoma. Am J Surg Pathol 2001;25(11):1397-1404.
14. Yang XJ, Wu CL, Woda BA, Dresser K, Tretiakova M, Fanger GR, et al. Expression of alphamethylacyl-CoA racemase (P504S) in atypical adenomatous hyperplasia of the prostate. Am J Surg Pathol 2002;26(7):921-925
15. Martens MB., Keller JH. Routine immunohistochemical staining for high-molecular weight cytokeratin 34βE12 and α-methylacyl CoA racemase (P504S) in postirradiation prostate biopsies. Modern Pathology 2006;19: 287-290.
16. Rubin MA, Zhou M, Dhanasekaran SM, Varambally S, Barrette TR, Sanda MG, et al. Alphamethylacyl coenzyme A racemase as a tissue biomarker for prostate cancer. JAMA 2002;287(13):1662-1670.
17. Jiang Z, Wu CL, Woda BA, Dresser K, Xu J, Fanger GR, et al. P504S/alphamethylacyl-CoA racemase: a useful marker for diagnosis of small foci of prostatic carcinoma on needle biopsy. Am J Surg Pathol 2002;26(9):1169-1174.
18. Beach R, Gown AM, De Peralta-Venturina MN, Folpe AL, Yaziji H, Salles PG, et al. P504S immunohistochemical detection in 405 prostatic specimens including 376 18-gauge needle biopsies. Am J Surg Pathol 2002;26(12):1588- 1596.
19. Boran C, Kandirali E, Yilmaz F, Serin E, Akyol M. Reliability of the 34βE12, keratin 5/6, p63, bcl-2, and AMACR in the diagnosis of prostate carcinoma. Urol Oncol 2011;29(6):614-623.
20. Farinola MA, Epstein JI. Utility of immunohistochemistry for alpha-methylacyl-CoA racemase in distinguishing atrophic prostate cancer from benign atrophy. Hum Pathol 2004;35(10):1272-1278.
21. Zhou M, Jiang Z, Epstein JI. Expression and diagnostic utility of alpha-methylacyl-CoA-racemase (P504S) in foamy gland and pseudohyperplastic prostate cancer. Am J Surg Pathol 2003;27(6):772-778.
22. Kahane H, Sharp JW, Shuman GB, Dasilva G, Epstein JI. Utilization of high molecular weight cytokeratin on prostate needle biopsies in an independent laboratory. Urology 1995;45(6):981- 986.
23. Signoretti S, Waltregny D, Dilks J, Isaac B, Lin D, Garraway L, et al. p63 is a prostate basal cell marker and is required for prostate development. Am J Pathol 2000;157(6):1769- 1775
24. Varma M, Linden MD, Amin MB. Effect of formalin fixation and epitope retrieval techniques on antibody 34betaE12 immunostaining of prostatic tissues. Mod Pathol 1999;12(5):472-478.
25. Lo Muzio L, Santarelli A, Caltabiano R, Rubini C, Pieramici T, Trevisiol L, et al. p63 overexpression associates with poor prognosis in head and neck squamous cell carcinoma. Hum Pathol 2005;36(2):187-194.
26. Marchini S, Marabese M, Marrazzo E, Mariani P, Cattaneo D, Fossati R, et al. DeltaNp63 expression is associated with poor survival in ovarian cancer. Ann Oncol 2008;19(3):501- 507.
27. Bismar TA, Demichelis F, Riva A, Kim R, Varambally S, He L, et al. Defining aggressive prostate cancer using a 12-gene model. Neoplasia 2006;8(1):59-68.
28. Mucci LA, Pawitan Y, Demichelis F, Fall K, Stark JR, Adami HO, et al. Testing a multigene signature of prostate cancer death in the Swedish Watchful Waiting Cohort. Cancer Epidemiol Biomarkers Prev 2008;17(7):1682-1688.
29. Narahashi T, Niki T, Wang T, Goto A, Matsubara D, Funata N, et al. Cytoplasmic localization of p63 is associated with poor patient survival in lung adenocarcinoma. Histopathology 2006;49(4):349-357.
30. Ferronika P, Triningsih FX, Ghozali A, Moeljono A, Rahmayanti S, Shadrina AN, et al. p63 Cytoplasmic Aberrance is Associated with High Prostate Cancer Stem Cell Expression. Asian Pacific J Cancer Prev 2012;13(5):1943-1948.
31. Parsons JK, Gage WR, Nelson WG, De Marzo AM. p63 Protein expression is rare in prostate adenocarcinoma: Implications for cancer diagnosis and carcinogenesis. Urology 2001;58(4):619-624.
32. Reiner T, De las Pozas A, Parrondo R, Perez-Stable C. Progression of prostate cancer from a subset of p63-positive basal epithelial cells in FG/Tag transgenic mice. Mol Cancer Res, 2007;5(11):1171-1179.
33. Fabbro M, Henderson BR. Regulation of tumor suppressors by nuclear-cytoplasmic shuttling. Exp Cell Res 2003;282(2):59-69.
34. Boldrup L, Coates PJ, Gu X, Nylander K. DeltaNp63 isoforms regulate CD44 and keratins 4, 6, 14 and 19 in squamous cell carcinoma of head and neck. J Pathol 2007;213(4):384-391.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30HealthcareA STUDY OF FOOT DEFECTS, DEFORMITIES AND DISEASES AMONG SHOD AND BAREFOOT MIDDLE AND LONG DISTANCE RUNNERS- CROSS SECTIONAL STUDY
English1523Watson ArulsinghEnglish Ganesh S. PaiEnglishObjective: To compare foot defects, deformities and diseases in middle, long distance shod and barefoot Runners.
Method: 51 barefoot runners, 61 shod runners and 65 healthy controls were screened for foot defects, deformities and diseases in this study using validated clinical tools.
Results: Foot defects vary significantly among the three groups compared as p value was 0.001 showed high significance. When foot deformities are concerned, they vary significantly among the three groups compared as the p value was 0.001. Whereas foot diseases vary significantly among the three groups compared as p value was 0.001.
Conclusion: The analysis of this study revealed that the prevalence foot defects, deformities and diseases have been found to be highly significant among three groups.
EnglishTruncated navicular height, Hallux valgus, Foot infection, Corns, Ingrown toe nailINTRODUCTION
Millions of runners across world take to the streets, tracks and trails every day. People usually run for health, for fitness, for stress relief and for fun. Despite these differences, all runners are susceptible to foot problems. Common foot and ankle conditions in runners include blisters, foot fungus, heel pain, hallux valgus, rigidus, stress fracture and achilles tendonitis, ankle sprain, neuroma, ingrowing toe nail, black toe, plantar wart and burning foot, corns1,2,3. M.kuchi et al4 observed a significant morphological changes in foot between runners and non runners. Aydog et al5 who had explored the morphological features of foot between runners, wrestlers, weight lifters, hand ball, gymnasts players and non runners reported that arch index of foot had varied significantly between wrestlers ,soccer players, handball players, weightlifters, gymnasts, and non-athletic controls. Morimoto and Okada6 had found long distance runners to have lower dorsal arch than throwers, jumpers and sprinters. They had reasoned it to sports specific mechanical stress, the effects of overall body build for the differences observed in foot morphology between long distance runners and non-athletes. Bertrand 7 (2007) found increased occurrence of hallux valgus over time through his study on historical population in France. Researchers8,9,10 reported that athlete’s foot does not occur among people who traditionally go barefoot. They claimed that wearing shoes could facilitate this problem. Some experts believe that most athletic shoes with inflexible soles, structured sides and super-cushioned inserts keep feet so restricted that they may actually be making your feet lazy, weak and more prone to injury. Doud et al 11 reported out of prospective study that habitually rearfoot strike (shod) had approximately twice the rate of repetitive stress injuries than individuals who habitually forefoot strike (barefoot runners). They found hip pain, knee pain, low back pain, tibial stress injuries, plantar fasciitis, and stress fractures were 2.7 times more likely to occur in rearfoot strikers. Yet their study did not explain reason for this general difference. As a result, barefoot training is gaining more attention among coaches, personal trainers and runners. K. D’Aou et al12 stated that footwear that fails to respect natural foot shape and function will ultimately alter the morphology and the biomechanical behaviour of the foot. Till date there was not a study which has exclusively compared the occurrence of foot deformities, defects and diseases among barefoot and shod runners. Thus the purpose of this study to explore the occurrence of defects, deformities, diseases among shod and unshod long, and middle distance runners.
MATERIALS AND METHODS
Materials used in this study were stadiometer, vernier caliper, weighing scale, goniometer ruler and validated life size photographs of hallux valgus deformity and foot diseases, colour ink, graph sheets, colour marker, pencil, knee hammer, scientific calculator and magnifying glass, Sony camera 16 mega fixal(10 optical zoom) 51 barefoot runners, 65 controls and 61 shod endurance runners overall 177 participants were screened for foot defects, deformities and diseases who fit into inclusion criteria across Dakshina kannda district, Karnataka. Alva’s institutional review board ethical approval was obtained. CTRI registration was done (CTRI/2013/06/003776Medical). Adult long, middle distance shod and barefoot runners with minimum three years of participation and age group between 18 to 55 years and controls of same age group were included. Both genders were included. Individual with congenital deformities of foot, trauma in the feet other than sports related, systemic disease affecting lower limb, having a history of diabetic, gout and any other neurologically affected foot were excluded. Screened foot defects were black toenail, thick toenail, Bunions, neuromas, march fracture, jones fracture. tarsal tunnel syndrome, blisters, corns, callosities, fissures, Ingrown toe nail, calcaneal prominence. Screened foot deformities were overriding toe, hallux valgus, curly toe, hammer toe, hallux flexus, hallux rigidus, pes planes, claw toe, mallet toe, foot splaying, calcaneo varus, calcaneo valgus, forefoot valgus, forefoot varus. Screened foot diseases were plantar warts, tinea pidea and toe nail Fungus. Hypothesis was that whether foot defects, foot deformities and foot diseases vary significantly among these three groups.
METHOD
Three groups were stratified for this study namely shod runners, barefoot runners and controls. Subjects were explained about the benefit of this study and procedure. Then consent was taken.
To Identify Hallux valgus deformity
The Manchester Scale13,14 was used to identify hallux valgus deformity. Life-size versions of laminated photographs were used. Subjects were asked to stand on an elevated platform. Life size photographs were kept alongside subject’s weight-bearing feet, and then hallux valgus deformity was confirmed. Figure 1 Illustrate the image of Life size photographs used to screen hallux valgus A. No deformity (grade 1), B. Mild deformity (grade 2), C. Moderate deformity (grade 3), D. Severe deformity (grade4).
To screen hallux rigidus of great toe
Coughlin MJ and his colleague’s criteria to screen hallux rigidus of great toe15 was adapted. To screen hallux rigidus, extension of first MTP (metatarsophalangeal joint) joint was measured with goniometer ruler while foot in plantigrade position. Subject was made to stand on the wooden box while goniometer’s immovable arm was placed parallel to the first metacarpal bone and movable arm placed to the bisection of the proximal and distal phalanx of the great toe. Then subjects were asked to do great toe dorsiflexion (Figure 2). If subject experiences pain with limited (< 450 ) great toe extension, he was sent for radiograph analysis to screen osteophyte formation and changes in MTP joint and was to be diagnosed and conformed by orthopaedic surgeon.
To screen forefoot angle
Kirsten and Irene’s method was used to identify fore foot and rear foot deformities16,17,18 The subject was asked to assume prone lying position with measuring foot and ankle extended approximately 6 inches off the plinth. The opposite extremity will be placed in slight knee flexion and with abduction, flexion and external rotation of the hip. Evaluator’s thumb was used to palpate the medial aspect of the talar head, which is slightly inferior and anterior to the medial malleolus and proximal to the navicular bone of extended foot. The index finger is used to palpate the lateral aspect of talar head, which is anterior to the lateral malleolus and toward the midline of the foot. During pronation and supination of subtalar joint movement, subtalar joint neutral position was obtained where the medial and lateral aspects of the head of the talus become prominent simultaneously. (Figure3). Examiner then applied a dorsiflexion loading force to the forefoot, with the thumb and index finger holding the foot in the toe sulcus across the lesser toes until a firm resistance was felt. Forefoot position at this point was determined by placing the stationary arm of the goniometer perpendicular to the calcaneal bisection and the movable arm parallel to the second to fifth metatarsal heads. If positive degrees obtained that is forefoot varus, neutral if it (0º), or if negative degrees obtained that is forefoot valgus (Figure4). Angle was determined as the angle between the perpendicular to the bisection of the calcaneus and an imaginary line drawn through the metatarsal heads.
To determine rear foot alignment
Subjects were made to assume same position adapted for forefoot angle measurement. The vernier caliper was positioned at the medial and lateral borders of the lower leg at 8 and 6 inches above the calcaneum, and both the midpoints were marked with a water soluble marker. (Figure 5,6,7). A vertical line was drawn between the two midpoints to create the bisection line in calf. To draw a calcaneal bisection line, midpoints at both the superior and inferior aspects of the calcaneum by palpating the medial and lateral borders of the calcaneum and midpoint was located by using a flexible ruler marking a dot at midpoints (Figure8). Then vertically connect this two midpoints to make posterior calcaneal bisection line. Then subject was asked to stand on the wooden box. Evalutor used palpation technique to feel for talar dome congruency, placed the subject’s foot in subtalar joint in neutral position and goniometer ruler was aligned parallel to bisection of lower leg against calcaneal bisection lines, the angle was recorded (Figure 9). More than 6 degree of calcaneal tilt from neutral was considered as rear foot varus and valgus in either direction.
To screen type of foot arch
To screen the type of foot arch, normalized truncated navicular height (NTNH) 19 was measured. Subjects were made to assume relaxed standing position with feet positioned shoulder width apart. Navicular tuberosity was marked with water soluble marker (Figure 11). Navicular height was measured using metal ruler placed perpendicular to navicular tuberosity to the supporting surface. Then subjects were made to stand on two graph sheets placed in front of them after dipping their feet in ink diluted tray for generating foot print (Figure 10). Demarcation of first MTP joint in foot print is made maintaining that position on the graph. To calculate truncated foot length, distance between the two lines perpendicularly drawn from first MTP joint and from the most posterior aspect of the heel calculated (Figure 12). Then navicular height was divided by truncated foot length to derive normalized foot arch height .Values are documented as normal arch foot if NTNH value were 0.22-0.31. If NTNH values were > 0.18 was documented as flat foot. Standardized photographs of various foot diseases which were approved by dermatologist the second author of this study was used to grade various foot diseases and defects are employed20,21Criteria for identifying corns, calluses and verrucas were followed as per guidelines given by Snider RK and others.22,23,24 callosities, corns, warts were differentiated by its location, appearance, type of onset, direct pressure, side to side pressure and confirmed by dermatologist who is the second author of this study. Tinel’s sign was tested to screen if there were tarsal tunnel syndrome (TTS). Figure 13 provides the image of heel wart, Figure 14 the image of callosities. Figure 15 gives the image of ingrown toe nail.Figure 16 shows the image of tinea pedia. Figure 17 shows the image of corn with hallux valgus.
STATISTICAL ANALYSIS AND RESULTS
Data was collected and comparison was made between the groups namely barefoot runners, shod runners and controls for screening foot defects, foot deformities and foot diseases using spss version16. To test homogeneity between three groups for gender Chi-square test was used Table 1. To test homogeneity for BMI and age, one way ANOVAs analysis was used Table 2, 3. Then comparison of foot defects, foot deformities and diseases across three groups was carried out Table 4,5,6. Mean values of foot defects, deformities and disease for three groups are given in Table 7.
DISCUSSION
51 barefoot runners were compared against 65 controls and 61 shod runners for foot defects, foot deformities and diseases. There were no other studies exclusively in the past carried out to compare the prevalence of foot defects, foot deformities and diseases among the three groups chosen for this study. All outcome measure tools used in this study are clinically well validated and proven up-to-date. Gender homogeneity was found among three groups as the chi square test p value is 0.409. Age range homogeneity was found among three groups analysed as one way anova test p value is 0.083. BMI has varied significantly among three groups analysed namely barefoot runners, shod runners and controls as one way anova test p value is 0.009. Mean foot defects observed among barefoot runners, shod runners and control were 0.9608±.662, 1.442±.1.02 and 0.338±.53 were found to be highly significant across three groups as one way anova test p value was 0.001. Mean foot deformities observed among three groups were 0.745±.796, 0.868±1.16 and 0.23±.42 were found to be highly significant across three groups as one way anova test p value were 0.001. Mean foot diseases among barefoot runners, shod runners and controls were 0.588±.75, 0.426±.66 and 0.107±.35 were found to be highly significant across three groups as one way anova test p value were 0.001. Thus null hypothesis stands rejected. In this study mean foot defects were more in shod runners to barefoot runners. As for foot deformities were concerned, more occurrences were found with shod runners to barefoot runners. Yet mean number of foot diseases were more with barefoot runners to shod runners group. Surprisingly in controls, very few occurrence of foot defects, deformities and diseases are found. This study results contradict the reports given by researchers8,9,10 in which they reported fungus infection was more with shod group. Yet APMA (2015)25 recommends athletes not to use barefoot pattern generally to avoid acquiring athletic foot, warts. As a result of this study, one can understand the influence of foot wear on the occurrence of foot defects explained by Bertrand 7 . This study results have supported the claims of M.kuchi et al4 and K. D’Aou, T. et al.12 Though there are number of foot conditions common for runners, this study exclusively stratified runners in to shod and barefoot groups in screening various foot disorders in order to shed more light in devising prophylaxis measures. When shod runner’s age and BMI were correlated to the occurrence of foot defects, deformities and diseases exhibited poor correlation. So did with barefoot runners. Number of barefoot runners was comparatively less in this study might be a limiting factor. BMI varied significantly among three groups when age range, gender participation in three groups not varied significantly, thus homogeneity might be compromised to some extent. But when BMI was correlated to the incidence of foot defects, deformities and diseases in each group, it exhibited positive correlation with shod runners group. But with barefoot runners group and controls, BMI negatively correlated. The reason is not known. Equal numbers of samples in each group with larger sample size is recommended for future studies. Though less number of female participated in this study, gender homogeneity was found across three groups analyzed here. Shoe components can be correlated to the occurrence of the foot disorders observed in this study for shod runners group. This study has the advantage of stratifying samples and also has included controls for comparison in order to shed clear light in this area of research.
CONCLUSION
Three groups namely barefoot runners, shod runners and controls were screened in this study for the prevalence foot defects, deformities and diseases. Result of this study revealed that foot defects, deformities and diseases have been found to be highly significant among three groups.
ACKNOWLEDGEMENT
Authors express sincere thanks to Professor A. Joseph Oliver Raj M.P.T. Alva’s college of Physiotherapy and Research center for his support and Professor Radakrishnan M.phil, (PhD) former Physical education coach of Alva’s Physical education college for rendering his full-fledged help in getting samples in due course of time for this study. Self funded project work as well as a part of Major PhD research.
Englishhttp://ijcrr.com/abstract.php?article_id=597http://ijcrr.com/article_html.php?did=5971. Joan M. Bedinghaus, Mark W. Niedfeldt, Over-thecounter foot remedies; Medical college of Wisconsin, Milwaukee,Wisconsin.,www.aafp.org/afp American Family Physician SEPTEMBER 1, 2001 / VOLUME 64, No 5;791- 794.
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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30HealthcareA STUDY ON EXCLUSION GROUP FROM THE INITIATION OF DOTS UNDER REVISED NATIONAL TUBERCULOSIS CONTROL PROGRAMME IN WEST BENGAL, INDIA
English2432Arupkumar ChakrabarttyEnglish Kazi Monjur AliEnglish Abhinandan GhoshEnglish Debidas GhoshEnglishBackground: Revised National Tuberculosis Control Program (RNTCP) in on from 1990s. But outcome is not satisfactory in many states including West Bengal. Our objective is to profile people coming at microscopy centre for sputum examination early and late. It tries to identify factors adversely influencing early sputum examination and causes of exclusion from initiation of Directly Observed Treatment Short Course (DOTS) therapy.
Methods: Survey was conducted on 577 persons with cough for minimum two weeks from 36 microscopy centres. Important variables explored were sputum positivity level, a proxy indicator of delay in seeking services and initiation of DOTS. Apart that, information on poverty level, religion, caste, mode of journey to facility was also captured.
Results: Patients coming late in the microscopy centre were expected to be high positive and those came earlier to be low positive. For both sex, late diagnosis (88.24% and 81.58%) was much more than early diagnosis (11.76% and 18.42%). Across all religions, late diagnosis was much higher than early diagnosis (Hindu 83.05%, Muslim 88.89% and others 100.0% for late diagnosis). Variables significantly influencing initial default of DOTS are age, sex, caste, religion, education, employment status, access to facility and service providers. Upper caste and above poverty line people are more complaint to DOTS.
Conclusion: Present study recommends developing an overall community mobilization strategy so that TB suspects reach facilities for early diagnosis and start DOTS. Stigma reduction strategy may be developed so that community does not hesitate to access the existing microscopy health care services.
EnglishDOTS, Initial defaulter, Treatment Compliance, Exclusion groupINTRODUCTION
Tuberculosis (TB) continues to be the leading communicable disease and second most reason of death after AIDS (1). It accounts for more deaths among women than all other causes of maternal mortality combined (2). Tuberculosis disproportionately affects poorer and marginalized sections of the society (3, 4). India introduced the Revised National Tuberculosis Control Program (RNTCP) in mid-1990s for the prevention, containment, and cure of TB infections in the country through World Health Organization (WHO) endorsed Directly Observed Treatment Short Course (DOTS) strategy. The RNTCP currently works in conjunction with ‘Stop TB Partnership’ with a goal of world wide reduction of TB prevalence by 50% within 2015 and less than 1 TB case per million population within 2050 (5). At the country level and as well as in the state of West Bengal; progress is much behind the target of ‘Stop TB Partnership’ (5, 6). RNTCP’s overarching objective is to “achieve and maintain a cure rate of at least 85 percent in new cases, and to achieve and maintain detection of at least 70 percent of sputum positive pulmonary TB patients” (6, 7). To comply fully the objective of RNTCP; the programme has to mobilize community to public facilities for sputum test as first and foremost strategy (5, 8). Health care seeking is a dynamic process that is influenced by socio-demographic, cultural and other factors.
Availability of a simple and rapid diagnostic TB test for use at the lowest level of health care and the involvement of all health providers in case finding activities are imperative for early TB case detection (9). In Taiwan, during the five-year study period, among the 78,118 new Pulmonary TB patients, the mean diagnosis and treatment times were 12 and 5 days and the median times 1 day and 0 days, respectively (10). Our previous study in this concern suggested that due to stigma and caste many people are delayed in accessing healthcare (11). Compounded with the above problems that community is not coming to facilities for sputum examinations or coming very late leading to very late diagnosis; problems are again multi-folded. When there is delay in seeking care, the patient is suffering for long time but did not turn up for sputum test. It is expected that longer cough duration means more sputum positivity on examination. No initiation of DOTS therapy will cause spread of disease in the community. So more sputum positivity will indicate more delay in seeking care. In best of our knowledge, there is no information available that reflects difference in socioeconomic profile between the two groups; who are coming to microscopy centre early and who are coming late. Hence, the objective of this study is to look at the people, detected sputum positive and two groups; one who are coming early for diagnosis and the other who are coming late through sputum examination at the microscopy centre. Also efforts are made to identify factors adversely affecting early seeking of sputum examination services under RNTCP and initiation of DOTS.
METHODOLOGY ADOPTED
Study setting
Selection of district: In West Bengal there are 20 districts and out of which three districts - Birbhum, Jalpaiguri and North 24 Parganas have been selected those geo-ethnographically represent the state. There are three sub-divisions – Jalpaiguri, Presidency and Bardhaman. From each sub-division one district has been selected to capture maximum variations - Birbhum for Scheduled Tribe (ST) population, Jalpaiguri for ST including North Bengal’s variations and North 24 Pgs for Scheduled Caste (SC) and urban variations together with factors related to riverine variety.
Selection of Tuberculosis
Unit (TU): Each TU covers around 0.5 million population. A total of 12 TUs have been selected – seven from North 24 Parganas, three from Jalpaiguri and two from Birbhum based on the population. TUs have been notified based on certain criteria like urban/rural, SC/ST, minority/majority and hard to reach/easy to reach areas. For North 24 Parganas, seven TUS have been selected, randomly one TU for each criteria; for Jalpaiguri randomly three TUs have been selected for first three criteria and for Birbhum two TUs have been selected for first two criteria.
Selection of Designated
Microscopy Centre (DMC): Each DMC covers 0.1 million population. Under the selected TUs again following above procedure; three DMCs have been selected from each TU. Therefore a total of 36 DMCs have been selected.
Sampling: When prevalence of suspected tuberculosis is 10% among persons attending in a medical OPD; we assume this as prevalence of tuberculosis among people with cough equal or more than two weeks. Considering 5% permissible error and design effect of 2, estimated sample size is 256. In the present study, 577 persons are included with cough equal or more than two weeks.
Selection of respondents and data collection: From the selected DMCs, on the day of data collection, we have collected available information of patients who have provided at least two cough samples in last three years. Some information as desired in the survey tool are collected by the laboratory technicians, but not mentioned in the laboratory register, through telephone or home visits. Most of the time, patients found sputum positive, have started DOTS or completed DOTS. Therefore, they are known to laboratory technicians. Personal contact and home visit have been used to collect data. 2506 people are identified by laboratory technicians as eligible respondents, but out of them, only 577 respondents have been reached and their information also has been collected.
Variables measured and its analysis plan: Important variables those have been captured from the laboratory registers are age, sex, sputum positivity level, started DOTS or not. In addition, information on Above Poverty Line (APL)/Below Poverty Line (BPL) status, religion, caste, mode of journey to DMC and others have also been captured. The most important dependent variables used under the study are sputum positivity level i.e. proxy indicator of delay in cares seeking and started DOTS or not i.e. treatment compliance. Apart from frequency, percentages, bivariate analysis is done through chi-square method and multinomial logistic regression was done to reflect on strength of association. Sputum test is done in microscopy and its positivity has been defined as low positive (scanty to 1+) as early diagnosis and high positive (> 1+) as late diagnosis. Patients coming late in the microscopy centre are expected to be high positive and those coming earlier are expected to be low positive.
Informed Consent
Informed consent was part of all interviews conducted. The proforma for consent was approved by the Ph.D. Committee, Dept. of Bio-Medical Laboratory Science and Management, Vidyasagar University.
Ethical Clearance
Data collection was done on human on issues of tuberculosis. The study protocol was reviewed by the State TB Cell, Health and Family Welfare Department, Government of West Bengal. Administrative approval in respect of ethical consideration was taken from that end (Memo No./ HTB/31-2008/1054 Dt. 25th August 2012).
RESULTS
Profile of the participants
There are 425 males (73.7%) and 152 females (26.3%) out of 557 respondents who have completed sputum tests twice. There are 413 Hindus (71.6%), 72 Muslims (12.5%) and 92 others (15.9%) like Christian, Jainism, Sikh etc. Majority of the participants falls within the age group of 21-40 years, 270 (32.6%) and 41-60 years, 188 (32.6%). Scheduled tribe (ST) constitutes 230 (39.9%), Scheduled Caste (SC) 208 (36.0%). General caste and Other Backward Caste (OBC) constitute together 139 (24.1%). Daily wage labours count maximum proportion 236 (40.9%) compared to government employee 43 (7.5%) and 157 (27.2%) are self employees. People who have tested sputum, among them 436 (75.6%) belong to Below Poverty Line (BPL). Results are summarized in table 1a and table 1b.
Delay in seeking sputum examination services and its covariates
Sputum test is done in DMC. Its positivity is here defined as low positive (scanty to 1+) as early diagnosis and high positive (> 1+) as late diagnosis. Patients coming late in the microscopy centre are expected to be high positive and those coming earlier are expected to be low positive. For both male and female, late diagnosis (88.24% and 81.58%) is much higher in proportion compared to early diagnosis (11.76% and 18.42%). Across all religions, late diagnosis is much higher than early diagnosis. For Hindu, Muslim and others; late diagnosis is 83.05%, 88.89% and 100.0% respectively. Similarly for other factors like caste, employment, literacy, type of service providers and mode of journey; participants have a tendency to opt for late diagnosis and their associations are statistically significant at 95% confidence interval except for mode of journey. The results are depicted in table 2. Covariates of late diagnosis of sputum positive cases are provided in figure 1.
Compliance of DOTS and its covariates
If sputum test is positive for one sample out of two tests done at DMC, DOTS must be started. Majority of the patients who are tested positive, have been put on DOTS. Among those who are positive in sputum test, around 10.84% of them have come back to the community without DOTS and have started spreading TB infection among household and other contacts. Covariates related to compliance with DOTS are provided in table 3 and covariates of non compliance in figure 2. Compared with SC, OBC and general people, STs are found to remain 9.2, 4.3 and 2.8 times more complied to initiate DOTS. Similarly people with higher age group (> 60 years) are less interested to initiate DOTS. Respectively people of age groups 41-60 years, 21-40 years and up to 20 years are 1.5, 1.6 and 1.2 times more complied to initiate DOTS that people of age more than 60 years (table 4).
DISCUSSION
Delay in sputum examination from microscopy centre
Important factors associated with diagnosis delay include age, reporting year, living with family and a positive sputum culture (p < 0.0001) (10). The results indicated that 78 i.e. 13.52% accessed sputum service examination early and 499 i.e. 86.48% accessed sputum examination services late. Our study has identified similar factors to have statistical significant relationship with either access to sputum examination services or initiation of DOTS. Current global TB control policy emphasizes case finding through sputum smear microscopy for patients who self report to primary health centres. Low case detection rates remain an obstacle to the long-term success of TB control programs. Current World Health Organization policy emphasizes passive case finding in contrast with the identification of cases through screening. This strategy has been based on the expectation that (i) passive detection of individuals will ensure to seek medical care is far more cost-effective than population-based screening. The failure of national TB programs to detect the vast majority of new infectious cases suggests that active screening strategies should be re evaluated in an attempt to improve case detection and thereby, increase access to TB treatment (12). The institutional and community norms leading to stigmatization on tuberculosis may hinder TB control. Stigma out of TB has adverse socioeconomic consequences, especially on women. Stigma is believed to delay access to TB diagnostic services and treatment compliance. There are some interventions that may reduce TB stigma (14). TB suspect referral of tuberculosis in West Bengal is around 157 per 0.1 million population, when the expected rate is 203 per 0.1 million (15). A study in Jalpaiguri, Birbhum and North 24 Parganas, 26.7% showed that people with cough equal or more than two weeks are susceptible to have tuberculosis (11). If people do not know that cough equal or more than two weeks may be symptom of tuberculosis, naturally they will not approach the facility for sputum test. This describes why suspect referral of tuberculosis in West Bengal is poor (15). It is found that stigma is significantly associated with duration of cough (Englishhttp://ijcrr.com/abstract.php?article_id=598http://ijcrr.com/article_html.php?did=5981. Herzog H. History of tuberculosis. Respiration (Herrlisheim) 1998; 65: 5–15.
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5. Ministry of Health and Family Welfare. Government of India, Central TB Division. TB India. 2012; 16-7.
6. Indian Institute of Health Management Research. Accessibility and utilization of RNTCP services by SC/ST population. 2003; Chapter 5, 1-5.
7. Story A, Hest RV, Hayward A. Developed countries need new strategies for controlling tuberculosis. BMJ 2006; 333(7558): 57–8.
8. Wendy L, Wobeser P, Yuan L. Expanding the epidemiologic profile: risk factors for active tuberculosis in people immigrating to Ontario. CMAJ 2003; 163(7): 823–8.
9. Yimer S, Holm-Hansen C, Yimaldu T, Bjune G. Health care seeking among pulmonary tuberculosis suspects and patients in rural Ethiopia: a community-based study. BMC Public Health 2009; 9: 454.
10. Lin HP, Deng CY, Chou P. Diagnosis and treatment delay among pulmonary tuberculosis patients identified using the Taiwan reporting enquiry system. 2002–2006; BMC Public Health 2009; 9:55.
11. Chakrabartty A, Ali KM, Ghosh D. A study on excluded groups from Revised National Tuberculosis Control Programme of West Bengal, India. Int J Current Res 2015; 7: 1292-11298.
12. Mercedes C, Becerra IF, Bayona J, Celi R, Sonya S, Kim JY. Expanding Tuberculosis Case Detection by Screening Household Contacts. Public Health Rep 2005; 120: 272.
13. Dye C, Watt CJ, Bleed D. Low access to a highly effective therapy: a challenge for international tuberculosis control. Bull World Health Organ 2002; 80: 437-44.
14. Courtwright A, Turner AN. Tuberculosis and stigmatization: pathways and interventions. Public Health Rep 2010; 125(4): 34-42.
15. Department of Health and Family Welfare, Government of West Bengal. Annual Bulletin of State TB Cell. 2013; Quarter 4: 32-4.
16. Van Rie A, Sengupta P. Measuring stigma associated with tuberculosis and HIV/AIDS in southern Thailand: exploratory and confirmatory factor analyses of two new scales. Psychol Health Med 2006; 11(3): 65-7.
17. State TB Cell. Department of Health and Family Welfare, Government of West Bengal. Performance indicators, RNTCP. 1st Quarter. 2014.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30HealthcareCLINICAL PROFILE REVIEW OF PATIENTS WITH THROMBOCYTOPENIA: A STUDY OF 100 CASES AT A TERTIARY CARE CENTRE
English3337Shah H. R.English Vaghani B. D.English Gohel P.English Virani B. K.EnglishIntroduction: With the widespread use of automated cell counters, clinicians in any field of medicine may encounter thrombocytopenia. The symptomatology of thrombocytopenia varies greatly and the underlying cause may be either inconsequential
(pseudo-thrombocytopenia) or life threatening.
Aims and Objectives: To evaluate different causes of thrombocytopenia along with study of clinical profile and laboratory parameters in patients with thrombocytopenia. Materials and Method: A total of 100 patients with thrombocytopenia admitted to Civil Hospital, Ahmedabad and were evaluated. Patients with platelet count EnglishPlatelet count, Bleeding manifestation, SpleenomegalyINTRODUCTION
Thrombocytopenia is defined as a subnormal number of platelets in circulatory blood. With the widespread use of automated cell counters, clinicians in any field of medicine may encounter thrombocytopenia. The symptomatology of thrombocytopenia varies greatly and the underlying cause may be inconsequential (pseudothrombocytopenia) or life threatening. Thrombocytopenia is caused by one of any three mechanisms:
1) Decreased bone marrow production,
2) Increased splenic sequestration or,
3) Accelerated platelet destruction In our geographical distribution the infections (e.g. malaria, dengue, enteric fever) and Megaloblastic anemia are commonly associated with thrombocytopenia, which is mild to moderate degree.
MATERIALS AND METHOD
A total of 100 patients with thrombocytopenia admitted to Civil Hospital, Ahmedabad and were evaluated. Criteria for Patient Selection:
1. Inclusion Criteria: Patient with platelet countEnglishhttp://ijcrr.com/abstract.php?article_id=599http://ijcrr.com/article_html.php?did=5991. Robert I. Handin, Harrisson’s principles of internal medicine 2005;15:337.
2. Shirley parker Levine Wintrobes clinical hematology 2006;11:581.
3. SK Sharma, Medicine update volume 17,2007:629.
4. Abrahamson, Page E., et al. “The incidence of idiopathic thrombocytopenic purpura among adults: a populationbased study and literature review.”European journal of haematology 83.2 (2009): 83-89.
5. Michel, Marc. “Immune thrombocytopenic purpura: epidemiology and implications for patients.” European Journal of Haematology 82.s71 (2009): 3-7.
6. Memon, Abdul Rauf, and Salahuddin Afsar. “Thrombocytopenia in hospitalized malaria patients.” Pakistan Journal of Medical Sciences 22.2 (2006): 141.
7. Liu, Shelan, et al. “Systematic review of severe fever with thrombocytopenia syndrome: virology, epidemiology, and clinical characteristics.” Reviews in medical virology 24.2 (2014): 90-102.
8. Nadir Ali at el, Pakistan Journal of Pathology, Dec 2004. 9. Harker and slichter, textbook of hematology,1972;435;4.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30HealthcareADIPOCYTOKINE VISFATIN - A LINK BETWEEN DIABETES MELLITUS AND PERIODONTITIS - A REVIEW
English3843ShamsiyaEnglish Rajasekar S.English Lakshmisree S.English Little MahendraEnglishVisfatin is a newly discovered member of adipokine family. It is a visceral adipokine, it has been found in skeletal muscle, liver, bone marrow and lymph. It was originally identified as a cytokine-like secreted protein that synergizes the effect of IL-7 and stem cell factor in promoting the growth and differentiation of B-cell lineage precursors. It is expressed in lymphocytes of peripheral blood and plays a role in lymphocytes maturation and inhibition of neutrophil apoptosis. It is an endocrine, autocrine as well as paracrine protein with many functions including enhancement of cell proliferation, biosynthesis of nicotinamide mono- and dinucleotide and induction of hypoglycemia. Visfatin has been shown to exert insulin mimetic
and pro-inflammatory effects, One of the fundamental functions of visfatin is the modulation of immune and inflammatory processes. It has been reported that visfatin activated nuclear factor-kappa B which has a crucial role in regulating immune responses. Up-regulation of visfatin has been also identified in a variety of pathophysiological conditions of the immune system including rheumatoid arthritis, psoriasis, clinical sepsis and acute lung injury.
Recently, there has been mounting body of studies investigating the association of visfatin with periodontal disease. This article gives an insight about visfatin and its correlation with periodontal disease.
EnglishVisfatin, Periodontal Disease, Diabetes mellitus, ImmunityINTRODUCTION
Periodontitis is an inflammatory condition of the supporting structures of teeth resulting from dental plaque biofilm attached to tooth surfaces. It is potentially an important nidus of systemic inflammation and its sequelae represents a unique opportunity for oral pathogens and their products to gain access to the systemic circulation.1 Diabetes mellitus is a group of metabolic disorders, characterised by hyperglycaemia, and excretion of sugar in the urine.1 Type 2 diabetes mellitus is the most common form of diabetes accounting for 90-95% of all cases and usually has an adult onset. Diabetes mellitus plays an important role in the pathogenesis of periodontal infections sharing a common pathway that involves an enhanced inflammatory response which can be observed at the local and systemic level.2 Periodontal infection itself represents a complication that may be involved in altering the systemic physiology in diabetic patients. A dysregulated immune response stemming from an inappropriate cytokine production may act as a possible mechanism underpinning the cross-susceptibility between periodontal disease and diabetes. 3,4 Another confounding factor related to periodontitis and type 2 diabetes mellitus is obesity or fatness which refers to excessive accumulation of body fat, caused by the consumption of more calories than the body can utilize.6,7 Obesity may be considered as a low – grade systemic inflammatory disease. Obese children and adults have elevated serum markers of inflammation and are closely associated with chronic inflammatory diseases. These findings explain the basis for association between obesity and periodontal disease.8 Currently obesity, particularly central obesity, heightens the pathogenesis of type 2 DM. Additionally, factors produced by adipose tissue (AT), referred to as adipocytokines, can influence the degree of insulin resistance as well as inflammation, due to their duality of function.7 Visfatin is a recently discovered adipokine, synthesized and secreted primarily by visceral fat.9 It is 52-kDa protein encoding a polypeptide of 491 amino acids.10 Visfa tin may be considered as a multifunctional protein acting as a hormone, cytokine and/or enzyme capable of exerting several pro-inflammatory functions11. Visfatin levels are elevated in a wide variety of inflammatory conditions like rheumatoid arthritis and any acute and chronic inflammation. In periodontal inflammation, there is upregulation of IL-1, IL-6, TNF-α(tumor necrosis factor-α) etc., that has a profound effect on the expression of visfatin11. Elevated levels of proinflammatory cytokines and visfatin can worsen insulin resistance and thereby impair glycemic control. Thus, periodontal disease may have a significant impact on the metabolic status in type 2 diabetes mellitus.12
PATHOGENESIS OF PERIODONTAL DISEASE
Periodontitis is a complex bacteria-induced infection, characterised by inflammatory host response to plaque microbiota and their by-products.18 Periodontal microbes colonizing the subgingival environment express various structural and metabolic substances, for instance, lipopolysaccharide (LPS). This is a surface component and a well-known virulence factor of these Gram negative subgingival bacteria, which has the ability to trigger the host cells to release cytokines and other mediators of inflammation, in an attempt to eliminate the infectious agents and initiate a defence mechanism. The chronic inflammation in periodontal tissues stems from inappropriate host-microbial interaction resulting in excessive production of proinflammatory cytokines (e.g. IL(interleukin)-1β, TNF(tumor necrosis factor)-α, IFN(interferon)-γ and IL-6), leading to tissue destruction. Thus, LPS plays a key role in activation and perpetuation of tissue destruction in periodontal disease. 14 Although the bacterial plaque is fundamental for periodontal disease initiation and propagation, the host defensive responses represented by inflammatory and immune reactions are the essential determinants of disease occurrence. Host related risk factors such as smoking, systemic disease, genetics, bacterial composition of microbial plaque and socioeconomic factors may exacerbate the host protective mechanisms against bacterial challenge and thereby increase the destructive nature of the processes.15
PATHOGENESIS OF DIABETES MELLITUS
Body glucose homeostasis is mainly reliant on insulin (a hormone secreted by pancreatic β-cells). Diabetes mellitus, ensues from defects in insulin secretion, insulin action, or both resulting in the inability of glucose to be transported from the bloodstream into the tissues, which in turn, results in high blood glucose levels and excretion of sugar in the urine. 1 The most likely cause of insulin secretion deficiency is the dysfunction in the pancreatic β-cells whilst the hypo responsiveness of the tissues to insulin action (termed Insulin Resistance IR) may represent one of the main complications of obesity.16 Indeed, the regulation of insulin sensitivity and resistance depends on a number of factors including adipokines, inflammatory mediators, genetic factors and environmental stresses.6 During the initial stages in the natural history of type 2 diabetes mellitus, the body increases insulin output which results in hyperinsulinaemia to compensate for the reduction in insulin action and maintain normal glucose tolerance. As the insulin resistance worsens, the body is unable to control any further rise in metabolic load. There is a decline in insulin production affiliated with peripheral insulin resistance and diminished β-cell function. Ultimately, insulin secretions become diminished and inadequate to recompensate for the insulin resistance, thereby driving to impaired glucose tolerance and overt type 2 diabetes mellitus.17
PERIODONTITIS ↔TYPE 2 DIABETES MELLITUS RELATIONSHIP
There has recently been much emphasis on the ‘two-way’ relationship between diabetes and periodontitis. The exacerbation and dysregulation in the inflammatory responses play a central role in interrelationship between periodontal disease and diabetes. Hyperglycaemia drives numerous proinflammatory effects that influence various body tissues including the periodontium, leading to localized dysregulated immuno-inflammatory reactions.17
The influence of diabetes on the periodontium has been thoroughly investigated. Although it is difficult to make definitive conclusions about the specific effects of diabetes on periodontium, a variety of changes have been described, including a tendency toward reduced salivary flow, burning mouth, enlarged gingiva, sessile or pedunculated gingival polyps, polypoid gingival proliferations,
abscess formation, periodontitis, and loosened teeth. Perhaps the most striking changes in uncontrolled diabetes are the reduction in defence mechanisms and the increased susceptibility to infections leading to destructive periodontal disease. Diabetes does not cause gingivitis or periodontal pockets, but there are indications that it alters the response of the periodontal tissues to local factors, hastening bone loss and retarding postsurgical healing of the periodontal tissues.1
HYPERGLYCEMIA, ADVANCED GLYCATION END PRODUCTS (AGES) and
Binding of AGEs to its receptor (RAGE) resulted in the upregulated production of proinflammatory mediators such as IL-1β, TNF-α and IL-6. AGE formation results in the production of ROS and enhances oxidant stress, and the subsequent endothelial cell changes that occur contribute to the vascular injury implicated in many diabetes complications. Apoptosis may also play a role in the increased susceptibility to periodontitis associated with diabetes, and apoptosis of matrix-producing cells may limit the opportunities for repair in inflamed tissues.18
IMPACT OF PERIODONTITIS ON DIABETES RELATED INFLAMMATORY STATE AND INSULIN RESISTANCE
In untreated severe periodontal disease, the cumulative surface area of ulcerated pocket epithelium has been estimated to range from 8 to 20 cm2 , which approximates the size of the palm of an adult hand.19 Bacteremia and endotoxemia can be induced by dental procedures, as well as by usual daily activities (such as chewing), leading to an elevated inflammatory state and stimulating increase in the levels of serum inflammatory markers. Chronic inflammation, through the action of inflammatory mediators is found to be associated with the development of insulin resistance which is influenced by genetically modified environmental factors, including decreased physical activity, poor nutrition, obesity and infection.20 Patients with inflammatory periodontal diseases often have elevated serum levels of proinflammatory cytokines mainly IL-6, IL-1, TNF-α and PGE-2. In diabetic patients with periodontitis, the hyperinflammatory immune cells can exacerbate the elevated production of proinflammatory cytokines which increases insulin resistance leading to greater risk of poor glycemic control when compared to diabetic patients without periodontitis.17 The inflammatory mediators originating from periodontal sources can interact systemically with lipids, free fatty acid and advanced glycation end products (AGEs), all of which are characteristics of diabetes. This interaction induces or perpetuates activation of the intercellular pathways, such as I kappa-β, Nuclear factor kappa β and the Protein jun N-terminal kinase axes, all of which are associated with insulin resistance. The activation of these inflammatory pathways in immune cells (monocytes or macrophages), endothelium cells, adipocytes and muscle cells promotes and contributes to an increase in the overall insulin resistance, making it difficult to achieve metabolic control in patients with both type 2 diabetes and periodontitis.21
VISCERAL ADIPOSITY, OBESITY, INSULIN RESISTANCE, TYPE 2
DIABETES MELLITUS
In obesity, the initial deposition of triglycerides occurs in subcutaneous adipose tissue and as this increases, insulin resistance will arise and limit further subcutaneous lipid accumulation. Triglycerides will then be diverted to the visceral fat depot as well as to ectopic sites. This leads to a substantial rise in insulin resistance and the prevalence of its associated disorders. Supporting studies indicate that in lean subjects the prime determinant of insulin resistance is BMI(Body mass index), that is, subcutaneous fat, whilst in overweight and obese subjects, it is waist circumference and visceral adiposity. Accumulation of fat in abdomen regions has major implications for metabolism, particularly for insulin sensitivity.9 Visceral adiposity is considered a risk factor for type 2 diabetes mellitus in adults, as well as in first degree relatives of patients with type 2 diabetes mellitus with normal glucose levels. Adipocytokines, hormones secreted by the visceral adipocytes, generate the insulin resistant state and the chronic inflammatory profile that frequently goes along with visceral obesity
VISFATIN
THE DISCOVERY, STRUCTURE AND TISSUE DISTRIBUTION OF VISFATIN
Visfatin is a newly discovered member of adipokine family with the unique particularity within the group of having two variant forms, identical in sequence and coded by the same gene, but with different localizations - the first is intracellular nicotinamide phoshoribosil transferase (iNampt), and the second extracellular (eNampt). The intracellular form of visfatin is ubiquitously expressed and it was proved so far to synthesize NMN, an intermediate of NAD, through its phosphoribybosiltransferase activity. The extracellular form was found to be actively secreted by both white adipocytes 9 and brown adipocytes, justifying its inclusion in the adipokine group. The extracellular form of Nampt/visfatin is synthesized and released to the extracellular milieu, where it could exert a variety of actions in a paracrine or endocrine manner. Structurally, extracellular visfatin shows a slightly higher molecular weight than the intracellular isoform and seems to undergo post-transcriptional modifications.10 Despite the fact that visfatin is a visceral adipokine, it has been found in skeletal muscle, liver, bone marrow and lymph. Visfatin was originally identified as a cytokine-like secreted protein that synergizes the effect of IL-7 and stem cell factor in promoting the growth and differentiation of B-cell lineage precursors. It was originally called Pre-B cell colony enhancing factor (PBEF) which is protein with a enzymatic activity10 and acts as a nicotinamide phosphoribosyltransferase (Nampt).10It is expressed in lymphocytes of peripheral blood and plays a role in lymphocytes maturation and inhibition of neutrophil apoptosis.22 Visfatin is a 52 kDa large protein, and its gene PBEF/ Visfatin is located on chromosome 7q22.2. It consists of 11 exons and 10 introns and is 34.7 kb large. Fukuhara et al. 9 presented Visfatin as a newly identified adipocytokine with many possible effects in physiological regulation in humans and a possible role in the development of some pathological conditions. Plasma Visfatin levels positively correlated with obesity development and had insulin-mimetic activity.
VISFATIN IN REGULATION OF INSULIN SIGNALLING
A very important finding is Visfatin’s insulin-mimetic activity. The insulin-mimetic activity was explored in various experiments. Visfatin lowered plasma glucose level in mice. In heterozygous mice with mutated Visfatin gene, slightly higher plasma glucose levels were observed than in wild type individuals. The effect of Visfatin on cultured cells is found to be similar to that of insulin. Visfatin not only influenced glucose uptake into 3T3-L1 adipocytes and L6 myocytes, but also suppressed glucose release from H4IIEC3 hepatocytes. 9 Further it was described that Visfatin binds to insulin receptor in a different binding site than insulin. Visfatin induced the phosphorylation of insulin receptor, IRS1 and also IRS2 (insulin receptor substrate).9 Visfatin could act as an attractive target molecule with insulin-mimetic activity, which is non-competitive with insulin, in pharmacotherapy of insulin-resistant conditions. It is not surprising that Fukuhara et al., considered the role of Visfatin in some metabolic disorders related to glucose homeostasis.9
VISFATIN AND TYPE 2 DIABETES MELLITUS
Visfatin is an endocrine, autocrine as well as paracrine protein with many functions including enhancement of cell proliferation, biosynthesis of nicotinamide monoand dinucleotide and induction of hypoglycemia. Visfatin has been shown to exert insulin mimetic and proinflammatory effects, also functioning as an intracellular enzyme to produce NAD.10 The observation that visfatin has insulin-mimetic functions has raised the hypothesis that a dysregulation of the activity of this molecule may contribute to the metabolic syndrome and diabetes. Chen M. P. et al., (2006) in their study investigated whether plasma visfatin level is altered in patients with type 2 diabetes mellitus. Plasma visfatin was found to be elevated in patients with type 2 diabetes mellitus when compared to age and sex matched controls. Increasing concentrations of visfatin were independently and significantly associated with type 2 diabetes mellitus.2
VISFATIN AND OBESITY
Human body contains two types of adipose tissue – subcutaneous and visceral fat. Visceral fat is significantly related to metabolic disorders, especially metabolic syndrome, and represents a strong risk factor. Metabolic syndrome is associated with the central obesity, type 2 diabetes mellitus, insulin resistance, hypertension and higher cardiovascular risk. Obesity has also been associated with increased accumulation of macrophages in visceral fat and the amount of macrophages is positively correlated with the total fat mass of the body.
Fukuhara et al (2005) 9 reported that plasma Visfatin levels correlated strongly with the amount of visceral fat, but only mildly with the amount of subcutaneous fat in their experiment on 101 male and female human subjects. They also analyzed the mRNA Visfatin expression in the visceral and subcutaneous fat in KKAy mice which are models for obesity and type 2 Diabetes. In the time period, when the mice become obese (between 6 and 12 week of age), Fukuhara et al. found increased levels of plasma Visfatin which correlated with the increase of mRNA Visfatin expression in visceral fat. On the contrary, no significant changes were found in mRNA expression in subcutaneous fat9
VISFATIN AND IMMUNE AND INFLAMMATORY PROCESS
One of the fundamental functions of visfatin/PBEF/ Nampt is the modulation of immune and inflammatory processes. Moschen et al (2007)10 has revealed that human leukocytes can be activated by visfatin to produce several pro and anti-inflammatory cytokines. While stimulation of CD14+ monocytes by visfatin leads to the production of IL-1β, TNF-α and IL-6, on the other hand, anti-inflammatory cytokines such as IL-1Ra and IL-10 might also be produced by stimulation of monocytes by visfatin. Moreover, this adipokine enhanced the surface expression of the co-stimulatory molecules CD54, CD40 and CD80 in CD14+ monocytes. Furthermore, it has been noted that visfatin/PBEF/Nampt was able to activate antigen presenting cells (APCs) and enhance phagocytosis in monocytes.10 In addition, trafficking CD14+ monocytes and CD19+ B-cells into sites of inflammation is another important function of visfatin which is deemed to be a strong chemotactic factor for these cells.10 Moreover, it has been reported that visfatin activated nuclear factor-kappa B which has a crucial role in regulating immune responses. 9 Indeed, it has been illustrated that serum visfatin levels positively correlated with IL-6 and CRP levels in human serum, which in turn corroborated the significance of visfatin as inflammatory cytokine. Up-regulation of visfatint has been also identified in a variety of pathophysiological conditions of the immune system including rheumatoid arthritis, psoriasis , clinical sepsis and acute lung injury.10
VISFATIN AND PERIODONTAL DISEASE
Recently, there has been mounting body of studies many number of trials were have been done investigating the association of visfatin with periodontal disease. A pilot study exploring the gene expression signature in pathological gingival tissues has revealed Visfatin as one of the top 20 genes that have been distinguished in periodontitis lesions. Moreover, stimulating monocytic cell line with P.gingivalis and E.coli LPS has yielded a differential up-regulation in Visfatin gene expression by E.coli LPS when compared with P.gingivalis LPS. 20 Pradeep A R et al., (2011) 24 assessed gingival crevicular fluid and serum visfatin concentration in subjects with periodontal health and disease. A total of 40 individuals (20 males and 20 females; age range: 23 to 53 years) were selected and divided into three groups based on the gingival index, probing depth, clinical attachment level, and radiologic parameters (bone loss). GCF and serum samples were collected to estimate levels of visfatin using an enzyme-linked immunosorbent assay kit. Mean visfatin concentrations increased in GCF and serum with the severity of disease from healthy to gingivitis to periodontitis groups and differed significantly (P Englishhttp://ijcrr.com/abstract.php?article_id=600http://ijcrr.com/article_html.php?did=6001. Newmann M G, Takei H H, Klokklevold R P et al. Carranza’s clinical periodontology.W B Saunders company 2006;10th edition.
2. Brian Mealey. Periodontal disease and diabetes: a two way street; Journal of American Dental Association: 2006;137(10 supple):26S-31S.
3. Amano. Host–parasite interactions in periodontitis: microbial pathogenicity and innate immunity:Periodontology 2000 October 2010;Volume 54(1): 9–14.
4. Philip M. Preshaw. Host response modulation in periodontics: Periodontology 2000 October 2008;Volume` 48: (1): 92-110.
5. Giulietti A, Van Etten E, Overbergh L, Stoffels K, Bouillon K, Mathieu C. Monocytes from type 2 diabetic patients have a pro-inflammatory profile. 1, 25-Dihydroxyvitamin D (3) works as anti-inflammatory: Diabetes Res Clin Pract.2007 Jul;77:47-57.
6. Wellen K E, Hotamisligil G S. Inflammation, stress, and diabetes: J Clin Invest. 2005 May; 115:1111-9.
7. Kopelman P. Obesity as a medical problem.Nature. 2000; 404:635-643.
8. Caroline FD. Overweight and Obesity as Risk Indicators for Periodontitis in Adults. Journal of Periodontology 2005; 76:1721-1728.
9. Atsunori Fukuhara, Morihiro Matsuda, Masako Nishizawa, Katsumori Segawa, Masaki Tanaka, Kae Kishimoto et al. Visfatin: a protein secreted by visceral fat that mimics the effect of insulin. Science.2005 Jan 21;307: 426-30.
10. Moschen A R, Kaser A, Barbara Enrich, Birgit Mosheimer, Milan Theurl, Harald Niederegger and Herbert Tilg. Visfatin, an Adipocytokine with Proinflammatory and Immunomodulating properties: J Immunol 2007; 178:1748- 1758.
11. S Ognjanovic, S Bao, S Y Yamamoto, J Garibay-Tupas, B Samal and G D Bryant Greenwood. Gnomic organisation of the gene coding for human. J mol.endocrinol 2001;26:107- 117.
12. Brian L Mealey and Thomas Oates. AAP-Commissioned Review Diabetes Mellitus and Periodontal Diseases: J Periodontol August 2006 ;77:1289-1300.
13. Socransky SS. Haffajee AD. Cugini MA, Smith C, Kent Jr. Microbial complexes in subgingival plaque: J Clin Periodontol 1998; 25: 134-144.
14. Richard P. Darveau and Sumita Jain. Contribution of Porphyromonas gingivalis lipopolysaccharide to periodontitis: Periodontology 2000 2010; Vol. 54:53-70.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30HealthcareANAESTHESIA FOR ABDOMINO - PERINEAL RESECTION IN A PATIENT WITH PREVIOUS PARALYTIC POLIOMYELITIS
English4446Pratibha S. D.English Shivanand L. K.English Renuka H.EnglishPoliomyelitis (also called infantile paralysis or acute anterior poliomyelitis) is an acute viral infectious disease that can present in two forms: asymptomatic infection or paralytic disease. A 45year old man, ASA(American society of anaesthesiologist) physical status II, 168cm tall and weighing 66kg was scheduled for Abdomino-perineal resection for Carcinoma - rectum. Medical history included paralytic poliomyelitis since childhood with hypoplastic lower limbs and kyphoscoliosis. General anesthesia was planned as patient refused for regional technique. General anaesthesia was effectively performed for polio patients with kyphoscoliosis by meticulous neuromuscular monitoring and titrated dose of drugs.
EnglishPoliomyelitis, Kyphoscoliosis, General anaesthesia, Neuromascular monitoringINTRODUCTION
Post polio syndrome1 is a disorder related to the recurrence of neuromuscular symptoms in survivors of paralytic poliomyelitis. Poliomyelitis (also called infantile paralysis or acute anterior poliomyelitis) is an acute viral infectious disease that can present in two forms: asymptomatic infection or paralytic disease. Paralytic disease2 is characterized by the sudden onset of flaccid paralysis associated with fever. It usually affects the lower limbs causing muscular weakness which results in reduction or loss of neurological reflexes. sensory system will be intact. Poliovirus damages the reticular activating system, many anesthetic drugs have action on this site . This may account for the extreme sensitivity these patients demonstrate to anesthetic medications as well as to the increased potential for delayed awakenings and other postoperative complications. Therefore it is of utmost importance to be careful about pharmacologic dosing of opioids and neuromuscular agents. Perioperative and postoperative issues related to aspiration risk, cold intolerance and positioning need timely intervention. CASE REPORT A 45year old man, ASA(American society of anaesthesiologist) physical status II, 168cm tall and weighing 66kg was scheduled for Abdomino-perineal resection for Carcinoma - rectum. His medical history included paralytic poliomyelitis since childhood with hypoplastic lower limbs and kyphoscoliosis, but did not include respiratory insufficiency necessitating assistive devices.
Preoperative blood pressure was 136/68 mm Hg, pulse was 86/min, respiratory rate was 14/min, temperature was 37.2°Cand oxygen saturation was 100% on room air. Airway assessment demonstrated a Mallampati class II. Spine examination revealed kyphoscoliosis, with irregular intervertebral spaces. Serum electrolytes, blood sugar, urea, creatinine and complete blood cell count indices were all within normal limits. The chest radiograph did not show any acute disease but showed kyposcoliosis. His electrocardiogram(ECG) was within normal limits. Results of the physical examination revealed bilateral lower extremity muscle weakness, necessitating the use of a cane and leg braces. He denied any history related to deficiencies with the respiratory muscles, including difficulty with breathing, swallowing or sleep apnoea. Colonoscopy done and biopsy revealed adenocarcinoma –colon (moderately differentiated). General anesthesia was planned as patient refused for regional technique. Premedication IV was given with midazolam-1mg ,Glycopyrolate -0.2mg,Pantoprazole- 40mg,Ondansetron-4mg and fentanyl-100 µg. Monitors included NIBP(non invasive blood pressure), ECG, Pulse oxymetry, ETCO2 (end tidal carbon dioxide ) respiratory gas analyzer, temperature, urine output and neuromuscular monitor. Induced with inj propofol 100mg IV, Intubated with cuffed portex 8.5 No endotracheal tube with inj. Vecuronium 6 mg iv . Maintained with oxygen, nitrous oxide, isoflurane and inj vecuronium with neuromuscular monitoring to maintain surgical plane of anaesthesia. Measures to maintain temperature were taken. Surgery lasted for 5hours.
Figure 2: Neuromascular Monitoring
End of surgery TOF (train of four) ratio in NMM (Neuro muscular monitoring) -0.9. Reversed with glycopyrolate (0.5 mg iv) and neostigime (2.5 mg iv) . Patient was conscious oriented, responded to oral commands but was unable to lift the head for more than 5secs and had inadequate hand grip. Patient was put on t-piece 5lts oxygen and monitored for 4hrs and extubated once extubation criteria were met. Patient was shifted to intensive care unit for observation for 24 hours.
DISCUSSION
An estimated 60% of those who had paralytic poliomyelitis are affected by postpolio syndrome. Postpolio syndrome is diagnosed in patients with a history of paralytic polio who have had a neurologic recovery of at least 15 years, followed by a gradual or new onset of muscle weakness, pain or other neurological symptoms. The most common symptoms of postpolio syndrome are fatigue, muscle pain, respiratory difficulties, intolerance to cold and difficulty in swallowing. The choice of using a general anesthetic versus a regional anesthetic should be based on the preoperative assessment, surgery and patient consent3 . It is unknown whether the motor neurons of patients with postpolio syndrome are more vulnerable to the effects of local anesthetics and if these patients may be more sensitive to overall toxic concentrations. Up to 42% of patients with postpolio syndrome4 have respiratory muscle involvement ranging from laryngeal muscle weakness to vocal cord paralysis. Dysphagia is present in 10% to 20% of these patients. This should alert the anesthetist to the increased potential of postoperative apnea and aspiration. The careful titration of opioids and muscle relaxants is necessary because of the increased sensitivity to these medications. Depolarizing muscle relaxant poses potential risk of hyperkalemia, severe myalgia and prolonged duration of action5 . There is a potential of increased sensitivity to nondepolarizing neuromuscular agents, necessitating careful neuromuscular monitoring. Careful positioning is essential because of potential chronic pain. Patients typically have a profound cold intolerance. Care should include warming the ambient air of the operating room, using warming blankets and warming intravenous fluids as indicated as well as continued warming efforts in the postoperative period to avoid shivering.
CONCLUSION
General anaesthesia was effectively performed for polio patients with kyphoscoliosis by meticulous neuromuscular monitoring and titrated dose of drugs. The decision to perform regional anesthesia in patients with preexisting neurologic deficits should be based on the risks and potential benefits of each individual case.
Source of funding: None
Conflict of interest: Nil
ACKNOWELEDGMENT
Authors would like to thank BLDEU Medical college for giving an opportunity. They also extend their gratitude to their colleagues for continuous support for during the case. Authors also thanks all the authors of articles from which information is cited in this paper.
Englishhttp://ijcrr.com/abstract.php?article_id=601http://ijcrr.com/article_html.php?did=6011. Donna Wheeler, Anesthetic Considerations for Patients with Postpolio Syndrome: A Case Report; AANA Journal; October 2011;Vol. 79, No. 5; 408-410.
2. Lambert DA, Giannoulin E, Schmidt BJ. Postpolio syndrome and anesthesia. Anesthesiology. 2005;103(3):638-644.
3. Costello JF, Balki M. Cesarean delivery under ultrasoundguided spinal anesthesia [corrected] in a parturient with poliomyelitis and Harrington instrumentation. Can J Anesth. 2008;55(9):606-611.
4. Suneel PR, Sinha PK, Unnikrishnan KP, Abraham M. Anesthesia for craniotomy in a patient with previous paralytic polio. J Clin Anesth. 2008;20(3):210-213.
5. Cherng C. Uneventful use of succinylcholine in six patients with post-polio syndrome. Br J Anaesth Online. 2008;101(1).
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524176EnglishN-0001November30HealthcareFINE NEEDLE ASPIRATION CYTOLOGY OF DE QUERVAIN'S THYROIDITIS - A RARE CASE REPORT
English4750R. Vimal ChanderEnglish Sonti SulochanaEnglish S. ChitraEnglishIntroduction: De Quervain’s thyroiditis, also called subacute thyroiditis, accounts for 5 % of the thyroid disorders, clinically characterised by painful diffuse enlargement of the thyroid, and is usually self-remitting.
Case Report: We report a case of a 28 year old male presenting with painful enlargement of right lobe of thyroid gland with a diagnosis of De Quervain’s thyroiditis on fine needle aspiration cytology.
Discussion: This is to illustrate that De Quervain’s thyroiditis has to be considered in the differential diagnosis of painful asymmetrical enlargement of thyroid, especially when there are numerous epithelioid granulomas with multinucleated giant cells along with the absence of antithyroid antibodies and rapid response to steroid therapy.
EnglishThyroiditis, Subacute thyroiditis, De Quervain’s, Granulomatous thyroiditisINTRODUCTION
Subacute thyroiditis is a rare self-remitting inflammatory disease of the thyroid, usually caused by viral infection. [1] It accounts for 5 % of the thyroid disorders. On examination, the thyroid is diffusely enlarged and tender. The diagnosis in most cases is self evident based on history, clinical examination, laboratory findings and clinical course of the disease. Rarely, it may present as a nodule or single lobe enlargement. Here we report a case of De Quervain’s thyroiditis in a 28 year old male presenting with enlarged right lobe of the thyroid.
CASE REPORT
A 28 year old male presented with progressively enlarging swelling in front of the neck for the past 2 years associated with pain. He gave history of fever with sore throat prior to the onset of the swelling. He is not a known diabetic, tuberculosis or other co-morbid conditions. On examination, right lobe of the thyroid was diffusely enlarged and mildly tender. [Figure 1] Cervical lymph nodes were not palpable. Thyroid function tests revealed elevated free Triiodothyronine (free T3) levels (9.2 pg/ml, Normal range: 2.3- 4.2 pg/ml) and free thyroxine (free T4) levels (3.41 ng/l, Normal range: 0.8-1.8 ng/l) and markedly reduced Thyroid stimulating hormone (TSH) levels (0.02 mIU/l, Normal range: 0.3-3.04 mIU/l). Antithyroglobulin antibodies were found to be negative. Ultrasonogram of the neck showed normal left lobe of thyroid and enlarged right lobe with multiple hypoechoic nodules with increased surrounding vascularity. Fine needle aspiration cytology of thyroid was then done. Cytology showed cellular smears with clusters of follicular epithelial cells, some of the cells showing Hurthle cell change, along with numerous clusters of epithelioid histiocytes, macrophages, few lymphocytes and focal areas of neutrophilic debris in the background. [Figures 2 to 6] An impression of De Quervain’s thyroiditis was then made. He was then treated with prednisone 40 mg/day for 10 days and gradually tapered over the next 8 weeks. On follow up, the patient reported resolution of pain and reduction in the size of the swelling. Follow up thyroid function tests after 3 months were found to be within normal limits.
DISCUSSION
De Quervain’s thyroiditis, also called as granulomatous thyroiditis or giant cell thyroiditis, is a rare form of thyroiditis which is spontaneously remitting and considered to be of viral etiology.[1] It presents typically in adults following an upper respiratory tract infection with fever and followed by diffuse and painful enlargement of thyroid.[2] Disruption of thyroid follicles due to inflammation initially releases the preformed thyroid hormones into the circulation producing a transient phase of hyperthyroidism, during which period the thyroid hormones T3 and T4 levels are increased and thyroid stimulating hormone (TSH) values are decreased. Thyroid function returns to normal by 6 to 8 weeks and may be followed by hypothyroidism, which is usually transient.[3] High titres of anti-thyroglobulin and anti-microsomal antibodies, which are so characteristic of Hashimoto thyroiditis, are not seen in De Quervain’s thyroiditis. In a few cases, thyroid may be asymmetrically enlarged which may raise the suspicion of neoplasia and hence may be referred for fine needle aspiration cytology.[4],[5] Cytological features include numerous clusters of epithelioid histiocytes along with multinucleated giant cells along with lymphocytes and degenerating follicular epithelial cells, some may show Hurthle cell change, in a dirty background containing cell debris and colloid. Multinucleated giant cells are numerous and is a more striking finding. Scant unremarkable macrofollicle fragments and colloid are usually present.[6] Granulomas may also be seen in the thyroid as a histiocytic response to hemorrhage, usually as a reaction to spilled colloid adjacent to a neoplasm following aggressive clinical examination (palpation thyroiditis). It can also be seen in fungal infections, sarcoidosis, some types of vasculitis or rarely as a foreign body giant cell reaction.[7],[8] Multinucleated giant cells are also seen in autoimmune thyroiditis, which can be confirmed by increased titres of anti-microsomal and anti-thyroglobulin antibodies.[9] Aspiration of intact follicles (pseudo-giant cells) should not be mistaken for multinucleated giant cells. Multinucleated giant cells along with epithelioid cells and lymphocytes, seen in tuberculosis, a rare infection affecting the thyroid gland, should also be kept in mind as a differential diagnosis in such situations. Tuberculosis of thyroid may present as multiple caseating granulomas, cold abscess with multiple sinuses or as a chronic fibrosing type. Especially, the chronic fibrosing tuberculous lesion of the thyroid may be difficult to distinguish from De Quervain’s thyroiditis. In such cases, demonstration of acid fast bacilli by Zeihl-Neelsen staining would be more useful for confirmation of diagnosis, though it may be often negative in tissue sections. This along with any other clinical manifestations of tuberculosis would be helpful for confirmation.[10] The dirty background may be mistaken for necrosis and this along with degenerative atypia in the follicular epithelial cells may lead to an inappropriate suspicion of malignancy. Rarely, the pale elongated or folded nuclei of the epithelioid histiocytes may be potentially misinterpreted as papillary carcinoma nuclei.[11] Anaplastic carcinoma of thyroid may rarely contain osteoclast-like giant cells as a reactive population, which may cause a diagnostic confusion with a granulomatous process, but it can usually be ruled out owing to the absence of significant nuclear atypia in De Quervain’s thyroiditis.[12]
CONCLUSION
De Quervains thyroiditis is a rare form of inflammation of the thyroid and the differential diagnosis to be considered ranges from various nonneoplastic to neoplastic lesions. This case illustrates that De Quervain’s thyroiditis has to be considered in the differential diagnosis of painful asymmetrical enlargement of thyroid, especially when there are numerous epithelioid granulomas with multinucleated giant cells along with the absence of antithyroid antibodies and rapid response to steroid therapy.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
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