IJCP_July_2011 by IJCP

Indexed with IndMED

www.ijcpgroup.com

ISSN 0971-0876

Single Copy Rs. 300/-

Indian Journal of

CLINICAL PRACTICE 53-104 Pages

July 2011

Volume 22, Number 2

An Interesting Cause for Jaundice

Dr KK Aggarwal Group Editor-in-Chief

Indian Journal of

Online Submission

Clinical Practice

Volume 22, Number 2, July 2011

CoNtENtS

An IJCP Group Publication Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor Dr Deepak Chopra Chief Editorial Advisor

FROM THE DESK OF GROUP EDITOR-IN-CHIEF

Medical Therapy for Coronary Disease with Reduced Left Ventricular Function

KK Aggarwal

Dr KK Aggarwal CMD, Publisher and Group Editor-in-Chief Dr Veena Aggarwal Joint MD & Group Executive Editor Anand Gopal Bhatnagar Editorial Anchor

ORIGINAL STUDY

Evaluation of Efficacy and Safety of Liv.52 HB Capsules in Chronic Hepatitis B

Amit Banerjee, Pralhad S Patki

IJCP Editorial Board Dr Alka Kriplani Asian Journal of Obs & Gynae Practice Dr VP Sood Asian Journal of Ear, Nose and Throat Dr Praveen Chandra Asian Journal of Clinical Cardiology Dr Swati Y Bhave Asian Journal of Paediatric Practice Dr Vijay Viswanathan The Asian Journal of Diabetology Dr KMK Masthan Indian Journal of Multidisciplinary Dentistry Dr M Paul Anand, Dr SK Parashar Cardiology Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty Diabetology Dr Ajay Kumar Gastroenterology Dr Hasmukh J Shroff Dermatology Dr Georgi Abraham Nephrology Dr Sidharth Kumar Das Rheumatology Dr V Nagarajan Neurology Dr Thankam Verma, Dr Kamala Selvaraj Obs and Gyne Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

ORIGINAL ARTICLE

Urinary Iodine Excretion in Urine Samples Among Children in Dahod District, Gujarat

JR Damor, NG Padhiyar, GL Ninama

REVIEW ARTICLE

Heat-Related Illness

Jonathan A. Becker, Lynsey K. Stewart

CASE REPORT

An Interesting Cause for Jaundice

G Geetha, P Chitrambalam

Dengue Myopericarditis

Lubna Zafar, Anjum Parvez, Asif Hasan, Mohammad Asif

Organophosphate-induced Delayed Spastic Paraplegia and Distal Motor Neuropathy

Ibraheem Khan, Chandra Kant, Alok Goyal

Steatocystoma Multiplex with Oligodontia: A Clinical Report Bharat Kumar PV, Wilma Delphine Silvia CR, Bhanu Prakash, Santosh KV

Indian Journal of

Clinical Practice

Volume 22, Number 2, July 2011

Contents

Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Pvt. Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com

practice guidelines

AAP Revises Policy Statement on the Use of Postnatal Corticosteroids for Bronchopulmonary Dysplasia

Printed at IG Printers Pvt. Ltd., New Delhi E-mail: igprinter@rediffmail.com printer_ig@yahoo.com

photo quiz ÂŠ Copyright 2011 IJCP Publications Pvt. Ltd. All rights reserved. The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Pvt. Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

Editorial Policies The purpose of IJCP Academy of CME is to serve the medical profession and provide print continuing medical education as a part of their social commitment. The information and opinions presented in IJCP group publications reflect the views of the authors, not those of the journal, unless so stated. Advertising is accepted only if judged to be in harmony with the purpose of the journal; however, IJCP group reserves the right to reject any advertising at its sole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP group of a particular policy, product or procedure. We believe that readers need to be aware of any affiliation or financial relationship (employment, consultancies, stock ownership, honoraria, etc.) between an author and any organization or entity that has a direct financial interest in the subject matter or materials the author is writing about. We inform the reader of any pertinent relationships disclosed. A disclosure statement, where appropriate, is published at the end of the relevant article. Note: Indian Journal of Clinical Practice does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.

Rapidly Growing Mass in the Chest Wall

clinical algorithm

An Approach to the Treatment of Peptic Ulcer Disease

lighter reading

Lighter Reading

emedinews Section

From eMedinewS

Editorial & Business Offices Delhi

Mumbai

Kolkata

Bangalore

Chennai

Hyderabad

Dr Veena Aggarwal 9811036687

Nilesh Aggarwal 9818421222

E - 219, Greater Kailash, Part - 1, New Delhi - 110 048 Cont.: 40587513 editorial@ijcp.com drveena@ijcp.com drveenaijcp@gmail.com

Building No. D-10 Flat No 43, 4th Floor Asmita Co-operative Housing Society Marvey Road Near Charkop Naka Malad (W) Mumbai - 400 095 nilesh.ijcp@gmail.com

Sr. BM Ritu Saigal 9831363901

Sr. BM H Chandrashekar 9845232974

Sr. BM Venugopal 9849083558

Flat 5E, Merlin Estate Geetanjali 25/8, Diamond Harbour Road Kolkata - 700 008 Cont.: 24452066 ritu@ijcp.com

Arora Business Centre, 111/1 & 111/2, Dickenson Road (Near Manipal Centre) Bangalore - 560 042 Cont.: 25586337 chandra@ijcp.com

Sr. BM Chitra Mohan 9841213823 40A, Ganapathypuram Main Road Radhanagar Chromepet Chennai - 600 044 Cont.: 22650144 chitra@ijcp.com

Subscription Dinesh: 9891272006 subscribe@ijcp.com Ritu: 09831363901 ritu@ijcp.com

Sr.: Senior; BM: Business Manager

H. No. 16-2-751/A/70 First Floor Karan Bagh Gaddiannaram Dil Sukh Nagar Hyderabad 500 059 Cont.: 65454254 venu@ijcp.com

From the Desk oF Group eDitor-in-ChieF

Medical Therapy for Coronary Disease with Reduced Left Ventricular Function

Dr KK Aggarwal

Padma Shri and Dr BC Roy National Awardee Sr. Physician and Cardiologist, Moolchand Medcity President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group Editor-in-chief, eMedinewS Chairman Ethical Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) emedinews@gmail.com http://twitter.com/DrKKAggarwal Krishan Kumar Aggarwal (Facebook)

or most patients with left ventricular ejection fraction (LVEF) of 35% or less and coronary artery disease amenable to coronary artery bypass graft (CABG) surgery the new evidence suggests for an initial course of optimal medical therapy alone rather than medical therapy plus CABG surgery. This is based upon the significant morbidity associated with CABG surgery. CABG surgery, however, may be preferred by patients who are willing to accept the increased risk of morbidity related to surgery in exchange for a potential mortality benefit versus optimal medical therapy alone. CABG surgery should also be considered for patients with ongoing anginal symptoms despite optimal medical therapy. The Surgical Treatment for Ischemic Heart Failure trial, a randomized trial, compared the combination of optimal medical therapy and surgical revascularization with optimal medical therapy alone in patients with stable coronary heart disease (CHD), LVEF of 35% or less, and coronary artery disease amenable to CABG surgery. Compared with optimal medical therapy alone, optimal medical therapy plus CABG surgery resulted in no significant improvement in the primary outcome of all-cause mortality at a median follow-up of 56 months. In the past, most observational studies have shown that surgical revascularization of hibernating myocardium improves both survival and left function. This is based on the fact that 50% of patients with left ventricular systolic dysfunction due to CHD have a significant amount of viable (e.g., hibernating) myocardium. And much more in this issue ... n

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

oriGinAl stuDy

Evaluation of Efficacy and Safety of Liv.52 HB Capsules in Chronic Hepatitis B Amit Banerjee*, Pralhad S Patki**

AbstrACt The present study was planned to evaluate the clinical efficacy and safety of Liv.52 HB capsules in the treatment of chronic hepatitis B in a double-blind, randomized and placebo-controlled clinical study. A total of 28 male and female patients aged between 18-65 years with positive hepatitis B surface antigen for at least six months and those willing to give informed consent were included in the study. A detailed medical history and symptomatic evaluation was done. Biochemical investigations included total bilirubin, aspartate and alanine aminotransferase, serum alkaline phosphatase and total proteins. Clinical examinations were repeated every four weeks for 24 weeks and biochemical investigations were repeated only after 24 weeks. All the patients were randomized into either Liv.52 HB group (n = 14) or placebo group (n = 14). The two groups were similar with regards to the demographic data, serological parameters and biochemical investigations. The Liv.52 HB group received two capsules twice-daily and placebo group received two capsules twice-daily for 24 weeks. Statistical analysis was carried out using GraphPad Prism, Version 4.03 for windows, Graphpad Software. All the patients completed the study and their data was available for analysis. Significant evidences of hepatoprotective effect of Liv.52 HB in patients with hepatitis B virus infection in terms of clinical response and reduction in biochemical parameters were observed after 24 weeks of treatment. Though, the trial has limitations, the treatment group showed significant clearance of surface antigen as compared to placebo group. The clinical and biochemical recovery in Liv.52 HB group was faster as compared to placebo group. There were no clinically significant adverse reactions either reported or observed during the entire study period. The overall compliance to the treatment was good and no treatment discontinuations were reported. The results of the present study show clinical benefits of Liv.52 HB and appear promising in the management of hepatitis B. Key words: Chronic hepatitis B, Liv.52 HB, placebo

ver since the identification of Australian antigen in 1967, which is now known as hepatitis B surface antigen (HBsAg), hepatitis B infection has emerged as one of the top 10 leading causes of death in the world. Prevalence of HBsAg in India varies from 1 to 13%, with an average of 4.7%.1-3 Hepatitis B virus (HBV) is present in the blood, saliva, semen, vaginal secretions, menstrual blood and to a lesser extent, sweat, breast milk, tears and urine of infected individuals. A highly resilient virus, HBV is resistant to breakdown, can survive outside the body and is easily transmitted through contact with infected body fluids. In areas of high endemicity, the most common route of transmission is perinatal or *Professor and Head, Dept. of Medicine Medical College, Kolkata **Head, Medical Services and Clinical Trials R&D Center, The Himalaya Drug Company, Makali, Bangalore Address for correspondence Dr Pralhad S Patki Head, Medical Services and Clinical Trials R&D Center, The Himalaya Drug Company, Makali Bangalore - 562 123 E-mail: dr.patki@himalayahealthcare.com

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

the infection is acquired during the preschool years. In areas of intermediate endemicity, transmission is either perinatal or horizontal.4,5 The route of transmission has important clinical implications, because there is a very high probability of developing chronic hepatitis B (CHB), if the infection is acquired perinatally or in the preschool years.6 The use of unsafe injections poses a particular public health problem in developing countries.7 Contaminated needles cause 8-16 million HBV infections each year, compared with 2.3-4.7 million hepatitis C virus infections and 80,000-1,60,000 human immunodeficiency virus infections.8 In areas of low endemicity, most HBV infections are acquired by horizontal transmission in early adult life, i.e., through intravenous drug use or unprotected sexual activities.5 There are two types of CHB namely hepatitis B e antigen (HBeAg)-positive and HBeAg-negative. Both types are associated with active HBV replication and could produce active liver disease. HBeAg-positive CHB consists of immunoreactive and immunotolerant phases.9 59

original study The immunoreactive phase is mostly seen in adults, with patients having elevated liver enzymes and high levels of viral DNA. The immunotolerant phase is usually seen in children who are infected at birth. They have normal liver enzymes, despite having very high levels of viral replication. The immunotolerant phase may change into the immunoreactive phase. The latent period may be 20-30 years for those who are infected at birth and much shorter for those who have been infected in adolescence or adulthood.10 Seroconversion from HBeAg-positive to HBeAg-negative and hepatitis B e antibody (HBeAb)-positive states are followed by biochemical, biological and histological resolution.11 In most patients, this is a transient phase to the inactive carrier state. The biochemical, virological and histological abnormalities will persist in 1-5% of patients in spite of seroconversion. This group of patients is called HBeAg-negative CHB. Although CHB infection is highly preventable through vaccination, once it has been established, the sole option for long-term liver disease is treatment. The goals of treatment are sustained viral suppression, normalization of serum glutamic pyruvic transaminase (SGPT) levels and improvement in liver histology leading to long-term reduction in the risk of cirrhosis and hepatocellular carcinoma.12 Ongoing therapies of hepatitis B are interferon, lamivudine and most recently adefovir dipivoxil, have limited long-term efficacy. Improvement in treatment options will reduce morbidity and mortality for chronically infected individuals.13 Ayurveda, an indigenous system of medicine in India, has a long tradition of treating liver disorders with plant drugs. In the present study, Liv.52 HB capsule was evaluated for its efficacy and safety in management of CHB. It is a herbal formulation consisting of 125 mg each of hydroalcoholic extracts of the herbs Cyperus rotundus and Cyperus scariosus. Aim of the Study The present study was planned to evaluate the clinical efficacy and safety of Liv.52 HB capsules in the treatment of CHB. Study Design A double-blind, randomized and placebo-controlled clinical study conducted at Medical College, Kolkata, India. The study protocol, case report forms, regulatory 60

clearance documents, product-related information and informed consent form were submitted to the ‘Institutional Ethics Committee’ and were approved by the same. Material and Methods Inclusion Criteria 

 

Patients with positive HBsAg for at least six months. Patients willing to give informed consent. The SGPT levels of these patients should be within six times the upper limit of the normal at the screening visit.

Exclusion Criteria 



Patients with severe decompensated liver disease (defined by serum albumin ≤36 g/dl, bilirubin ≥15 g/dl, prothrombin time ≥2 second prolonged or a history of ascites, variceal hemorrhage or hepatic encephalopathy) and pancytopenias (defined as hemoglobin <11 g/dl, white cell count <4,000/mm3). Co-infection by hepatitis C virus, history of hepatocellular carcinoma, severe hypertension, serious cardiac failure of Grade III or more, renal failure, endocrine disorders (hyperthyroidism, hypogonadism or Cushing’s syndrome), patients on corticosteroids, methotrexate or heparin, diabetes, bone malignancy with pathological fractures. Patients with a history of using interferon or antiviral agents. Women of childbearing age not willing to follow the adequate contraceptive method and lactating women.

Study Procedure

A total of 28 male and female patients aged between 18-65 years were recruited. At the initial randomization visit, a detailed medical history and symptomatic evaluation was done, to score the severity and grading of symptoms such as icterus for evidence of clinical jaundice, anorexia, nausea and vomiting, fatiguability and weight loss. All the patients were routinely screened and subjected to biochemical investigations: Total bilirubin, serum glutamic oxaloacetic transaminase (SGOT) and SGPT, serum alkaline phosphatase (ALP) and total proteins. Clinical Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

original study examinations were repeated every four weeks for 24 weeks and biochemical investigations were repeated only after 24 weeks. All the patients were randomized arbitrarily using random table into either Liv.52 HB group (n = 14) or placebo (n = 14). The two groups were similar with regards to the demographic data, serological parameters and biochemical investigations. The Liv.52 HB group received two capsules twice-daily and placebo group received two capsules twice-daily for 24 weeks. Primary endpoints: HBsAg clearance. Secondary endpoints: HBV DNA levels and SGPT normalization to 40 IU/l at the end of treatment. Statistical Analysis

Statistical analysis was carried out using GraphPad Prism, Version 4.03 for windows, Graphpad Software, San Diego, California, USA. Biochemical parameters were analyzed using paired t-test for within the group comparison and unpaired t-test for between the group comparisons. The values are expressed as mean ± SD. Serological parameters were analyzed using Fisher’s exact test. The minimum level of significance was fixed at a 95% confidence limit and a 2-sided p value of <0.05 was considered significant. Adverse Events All adverse events, either reported or observed by patients, were recorded with information about severity, date of onset, duration and action taken regarding the study drug. Relation of adverse events to the study medication was predefined as ‘Unrelated’ (follows a reasonable temporal sequence from the administration of the drug), ‘Possible’ (follows a known response pattern to the suspected drug, but could have been produced by the patient’s clinical state or other modes of therapy administered to the patient), and ‘Probable’ (follows a known response pattern to the suspected drug that could not be reasonably explained by the known characteristics of the patient’s clinical state). Patients were allowed to voluntarily withdraw from the study, if they so desired without assigning reasons. For patients withdrawing from the study, efforts were made to ascertain the reason for dropout. Noncompliance (defined as failure to take <80% of the medication) was not regarded as treatment failure, and reasons for noncompliance were noted. Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Results Twenty-eight patients (18 males and 10 females) with a mean age of 35.90 ± 10.60 years participated in this double-blind, placebo-controlled clinical study (Table 1). There was no statistical difference in the demographic characters between the Liv.52 HB group and placebo groups. All the patients completed the study and their data was available for analysis. Significant evidence of hepatoprotective effect of Liv.52 HB was seen in patients with HBV infection, in terms of clinical response, reduction in biochemical and serological parameters. The clinical effects of Liv.52 HB started to appear as early as 12 weeks and by 24 weeks most of the patients showed a significant improvement in appetite. Clinical reduction of icterus was observed as early as 12 weeks. The effect was also linked with the disappearance of nausea and vomiting from the 12th week onwards. As appetite improved, the easy fatiguability of patients was reduced from the 12th week onwards. After starting treatment patients did not display further evidence of weight loss. It was evident that Liv.52 HB showed a hepatoprotective activity in controlling the early symptoms of HBV infection (Table 2). Though improvements in clinical symptoms were observed in the placebo group, the values were not clinically significant (Table 3). Investigations on the biochemical parameters demonstrated evidence of a significant improvement in bilirubin, albumin, SGPT and ALP levels in Liv.52 HB treated patients. The mean total bilirubin of 4.361 ± 3.704 mg/dl at entry was reduced to 0.910 ± 0.406 mg/dl after end of the treatment with significance of p < 0.017 and albumin was also improved from 3.591 ± 0.404 g/dl to 4.106 ± 0.342 g/dl after end of the treatment with significance of p < 0.015. SGPT and ALP also showed a significant reduction after the end of the treatment with significance of p < 0.005 and p < 0.019, respectively. Though there Table 1. Demographic Details Parameters

n = 28

Age (years)

35.90 ± 10.60

Male:Female

18:10

H/o smoking

H/o alcohol consumption

Diet (veg/nonveg)

16/12

original study Table 2. Results of Clinical Observations with Liv.52 HB Treatment (Mean ± SD) Clinical symptoms

At entry

Post-treatment 4 weeks

8 weeks

12 weeks

16 weeks

20 weeks

24 weeks

Appetite

0.58 ± 0.14

0.88 ± 0.09

1.08 ± 0.11

1.69 ± 0.22*

1.98 ± 0.20*

2.18 ± 0.12*

2.48 ± 0.04*

Nausea and vomiting

0.62 ± 0.12

0.51 ± 0.08

0.36 ± 0.09

0.24 ± 0.04†

0.12 ± 0.03*

0.06 ± 0.00*

0.02 ± 0.00*

Fatigue

0.75 ± 0.07

0.58 ± 0.14

0.49 ± 0.11

0.38 ± 0.16*

0.31 ± 0.06*

0.23 ± 0.09*

0.16 ± 0.01*

Weight

0.78 ± 0.11

0.54 ± 0.06

0.46 ± 0.09

0.39 ± 0.04*

0.30 ± 0.09*

0.24 ± 0.08*

0.22 ± 0.04*

Jaundice

1.92 ± 0.07

1.18 ± 0.09

0.95 ± 0.08

0.75 ± 0.12*

0.45 ± 0.04*

0.12 ± 0.03*

0.08 ± 0.02*

*p < 0.001 as compared to ‘at entry’ values.

†p

< 0.05 as compared to ‘at entry’ values.

Table 3. Results of Clinical Observations with Placebo Treatment (Mean ± SD) Clinical symptoms

At entry

Post-treatment 4 weeks

8 weeks

12 weeks

16 weeks

20 weeks

24 weeks

Appetite

0.59 ± 0.06

0.62 ± 0.03

0.78 ± 0.11

0.82 ± 0.17

0.91 ± 0.12

0.96 ± 0.12

1.01 ± 0.12

Nausea and vomiting

0.56 ± 0.14

0.48 ± 0.11

0.43 ± 0.03

0.35 ± 0.00

0.29 ± 0.12

0.25 ± 0.04

Fatigue

0.65 ± 0.06

0.61 ± 0.04

0.59 ± 0.11

0.53 ± 0.09

0.46 ± 0.01

0.41 ± 0.09

0.36 ± 0.11

Weight

0.68 ± 0.09

0.62 ± 0.08

0.58 ± 0.09

0.52 ± 0.08

0.48 ± 0.04

0.44 ± 0.02

0.42 ± 0.08

Jaundice

1.92 ± 0.08

1.74 ± 0.12

1.58 ± 0.08

1.35 ± 0.03

1.18 ± 0.02

1.06 ± 0.12

1.02 ± 0.07

Table 4. Effect of Liv.52 HB on Biochemical Parameters (Mean ± SD) Parameters

Placebo (n = 14) Initial

After treatment

Initial

After treatment

Bilirubin (mg/dl)

1.912 ± 1.908

1.229 ± 0.657 (NS)

4.361 ± 3.704

0.910 ± 0.406 (p < 0.017)

Albumin (g/dl)

3.544 ± 0.604

3.718 ± 0.662 (NS)

3.591 ± 0.404

4.106 ± 0.342 (p < 0.015)

Total protein (g/dl)

7.035 ± 0.799

6.965 ± 0.041 (NS)

6.760 ± 0.515

6.530 ± 0.279 (NS)

Fall in SGOT levels (U/l)

55.23 ± 118.0

99.70 ± 146.5 (NS)

Fall in SGPT levels (U/l)

40.00 ± 78.08

179.5 ± 228.1 (p < 0.005)

Fall in ALP levels (U/l)

32.27 ± 53.78

99.78 ± 63.55 (p < 0.019)

was reduction in SGOT and total protein levels the values were not statistically significant in Liv.52 HB treated patients. However, in placebo group, there was no improvement in bilirubin levels. There was reduction in the levels of albumin and total protein but the values were not statistically significant (Table 4). Before the treatment, HBsAg was detected in all the patients. HBsAg became undetectable in Liv.52 HB in nine of the 14 patients after 24 weeks of treatment and this difference was statistically significant (p < 0.02). Only two patients were HBsAg negative at the end of 24 weeks of treatment in placebo group. At entry, 10 of the 14 patients were detected positive for HBV DNA and after 24 weeks of treatment with Liv.52 HB, all the 10 cases were negative for the same (p < 0.05). Only four patients showed negative for HBV DNA out of 10 patients in 62

Liv.52 HB (n = 14)

the placebo group at the end of treatment (Table 5). Clinical characteristics, biochemical investigations and serological parameters showed that the group receiving Liv.52 HB had significantly better results than those receiving placebo. There were no clinically significant adverse reactions either reported or observed during the entire study period. The overall compliance to the treatment was good and no treatment discontinuations were reported. Discussion Despite the existence of safe and efficient vaccines against HBV infection for almost 20 years,14 it remains a major public health problem worldwide with 400 million chronic carriers, who are exposed to Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

original study Table 5. Serological Parameters at the End of the Treatment Parameters HbsAg HbeAg HBV DNA

Placebo (n = 14)

Liv.52 HB (n = 14)

Present

Absent

Present

Absent

Present

Absent

the risk of developing liver cirrhosis and hepatocellular carcinoma.15 The currently available treatments for CHB come with their own limitations. Conventional therapies like Îą-interferon and lamivudine, which are costly at present and whose use are associated with dose-limiting side effects16-18 in the management of CHB. The issues to be considered include efficacy, safety, resistance and cost.19 The beneficial results observed in this study in Liv.52 HB group compared to placebo could be due to synergistic actions of the herbs, C. rotundus and C. scariosus present in the study drug. The roots and rhizomes of C. rotundus is used in different diseases like chronic diarrhea, inflammation, skin rashes and excess bleeding. It has also antiestrogenic, antimicrobial, anthelmintic, antihistaminic, antiemetic, antipyretic and antidiabetic activities.20 The roots of C. scariosus have a folkloric reputation as a cordial, tonic desicant, emmenagogue, diaphoretic and diuretic. It is an important ingredient of several prescriptions used in indigenous system of medicine to treat a variety of diseases including diarrhea, epilepsy, fever, gonorrhea, syphilis and liver damage.21 Conclusion The present study shows significant evidence of hepatoprotective effect of Liv.52 HB in patients with hepatitis B infection in terms of clinical response and reduction in biochemical parameters. Though, the trial has limitations, the treatment group showed significant clearance of surface antigen as compared to placebo group. The clinical and biochemical recovery in Liv.52 HB group was faster as compared to placebo group indicating the activity of the Liv.52 HB in patients infected with HBV. There were no clinically significant adverse reactions either reported or observed during the entire study period. The overall compliance to the treatment was good and Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

p value p < 0.02 p < 0.05 p < 0.05

no treatment discontinuations were reported. The results of the present study showing clinical benefit of Liv.52 HB appear promising in the management of hepatitis B infection. References 1. Thyagrajan SP, Jayaram S, Mohanavalli B. Prevalence of HBV in general population of India. In: Hepatitis B in India: Problems and Prevention. Sarin SK, Singhal AK (Eds.), CBS, New Delhi 1996:5-16. 2. Tandon BN, et al. Indian J Med Res 1991;93:337-9. 3. Jain RC, et al. J Assoc Physicians India 1992;40(6): 390-1. 4. Lok AS. N Engl J Med 2002;346(22):1682-3. 5. Gust ID. Gut 1996;38(Suppl 2):S18-23. 6. Chen CJ, et al. J Gastroenterol Hepatol 2000;15(Suppl): E3-6. 7. Simonsen L, et al. Bull World Health Organ 1999;77(10):789-800. 8. Kane A, et al. Bull World Health Organ 1999;77(10): 801-7. 9. Montazeri G. Arch Iran Med 2006;9(1):1-10. 10. Lok AS, et al. Gastroenterology 1987;92(6):1839-43 11. Hsu YS, et al. Hepatology 2002;35(6):1522-7. 12. Jacobson IM. Am J Gastroenterol 2006;101(Suppl 1): S13-8. 13. Conjeevaram HS, Lok AS. J Hepatol 2003;38(Suppl 1): S90-103. 14. Szmuness W, et al. Hepatology 1981;1(5):377-85. 15. Lee WM. N Engl J Med 1997;337(24):1733-45. 16. Fontaine H, et al. Transplant Proc 2001;33(3):2327-9. 17. Kerl K, et al. Br J Dermatol 2003;149(3):656. 18. Schaefer M, et al. Hepatology 2003;37(2):443-51. 19. Xu XW, Chen YG. Hepatobiliary Pancreat Dis Int 2006;5(3):350-9. 20. Pal DK, Dutta S. Indian J Pharm Sci 2006;68(2):256-8 21. Gilani AH, et al. Arch Pharm Res 1994;17(3):145-9.

oriGinAl ArtiCle

Urinary Iodine Excretion in Urine Samples Among Children in Dahod District, Gujarat JR Damor*, NG Padhiyar**, GL Ninama†

AbstrACt Aim: To measure urinary iodine excretion level and to assess the iodine level in salt sample. Study design: Cross-sectional study done in 30 randomly selected wards/villages of Dahod district. Materials and method: The IDD survey at the Dahod district was conducted by population proportionate to size (PPS) cluster sampling. A sample of 90 children (45 boys and 45 girls) of age group of 6-12 years from the school was taken. In each cluster, seven urine samples of boys and seven samples of girls were collected and sent to the public health laboratories. From each cluster, salt samples were collected from a minimum of 10 houses and tested with the use of spot salt testing kit for the presence of iodine. Results: The median urinary iodine level was 115 μg/dl. Age-wise distribution of urinary iodine showed that the proportion of children with urinary iodine excretion <100 μg/dl was lowest in the 6-year age group, whereas the highest proportion was in the 10-year age group. Out of 300 salt samples, 207 samples (69%) had >15 ppm (parts per million) iodine; four samples (1.3%) had <15 ppm iodine. This means that the use of iodized salt was 70.3%. Conclusion: The lowest urinary iodine excretion was seen in age group of six years whereas highest urinary iodine excretion was seen in age group of 10 years. In 69%, salt samples had >15 ppm iodine present and in 1.3%, samples had <15 ppm iodine present. Thirty percent of salt samples were noniodized. Key words: Iodine deficiency disorders, salt samples, urinary iodine excretion

odine is an essential micronutrient with an average daily requirement of 100-150 µg for normal human growth and mental development. Inadequate or poor intake of iodine can result in physical and mental retardation. It affects people of all ages, both sexes and of different socioeconomic backgrounds. The disorders caused due to deficiency of nutritional iodine in the food or diet are called iodine deficiency disorders (IDDs).1

According to Public Health Standards, an area is declared to be iodine deficient, if 5% or more of school-going children suffer from goiter (enlargement of the thyroid gland situated in the neck). From this point of view, several districts in the state of Gujarat have the problem of iodine deficiency. *Associate Professor **Assistant Professor Dept. of Community Medicine †Assistant Professor Dept. of Microbiology Medical College and SSG Hospital, Vadodara Address for correspondence Dr JR Damor D-27, Akanksha Duplex Opposite Laxmikunj Society Laxmipura Road, Gorwa Vadodara - 390 016, Gujarat E-mail: jivrajdamor@yahoo.co.in

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Major activities of National Iodine Deficiency Disorders Control Programme (NIDDCP) are to conduct surveys to assess the magnitude of the IDDs, monitoring of iodized salt consumption, laboratory monitoring of iodized salt, urinary iodine salt concentration and health education and publicity.1 It is a well-established fact that with the exception of certain types of goiter, IDDs are permanent and incurable. But, these disorders can be easily prevented. The simplest method to prevent the broad-spectrum of IDDs is to consume iodized salt daily. This is the most effective and inexpensive mode to prevent these disorders. Iodized salt should ensure availability of not <150 µg of iodine per person per day. Since salt is consumed by all every day, the supply of iodized salt will ensure the availability of iodine for normal body function. The average consumption of iodized salt per person per day is about 10 grams. This consumption is in moderate amounts. The Central Government had issued a notification banning the sale of noniodized salt for direct human consumption in the entire country with effect from 17th May, 2006 under the Prevention of Food Adulteration Act 1954. 65

original article Starting with Bharuch district in 1982, the State Government brought the entire state under IDD Control Programme in a phased manner by the year 1994. Surveys conducted by the Preventive and Social Medicine (PSM) Dept. of the Govt. Medical Colleges in the state show that IDDs continue to be a health problem in several districts of the state. The high prevalence rate was found in Dangs, Bharuch and Valsad districts.2 The geographical difference reflects the difference in iodine content in drinking water and to some extent in milk.3 Aims and Objectives  To determine median urinary iodine excretion in samples of school children.  To assess iodine level in salt samples in households and at retail shops.  To assess the availability of iodized salt and information, education and communication (IEC) material at public distribution system shop. Materials and Method The survey for IDDs at Dahod district was conducted by population proportionate to size (PPS) cluster sampling. Selection of villages/wards by PPS was done from list of villages/wards along with the population from the latest census. The data are available for all districts of the country on CD from Registrar General <100 µg/dl

Office. A sample of 30 villages/wards had to be selected from the district. The method of sampling used was PPS systematic sampling. A sample of 90 children (45 boys and 45 Girls) of age group of 6-12 years from the school and in each cluster, seven urine samples of boys and seven samples of girls were collected and sent to the public health laboratories. From each cluster, salt samples were collected from a minimum of 10 houses and tested with the use of spot salt testing kit for the presence of iodine. Limitations: As it is a cross-sectional study, children who were not present in school at the time of study could not be examined. Results and Review of Literature The median urinary iodine level is 115 μg/dl. The proportion of samples with urinary iodine <50 μg/dl was found to be 15.6%, which is <20% (Table 1). Thus, this corresponds to the category of adequate iodine nutrition as per WHO guidelines for monitoring for IDDs. The age-wise distribution of urinary iodine showed that the proportion of children with urinary iodine excretion <100 μg/dl was lowest in the 6-year age group, whereas the highest proportion was found in the 10-year age group (Table 2). The gender-wise distribution of urinary iodine excretion showed that the proportion of children with >100 µg/dl

100% 90% 80%

Percentage

70%

63.2

55.9

53.4

56.7

52.5

60.3

57.6

57.1

36.8

44.1

46.6

43.3

47.5

39.7

42.4

42.9

Total

60% 50% 40% 30% 20% 10% 0% 6

Age (years)

Figure 1. Age-wise distribution of urinary iodine.

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

original article

Boys

15%

57%

Girls

30%

58%

25%

<20 µg/dl

50-99 µg/dl

<20 µg/dl

50-99 µg/dl

20-49 µg/dl

≥100 µg/dl

20-49 µg/dl

≥100 µg/dl

Figure 2. Gender-wise distribution of urinary iodine excretion. The gender-wise distribution of urinary iodine excretion shows that the proportion of children with urinary iodine excretion >100 μg/dl was almost similar among both the genders.

urinary iodine excretion >100 μg/dl was almost similar among both the genders (Table 3). A population based cross-sectional study evaluated the iodine status among primary school children of Dhankuta and Dharan in eastern Nepal. The median urinary iodine excretion in primary school children of Dhankuta and Dharan in eastern Nepal were 157.1 μg/dl and 180.3 μg/dl, respectively. The percentage of salt samples containing iodine >15 ppm (parts per million) was 81.3% in Dhankuta and 89.6% in Dharan.4 Horton et al

Table 1. Distribution of Urinary Iodine (n = 400) Number

<20 μg/dl

Urinary iodine level

3.9%

20-49 μg/dl

11.7%

50-99 μg/dl

112

27.3%

<100 μg/dl

176

42.9%

≥100 μg/dl

234

57.1%

Total

410

100%

Table 2. Age-wise Distribution of Urinary Iodine Age (years)

Samples collected

<20 μg/dl

20-49 μg/dl

50-99 μg/dl

<100 µg/dl

≥100 μg/dl

No.

3.5

8.8

24.6

36.8

63.2

3.4

11.9

28.8

44.1

55.9

3.4

17.2

25.9

46.6

53.4

1.7

8.3

33.3

43.3

56.7

5.1

6.8

35.6

47.5

52.5

5.2

13.8

20.7

39.7

60.3

5.1

15.3

22.0

42.4

57.6

Total

410

3.9

11.7

112

27.3

176

42.9

234

57.1

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

original article Table 3. Gender-wise Distribution of Urinary Iodine Excretion Gender

<20 μg/dl

Samples collected

20-49 μg/dl

50-99 μg/dl

<100 μg/dl

≥100 μg/dl

No.

Male

207

3.4

15.5

24.6

43.5

117

56.5

Female

203

4.4

7.9

42.3

117

57.6

Total

410

3.9

11.7

112

27.3

176

42.9

234

57.1

Table 4. Taluka-wise Urinary Iodine Excretion Taluka

Total samples taken

Median urinary iodine excretion (20 μg/dl)

<20 μg/dl

20-49 μg/dl

50-99 μg/dl

≥100 μg/dl

No.

Dahod

195

2.4

10.8

86.7

Devgadhbaria

150

2.1

4.2

68.8

Dhanpur

3.6

17.9

64.3

14.3

Fatehpura

5.5

14.5

Garbada

222.5

9.5

90.5

Jhalod

2.4

20.2

38.1

39.3

Limkheda

12.9

21.4

45.7

Total

410

115

3.9

11.7

112

27.3

234

57.1

The median urinary iodine excretion is <100 μg/dl for Dhanpur, Jhalod, Fatehpura and Limkheda and it is >100 μg/dl for the rest of the Talukas.

observed that median urinary iodine excretion was significantly and positively related to household availability of iodized salt for developing countries.5 In a study of more than 2000 school children aged 6-12 years from Rajkot district, India, the median urinary iodine excretion was 110 μg/dl. Iodine level >15 ppm was found in 81% of salt samples tested at household level.6 Urinary iodine excretion level was <100 μg/dl in 42.9% talukas and >100 μg/dl in 57.1% talukas (Table 4). Out of 300 salt samples, 207 samples (69%) had >15 ppm iodine present (Table 5). Iodized salt was available in majority of private shops (88.8%) in the villages (Table 6). Conclusion The proportion of samples with urinary iodine <50 μg/dl was found to be 15.6%, which is <20%. Thus this corresponds to the category of adequate 68

iodine nutrition as per WHO guidelines for monitoring for IDDs. The age-wise distribution of urinary iodine showed that the proportion of children with urinary iodine excretion <100 μg/dl was lowest in the 6-year age group, whereas the highest proportion was found in the 10-year age group. Sixty-nine percent contained >15 ppm iodine; 30% of the salt samples were noniodized. There was no genderwise difference in urinary iodine excretion. More than 50% talukas had urinary iodine excretion levels >100 μg/dl. Recommendations  In Dahod district, Gujarat, 30% salt samples were found to be noniodized hence, there is a need to create awareness among community people and school children about iodized salt by using IEC materials. To make available iodized salt in all public  distribution shops. Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

original article Table 5. Use of Iodized Salt at Household Level Cluster No.

0 ppm

<15 ppm

≥15 ppm

Total samples

Table 6. Distribution of Private Shop with Respect to Salt Iodization Status Name of Taluka

Salt

Total

Iodized

Noniodized

Fatehpura

Jhalod

Limkheda

Dahod

Devgadhbaria

Dhanpur

Garbada

Total

89 (29.7%)

4 (1.3%)

207 (69%)

300

Total

Out of 300 salt samples, 207 samples (69%) contained >15 ppm iodine.



10% of private shops had noniodized salts, so there should be a strict implementation of ban on selling of noniodized salt.

Suggested Reading 1. Revised Policy Guidelines on National Iodine Deficiency Disorders Control Programme. National Rural Health Mission IDD & Nutrition Cell, Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India New Delhi, Revised Edition, October 2006. Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Iodized salt was available in majority of private shops (88.8%) in the villages.

2. State Nutrition cell, Government of Gujarat Document on Iodine deficiency Disorders Control Programme: Gujarat, 2008. 3. Pedersen KM, Laurberg P, Nohr S, Jorgensen A, Anderson S. Iodine in drinking water varies by more than 100-fold in Denmark. Importance for iodine content of infant formulas. Eur J Endocrinol 1999;140(5): 400-3. 4. Gelal B, Chaudhri RK, Nepal AK, Sah GS, Lamsal M, Brodie DA, et al. Iodine deficiency disorders among primary school children in eastern Nepal. Indian J Pediatr 2011;78(1):45-8. 5. Horton S, Miloff A. Iodine status and availability of iodized salt: an across-country analysis. Food Nutr Bull 2010;31(2):214‑20. 6. Chudasama RK, Verma PB, Mahajan RG. Iodinenutritional status and goiter prevalence in 6-12 years primary school children of Saurashtra region, India. World J Pediatr 2010;6(3):233-7. 7. Chudasama R, Patel UV, Patel RR, Verma PH. Iodine deficiency disorders in 6-12 years - old rural primary school children in Kutch District, Gujarat. Indian Pediatr 2010 Nov 30. pii: S097475590900853-1. [Epub ahead of print]. 8. Misra S, Kantharia SL, Damor JR. Prevalence of goitre in 6 -12 years school-going children of Panchmahal district in Gujarat, India. Indian J Med Res 2007;126(5):475‑9. 9. Biswas AB, Chakraborty I, Das DK, Biswas S, Nandy S, Mitra J. Iodine deficiency disorders among school children of Malda, West Bengal, India. J Health Popul Nutr 2002;20(2):180-3. 10. Kapil U, Sharma TD, Singh P. Iodine status and goiter prevalence after 40 years of salt iodisation in the Kangra District, India. Indian J Pediatr 2007;74(2):135-7.

review ArtiCle

Heat-Related Illness Jonathan A. Becker, Lynsey K. Stewart

AbstrACt Heat-related illness is a set of preventable conditions ranging from mild forms (e.g., heat exhaustion, heat cramps) to potentially fatal heat stroke. Hot and humid conditions challenge cardiovascular compensatory mechanisms. Once core temperature reaches 104°F (40°C), cellular damage occurs, initiating a cascade of events that may lead to organ failure and death. Early recognition of symptoms and accurate measurement of core temperature are crucial to rapid diagnosis. Milder forms of heatrelated illness are manifested by symptoms such as headache, weakness, dizziness, and an inability to continue activity. These are managed by supportive measures including hydration and moving the patient to a cool place. Hyperthermia and central nervous system symptoms should prompt an evaluation for heat stroke. Initial treatments should focus on lowering core temperature through cold water immersion. Applying ice packs to the head, neck, axilla, and groin is an alternative. Additional measures include transporting the patient to a cool environment, removing excess clothing, and intravenous hydration. Delayed access to cooling is the leading cause of morbidity and mortality in persons with heat stroke. Identification of at-risk groups can help physicians and community health agencies provide preventive measures. Key words: Heat exhaustion, heat cramps, heat stroke, core temperature, hyperthermia

eat-related illness represents a continuum of pathologic states and affects a diverse population. Over a 23-year period, it accounted for nearly 5,000 deaths in the United States.1 When the heat index is higher than 95°F (35°C), mortality increases in relation to elevation of temperature and duration of the heat wave.2 In most cases, these fatalities are preventable. Populations at risk include older persons, children, and persons who perform strenuous outdoor activities. Persons with heart and lung diseases, those with chronic mental disorders, and those taking medications that interfere with salt and water balance are also at increased risk.3 Early recognition of symptoms and rapid cooling are crucial, because heat stroke is a medical emergency.4,5 Definitions Milder forms of heat-related illness are associated with a core temperature less than 104°F (40°C)

and no central nervous system symptoms.6 Heat exhaustion is the inability to continue activity because of environmental conditions, and is postulated to be caused by a central mechanism that protects the body in times of overexertion.7 Heat stroke is characterized by an elevated core temperature of 104°F or above and central nervous system disturbances. Classic heat stroke often develops slowly over days. It predominantly occurs in older persons and those with chronic illness.3,5 Exertional heat stroke has a more rapid onset and is associated with higher core temperatures. It generally occurs in young, healthy persons and is characterized by hot skin with or without sweating and central nervous system alterations.6 Early recognition of the differences between heat stroke and milder forms of heat-related illness is crucial to avoid morbidity and mortality (Table 1).5-8 Thermoregulation

JONATHAN A. BECKER, MD, is an assistant professor in the Department of Family and Geriatric Medicine at the University of Louisville (Ky.). He is also director of the University of Louisville and Jewish Hospital Primary Care Sports Medicine Fellowship. LYNSEY K. STEWART, MD, is a fellow in the University of Louisville and Jewish Hospital Primary Care Sports Medicine Fellowship.

Source: Adapted from Am Fam Physician. 2011;83(11):1325-1330.

Conduction, evaporation, radiation, and convection play an integral part in cooling the body and maintaining normothermia. The direct transfer of heat from a warmer surface to a cooler surface is accomplished by conduction.6,8 The Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Review ARticle Table 1. Types of Heat-Related Illness Type

Symptoms

Signs

Initial treatment

Mild illness (e.g., cramps, exhaustion)

Diarrhea, dizziness, headache, irritability, loss of coordination, nausea/ vomiting, syncope, weakness

Core temperature < 104°F (40°C), normal mentation, goose flesh, pallor, tachycardia, hypotension

Move to a cool location, hydration, rest, sodium ingestion

Heat stroke

Confusion, dizziness, hallucination, headache, nausea/vomiting, syncope

Core temperature ≥ 104°F, altered mental Initiate on-site cooling, status, hot skin with or without perspiration, intravenous hydration, hypotension, seizure, tachycardia transport for emergency care

Information from references 5 through 8.

degree of conduction is dependent on the temperature gradient, the conductive properties of the object contacting the body, and what percentage of surface area is in contact.9 In the setting of heat-related illness, this concept becomes important when treating a patient with cold water immersion. As more body surface area is immersed, there is more conductive potential and treatment becomes more effective.10

vasoconstriction of the peripheral vasculature creating hypoperfusion.8 When a person’s core temperature is 104°F or greater, cellular damage occurs. There is a systemic inflammatory response, and increased cell wall permeability allows the release of endotoxins. These disruptions of homeostasis initiate a cascade of events that include tissue hypoxia, metabolic acidosis, and severe organ dysfunction.3,11-13

Perspiration is an evaporative mechanism that is dependent on sweat production and water vapor pressure gradient. In high ambient temperatures, heat loss is almost solely based on the rate of sweating. As humidity increases, evaporation becomes increasingly ineffective, thus perspiration serves as the most effective way humans release heat.6,8

Successive increments of increased exposure in a hot environment are necessary for persons to work safely at levels of heat that were previously intolerable or life threatening. Physiologic adaptations, such as improved sodium retention, increased glomerular filtration rate, and enhanced cardiovascular performance, can take several weeks.5 Heat shock proteins also assist cells in tolerating the heat.3,5 It may take athletes as long as 10 to 14 days of exercise training before the body can start adapting to large temperature fluctuations.8,9

Radiation is the process by which the body gains or loses heat without direct contact. Radiant energy is resorbed or reflected, which is why light-colored clothing can prevent heat-related illness by absorbing less heat.6 The body exchanges heat with the surrounding air by way of convection. The body gains heat from hot air, which comes in contact with the skin. Convective heat exchange increases with increasing air speed and larger gradient between air and skin temperature. Air circulation can be increased by use of air-conditioning or fans. Clothing that is more permeable to air or loose fitting also increases convective heat loss.5 Several acute physiologic alterations take place when the body is exposed to heat stress. Thermoregulation is coordinated by central nervous system centers in the hypothalamus and spinal cord, as well as peripheral centers in the skin and organs. Peripheral vasodilatation occurs to augment dermal blood flow, which allows convective heat loss into the surrounding air.6 In an effort to preserve central perfusion, there is Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Children are particularly prone to heat-related illness because of their greater surface area to body mass ratio compared with adults. This permits more heat transfer from the environment to the body. They also have a diminished ability to dissipate heat because of slower sweat rates, a higher temperature threshold for the initiation of sweating, and production of a more diluted sweat. Furthermore, they are slower to acclimatize to the heat and have less of a thirst response.8 Risk Factors Conditions and medications (Tables 2 and 3 1,3,6,14,15) that increase the risk of heat-related illness negatively affect the body’s ability to dissipate heat, acclimatize to the weather, or obtain adequate hydration.1,3 Older persons are at risk because of higher rates of medication use, immobility, and volume depletion. They have diminished cardiovascular compensation and an agerelated loss of heat shock proteins that impart further 71

Review ARticle Table 2. Risk Factors for Heat-Related Illness

Evalution of Heat-Related Illness

Age older than 65 years or younger than 15 years

Clinical signs/symptoms of heat-related illness

Cognitive impairment Heart and lung diseases

Obtain rectal temperature

Limited access to air-conditioning Mental illness Obesity

Rectal temp < 104°F (40°C) Rectal temp ≥ 104°F

Physical disabilities/impaired mobility Poor fitness level

Central nervous system Central nervous system signs/symptoms? signs/symptoms?

Sickle cell trait Strenuous outdoor activity during hottest daytime hours Urban residence or living on higher floors Information from references 1, 3, 6, 14, and 15.

Table 3. Medications and Substances that Contribute to Heat-Related Illness

Yes

Consider alternatives Central nervous system disease Febrile illness/sepsis

Yes

Mild forms of heatrelated illness: cramps, edema, syncope, exhaustion

Hypoglycemia

Alcohol

Diuretics

Hyponatremia

Alpha-adrenergic agonists Amphetamines·

Ephedra-containing supplements

Thyroid storm

Anticholinergics

Laxatives

Antihistamines

Neuroleptics

Benzodiazepines

Phenothiazines

Beta blockers

Stimulants

Calcium channel blockers

Thyroid receptor agonists

Cocaine

Tricyclic antidepressants

Seizure

Treat for mild heat-related illness: Observe for symptom resolution Monitor core temperature

Toxicity Symptoms resolve in < 30 minutes

Relative rest Remain in cool place Patient education

Symptoms persist ≥ 30 minutes or clinical deterioration Treat for heat stroke: Address airway, breathing, and circulation Initiate rapid cooling

Information from references 1, 3, 6, 14, and 15.

Start intravenous fluids Arrange for transport for emergency care

intolerance to extreme conditions.5 Medications impart risks, such as blunting cardiac output in times of stress, interfering with hydration, and inhibiting sweat.1,3

Figure 1. Algorithm for the initial evaluation of a patient with suspected heat-related illness.

Young, healthy persons who perform strenuous activity in hot and humid environments, such as athletes, military personnel, and persons who work outdoors, are at increased risk.1,6,14 Among high school athletes, persons who play football have a 10-fold increased risk of heat-related illness over persons playing any other sport, especially during preseason conditioning in the month of August.16 Persons who work outdoors have a 20-fold increased rate of heat-related death compared with persons in other forms of employment.17

these conditions can only be differentiated from early signs of heat stroke by obtaining an accurate measure of core temperature. A rectal temperature is the most reliable measurement because alternatives, including oral, tympanic, axillary, and skin temperatures, are less accurate.9,14 Core temperature and the presence or absence of central nervous system symptoms will help guide diagnosis and treatment (Fig. 1). In the absence of hyperthermia, the presence of central nervous system symptoms should prompt investigation for an alternative diagnosis.

Mild Heat-Related Illness

Heat Exhaustion

Mild forms of heat-related illness include cramps, edema, syncope, and exhaustion. If mental status is normal,

Common symptoms of heat exhaustion include headache, weakness, dizziness, goose flesh, nausea, Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Review ARticle vomiting, diarrhea, irritability, and loss of coordination. The skin may appear pale or ashen, with associated tachycardia or hypotension. Normal mentation is maintained. Patients with heat exhaustion should remove excess clothing and be moved to a shaded, cool environment. They should be placed in a supine position, preferably with their legs elevated. Oral fluids are preferred over intravenous fluids for rehydration in those who are conscious, able to swallow, and not losing fluids secondary to vomiting or diarrhea.9 Vital signs should be monitored, with transport to an emergency facility if symptoms do not improve after 20 to 30 minutes.3,6,9 Heat Cramps

Heat cramps, or exercise-associated muscle cramps, can occur in any setting, but are more common when exercising in hot and humid environments. Dehydration, depletion of electrolytes, and sodium losses from sweat all accelerate in this type of environment, especially in those who sweat profusely.18 Treatment includes rest, prolonged stretching of affected muscle groups, and oral sodium ingestion. Intravenous normal saline may be used for more rapid relief, especially for severe, diffuse cramping or when oral repletion is not possible.19 Heat Stroke Heat stroke is a true emergency that requires immediate recognition and treatment. It is defined by a pathologic elevation of core temperature of 104Â°F or greater and associated central nervous system disturbances.6,8,9,13,20 Physicians considering the diagnosis of heat stroke should obtain a rectal temperature as soon as possible. Although anhidrosis can occur in classic heat stroke, affected patients may continue to perspire.9,10,20 A broad constellation of clinical signs and symptoms can be observed in both forms of heat stroke. Treatment begins with stabilizing the patientâ&#x20AC;&#x2122;s airway, breathing, and circulation. Morbidity is greatly reduced with rapid cooling. If there are no other life-threatening complications, on-site cooling before transfer to the emergency department is preferred.8,9 Cold water immersion is the treatment of choice when available. It is associated with the lowest morbidity and mortality rates, and patients with exertional heat stroke treated with cold water immersion have a survival rate of almost 100 percent.10,21,22 Large cooling tanks are often 74

used at outdoor activities (e.g., football practice) or mass participation events. Although the cooling rates for cold water immersion have been shown to be superior, applying ice packs or cold, wet towels to the head, neck, axilla, and groin is an alternative option. Rapid air movement with a fan, in combination with spraying a moderate-temperature mist of water, encourages evaporative and convective cooling and is also effective.10 Intravenous hydration should be initiated as soon as possible to protect renal blood flow and avoid complications such as rhabdomyolysis. Patients evaluated in the community setting should be moved to a cool, shaded environment and have excess clothing removed while an ambulance is called.10,22 It is rare for a person to succumb within a few hours after heat stroke has ensued, but the action taken in this time may determine the degree of cell damage that portends recovery or progression to organ failure. Within 24 hours, those with heat stroke typically display evidence of muscle, kidney, and cardiac injury. Delayed or improper treatment is the likely cause of fatalities associated with hyperthermia.10,11 Prevention Regardless of the patient factors or method of cooling employed, rapid access to cooling is the most effective method to prevent heat stroke fatalities.9,14,23 Physicians can work with community leaders to identify older patients with chronic medical disease or physical disabilities who lack access to air-conditioning, and make cool facilities available during heat advisories. Spending time in air-conditioned areas is among the strongest factors in preventing heat-related deaths. Fans do not provide the same benefit.24 Athletic events should be held during cooler periods of the day and scheduled to avoid hot, humid months. Athletes, coaches, and parents should be educated about the early signs of heat-related illness, hydration, and initial treatments.6,9 Heat acclimatization is the best protection against heat-related illness. This involves a gradual progression of duration and intensity of exercise over 10 to 14 days.9 Proper hydration, lightweight and light-colored clothing, shaded rest areas, and rule adjustments to allow for frequent substitutions can also help protect young athletes.8 The Wet Bulb Globe Temperature, which takes into account temperature, humidity, and radiant thermal Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Review ARticle energy, is the preferred method for assessing weather conditions that precipitate heat-related illness; however, it may not be readily available. The heat index is the relationship between air temperature plus relative humidity and how a person’s body feels in that specific environment. A heat index chart25 may serve as a substitute in assessing the risk of heat-related illness on a given day.4 References 1. Centers for Disease Control and Prevention (CDC). Heat-related mortality–Arizona, 1993-2002, and United States, 1979-2002. MMWR Morb Mortal Wkly Rep. 2005;54(25):628-630. 2. Metzger KB, Ito K, Matte TD. Summer heat and mortality in New York City: how hot is too hot? Environ Health Perspect. 2010;118(1):80-86. 3. Glazer JL. Management of heatstroke and heat exhaustion. Am Fam Physician. 2005;71(11):2133-2140. 4. Jardine DS. Heat illness and heat stroke [published correction appears in Pediatr Rev. 2007;28(12):469]. Pediatr Rev. 2007;28(7):249-258. 5. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978-1988. 6. Howe AS, Boden BP. Heat-related illness in athletes. Am J Sports Med. 2007;35(8):1384-1395. 7. Martinez M, Devenport L, Saussy J, Martinez J. Drug-associated heat stroke. South Med J. 2002;95(8):799‑802. 8. Bytomski JR, Squire DL. Heat illness in children. Curr Sports Med Rep. 2003;2(6):320-324. 9. Armstrong LE, Casa DJ, Millard-Stafford M, Moran DS, Pyne SW, Roberts WO; American College of Sports Medicine. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556‑572. 10. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev. 2007;35(3):141-149. 11. Marshall SW. Heat injury in youth sport. Br J Sports Med. 2010;44(1):8-12. 12. Pease S, Bouadma L, Kermarrec N, Schortgen F, Régnier B, Wolff M. Early organ dysfunction course, cooling time and outcome in classic heatstroke. Intensive Care Med. 2009;35(8):1454-1458.

13. Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation [published correction appears in N Engl J Med. 1999;340(17):1376]. N Engl J Med. 1999;340(6):448-454. 14. Casa DJ, Armstrong LE, Ganio MS, Yeargin SW. Exertional heat stroke in competitive athletes. Curr Sports Med Rep. 2005;4(6):309-317. 15. Lopez RM, Casa DJ. The influence of nutritional ergogenic aids on exercise heat tolerance and hydration status. Curr Sports Med Rep. 2009;8(4):192-199. 16. Centers for Disease Control and Prevention (CDC). Heat illness among high school athletes–United States, 2005-2009. MMWR Morb Mortal Wkly Rep. 2010;59(32):1009-1013. 17. Centers for Disease Control and Prevention (CDC). Heat-related deaths among crop workers–United States, 1992-2006. MMWR Morb Mortal Wkly Rep. 2008;57(24):649-653. 18. Rodriguez NR, Di Marco NM, Langley S; American Dietetic Association; Dietitians of Canada; American College of Sports Medicine. American College of Sports Medicine position stand. Nutrition and athletic performance. Med Sci Sports Exerc. 2009;41(3):709‑731. 19. Bergeron MF. Exertional heat cramps. In: Armstrong LE. Exertional Heat Illnesses. Champaign, Ill.: Human Kinetics; 2003:91-102. 20. Sandor RP. Heat illness: on-site diagnosis and cooling. Phys Sportsmed. 1997;25(6):35-40. 21. Costrini A. Emergency treatment of exertional heatstroke and comparison of whole body cooling techniques. Med Sci Sports Exerc. 1990;22(1):15-18. 22. Proulx CI, Ducharme MB, Kenny GP. Effect of water temperature on cooling efficiency during hyperthermia in humans. J Appl Physiol. 2003;94(4):1317-1323. 23. Smith JE. Cooling methods used in the treatment of exertional heat illness. Br J Sports Med. 2005;39(8):503‑507. 24. Centers for Disease Control and Prevention (CDC). Heat-related deaths–four states, July-August 2001, and United States, 1979-1999. MMWR Morb Mortal Wkly Rep. 2002;51(26):567-570. 25. NOAA’s National Weather Service. Heat: A major killer. http://www.nws.noaa.gov/os/heat/index.shtml. Accessed September 1, 2010. (For complete article, visit www.aafp.org/afp)

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

CAse report

An Interesting Cause for Jaundice G Geetha*, P Chitrambalam**

AbstrACt We present herein the case of a 15-year-old boy who presented with progressive abdominal distension and yellowish discoloration of eyes. He was finally diagnosed as Rosai-Dorfman disease, a rare benign proliferative histiocytic disorder. Key words: Terry’s nails, Rosai-Dorfman disease

Case Report A 15-year-old boy was admitted with 2-week history of progressive abdominal distension, yellowish discoloration of eyes. He also had low grade fever with evening rise of temperature, swelling in the legs, passage of high-colored urine, clay colored stool, pruritus, easy fatigability, and loss of appetite and loss of weight. There was no previous history of bone pain, bleeding manifestations, neuropsychiatric manifestations, ENT, lung, renal or skin manifestations. The patient was suspected to have tuberculous lymphadenopathy, and was started on antituberculosis treatment (ATT) one month prior to the onset of the symptoms. He also underwent native treatment for jaundice. On examination, he was conscious, oriented, had anemia, jaundice, pitting pedal edema, posterior cervical lymphadenopathy on the left side (multiple, matted and each 1-2 cm in size), black discoloration of nails (Terry’s nails) (Fig. 1) and Kayser-Fleischer rings (KF rings) in the eyes. His abdomen was uniformly distended with full flanks, no dilated veins. He had hepatomegaly upto 4 cm below right costal margin, which had smooth surface and firm consistency, palpable spleen and free fluids abdomen. Other system examinations were normal.

*Postgraduate **Additional Professor Institute of Internal Medicine, MMC Chennai

Figure 1. Terry’s nails.

Investigations The investigations showed normal blood picture and renal function. Liver function tests (LFTs) showed obstructive pattern (direct bilirubin 19.2 mg/dl of total 22.2 mg/dl, serum alkaline phosphatase [ALP] 846 IU with reversal of albumin/globulin [A/G] ratio). USG abdomen and portal Doppler showed chronic liver disease, splenomegaly with multiple nodules and ascites. Ascitic fluid was exudative in nature. Fine needle aspiration cytology (FNAC) of cervical nodes revealed caseating tubercular lymphadenitis. Viral markers were negative for (hepatitis B-virus surface antigen [HBsAg], anti-HCV [hepatitis C virus] IgM). Chest X-ray was normal. Slit lamp examination confirmed the presence of KF ring. Serum copper was mildly elevated (196.3 µg/dl), but serum copper and 24-hour urinary copper was normal. Liver biopsy revealed portal triaditis and esophagogastroduodenoscopy (EGD) was normal. He had para-aortic lymphadenopathy on CT abdomen. Bone marrow aspiration showed few atypical mononuclear cells but was otherwise normal. On the basis of these results, we made a diagnosis of Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Case Report disseminated tuberculosis with drug-induced hepatitis and the patient was put on second-line ATT. Despite treatment, his general condition progressively deteriorated. So, a review of diagnosis was done. A cervical node biopsy was done, which revealed total effacement of architecture, infiltrated by large cells with clear cytoplasm and large vesicular nuclei, occasional multinuclear giant cells. These cells are admixed with numerous eosinophils, lymphocytes. Immunohistochemistry of the same biopsy showed, CD-15, CD-30, LMP, S-100 positivity, CD-14 negative, CD-68 positive in larger cells, CD-45 positive in surrounding lymphoid cells, CD-3, CD-20 negative. Hence, we came to the final diagnosis of a rare disease, sinus histiocytosis with massive lymphadenopathy; also known as Rosai-Dorfman disease (RDD). Discussion Rosai-Dorfman disease is a rare benign, proliferative histiocytic disorder. It is common in younger age group and is thought to occur as a result of immune dysregulation or response to a presumed infectious agent. The stimulation of monocytes/macrophages via macrophage colony-stimulating factor leads to immunosuppressive macrophages, which is a main pathogenesis of RDD. Clinically, the mean age of onset is second decade. It presents as massive painless lymphadenopathy, particularly in neck, associated with fever, leukocytosis, increased erythrocyte sedimentation rate (ESR), hypergammaglobulinemia. The prevalence in extranodal sites such as skin, nasal cavity, paranasal sinuses, orbit, bone, CNS is about 30-40%. Diagnosis is by histopathological examination. In Giemsa stained-smear, a polymorphous picture with the presence of predominantly histiocytes admixed

with variable population of lymphocytes, plasma cells, neutrophils and few eosinophils was seen. The histiocytes had moderate to abundant cytoplasm, large vesicular nuclei and showed with phagocytosis (emperipolesis) of plasma cell and lymphocytes. Immunohistochemistry shows CD68+, CD45+, S-100+, CD1aâ&#x20AC;&#x201C;ve. The common differential diagnoses include infectious lesions, reactive lymphoid hyperplasia with sinus histiocytosis, Langerhans cell histiocytosis, hemophagocytic syndrome and malignant lymphoma. The course of RDD is usually benign, indolent and selflimiting in most patients. Treatment does not appear to be necessary in the majority of patients since the disease does not usually threaten life or organ function. Surgery is generally limited to biopsy to confirm the diagnosis or, to relieve obstructive symptoms. Patients with progressive disease have been treated with corticosteroids, chemotherapy or radiotherapy with variable results. Suggested Reading 1. Rosai J, Dorfman RF. Sinus histiocytosis with massive lymphadenopathy. A newly recognized benign clinicopathologic entity. Arch Pathol 1969;87(1):63-70. 2. Wenig BM, Abbondanzo SL, Childers EL, Kapadia SB, Heffner DR. Extranodal sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease) of the head and neck. Hum Pathol 1993;24(5):483-92. 3. Foucar E, Rosai J, Dorfman R. Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease): review of the entity. Semin Diagn Pathol 1990;7(1):19â&#x20AC;&#x2018;73. 4. Middel P, Hemmerlein B, Fayyazi A, Kaboth U, Radzun HJ. Sinus histiocytosis with massive lymphadenopathy: evidence for its relationship to macrophages and for cytokine-related disorder. Histopathology 1999;35(6):525-33.

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

CAse report

Dengue Myopericarditis Lubna Zafar*, Anjum Parvez**, Asif Hasan**, Mohammad Asif†

AbstrACt Dengue is the most rapidly spreading mosquito-borne viral disease in the world. Cardiac involvement is a known but infrequent complication of dengue fever. We report the case of a 24-year-old female who presented with fever and acute pulmonary edema. She had positive dengue serology and echocardiography was suggestive of myopericarditis. Patient was managed conservatively with favorable outcome. Key words: Dengue fever, dengue serology, myopericarditis

Case Report A 24-year-old female with no previous medical or cardiac history presented at JNMCH, Aligarh, a tertiary care center in North India with complaints of fever and shortness of breath. The patient had high grade fever for six days prior to admission. It was associated with myalgia, retrobulbar pain, nausea and vomiting. She had been receiving oral antibiotics and antimalarials (Artemesinin-based combination therapy) on outpatient basis. One day before admission, she developed chest pain. It was retrosternal, moderate-severe in intensity, unassociated with exertion but aggravated during inspiration and coughing. She started experiencing sudden-onset dyspnea, which was increasing progressively, till admission. On examination, she was dyspneic and exhausted. Her heart rate was 140/min, regular and BP was 90/56 mmHg. The respiratory rate was 36/min and temperature was 101°F. Examination of the cardiovascular system revealed gallop rhythm, but no murmur or rub were present. She was using accessory *Assistant Professor **Associate Professor †Resident Dept. of Medicine, Jawaharlal Nehru Medical College Aligarh Muslim University, Aligarh Address for correspondence Dr Anjum Parvez D-7, Abdullah Apartment Near Abdullah Girls College Civil Lines, Aligarh, UP - 202 002 E-mail: anjumparvez66@yahoo.com

respiratory muscles and crepitations were present upto lung apices. The abdomen was soft, with no hepatosplenomegaly. There were no petechial rashes or bleeding from any site. The laboratory investigations of the patient revealed hemoglobin 8.1 g/dl, total leukocyte count 8,700/µl with 38% lymphocytes. The platelet count was 84,000/µl. The serum was negative for dengue antigen NS1 (nonstructural protein 1) but was positive for IgM and IgG antibodies. Serum creatinine at presentation was 2.0 mg/dl and blood urea was 70 mg/dl, which subsequently improved to 0.7 mg/dl and 26 mg/dl, respectively. The liver function tests showed total serum bilirubin of 1.6 mg/dl, serum aspartate aminotransferase (AST) 102 IU/l and serum alanine aminotransferase (AST) 56 IU/l. Urine examination and serum electrolytes were normal. Ultrasonography of abdomen did not reveal any abnormality. Electrocardiographic (ECG) showed sinus tachycardia at presentation and deep T wave inversion in leads V1-V6 the next day. Cardiac troponin I was qualitatively positive and the CPK-MB level was 52 IU/l. With the background of fever and positive dengue serology, when the patient developed significant ECG changes and raised cardiac enzymes, a provisional diagnosis of dengue myopericarditis was made and an urgent 2D echocardiography was done (Fig. 1). It revealed global hypokinesia with severely impaired left ventricular systolic function with ejection fraction of 30%. There was mild mitral regurgitation (MR) with Grade 1 aortic regurgitation (AR) along with evidence of minimal pericardial effusion. Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Case Report wherein for the purpose of triage, it was classified as DF with or without warning signs and severe dengue with associated plasma leakage, hemorrhage or organ impairment.

RV IVS RA LV MV CN15 16 cm DB72 V B4

MI <0.4

Figure 1. 2D echocardiography showing apical four chamber view revealing dilated LA and LV.

The patient was managed conservatively with high flow oxygen, inotropic support and diuretics as required in coronary care unit (CCU). She responded well to the treatment and her clinical and biochemical parameters improved. She was discharged after six days of in hospital stay, with repeat echocardiography planned on her subsequent visit. Discussion Dengue fever (DF) is caused by dengue virus (DENV) members of the Flaviviridae family. There are four (DEN 1 to DEN 4) serologically distinct, but closely related viruses that cause dengue. Dengue infection is transmitted to humans via bite of Aedes aegypti mosquito. Dengue is the most rapidly spreading mosquito-borne viral disease in the world. In the last 50 years, incidence has increased 30-fold with increasing geographic expansion to new countries and, in the present decade, from urban to rural settings. An estimated 50 million dengue infections occur annually and approximately 2.5 billion people live in dengue endemic countries of which 1.8 billion (>70%) live in South-East Asia Region and Western Pacific Region. Classically, symptomatic dengue virus infections were grouped into three categories: Undifferentiated fever, DF and dengue hemorrhagic fever (DHF). DHF was further classified into four severity grades, with Grades III and IV being defined as dengue shock syndrome (DSS). There have been several reports of difficulties in the use of this classification. Therefore in 2009, WHO suggested a new case definition for dengue, Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Cardiac manifestations of dengue are uncommon.1 The clinical presentations of patients vary considerably, from self-limiting tachy-brady arrhythmia to severe myocardial damage, leading to hypotension and pulmonary edema.2 Bradycardia is the commonest finding, although first and second degree atrioventricular (AV) block, poor R wave progression, ST elevation and nonspecific ST-T wave changes, partial right bundle branch block and rarely, atrial fibrillation, have been described.3 In a study conducted in Sri Lanka, a dengue endemic region, only five cases of myocarditis were reported in a study of 404 dengue cases.4 In India, Wali et al observed that persistent hypotension in patients of DHF/DSS may be attributed to reversible cardiac insult.5 Dengue myopericarditis has not been reported commonly in world literature. Nagaratnam et al described a series of three cases with myocarditis and pericarditis caused by the dengue virus.6 Wiwanitkit proposed a probable reason for the low incidence of dengue myocarditis, that it might be an uncommon presentation or it might be due to under diagnosis and neglecting to report.7 Our patient had clinical features and serology suggestive of DF. Since she was in pulmonary edema and had significant ECG changes, a provisional diagnosis of myocarditis was considered. An urgent echocardiography supported the diagnosis and revealed myopericarditis with reduced ejection fraction. She improved with oxygen therapy, diuretics and inotropes. Thus physicians should be aware of cardiac complications of DF and should have a high index of suspicion in patients with persistent hypotension. Otherwise the course of the disease may be fulminant and ultimately fatal, if not intervened early. Conclusion Dengue fever may have varied clinical presentations, of which cardiac involvement is an uncommon but a potentially fatal complication. Thus, prompt recognition of the condition is essential as urgent management is lifesaving in these patients. 79

Case Report References 1. Gulati S, Maheshwari A. Atypical manifestations of dengue. Trop Med Int Health 2007;12(9):1087-95. 2. Lee IK, Lee WH, Liu JW, Yang KD. Acute myocarditis in dengue hemorrhagic fever: a case report and review of cardiac complications in dengue-affected patients. Int J Infect Dis 2010;14(10):e919-22. 3. Bhatia V, Parida AK, Arora P, Mittal A, Pandey AK, Singh G, et al. Electrocardiographic and echocardiographic findings during the recent outbreak of viral fever in National Capital Region. Indian Heart J 2007;59(4):360‑2.

4. Kularatne SA, Gawarammana IB, Kumarasiri PR. Epidemiology, clinical features, laboratory investigations and early diagnosis of dengue fever in adults: a descriptive study in Sri Lanka. Southeast Asian J Trop Med Public Health 2005;36(3):686‑92. 5. Wali JP, Biswas A, Chandra S, Malhotra A, Aggarwal‑P, Handa R, et al. Cardiac involvement in dengue hemorrhagic fever. Int J Cardiol 1998;64(1):31-6. 6. Nagaratnam N, Siripala K, de Silva N. Arbovirus (dengue type) as a cause of acute myocarditis and pericarditis. Br Heart‑J 1973;35(2):204-6. 7. Wiwanitkit V. Dengue myocarditis, rare but not fatal manifestation. Int J Cardiol 2006;112(1):122.

Conference Calendar Family Medicine: An Evidence-based Approach to Patient Care Venue: Gallatin Gateway, Montana, United States August 4-6, 2011 Website: http://www.mceconferences.com/conferencedetail.php?conf_id=MT812 4th Passionate about Practice Conference 2011 Venue: Brisbane Convention and Exhibition Centre Brisbane, Queensland, Australia August 8-9, 2011

Website: http://www.elsa2011singapore.com 38th Annual Scientific Meeting of the Infectious Diseases Society for Obstetrics and Gynecology Venue: Chicago, IL, United States August 11-13, 2011 Website: http://www.idsog.org/annual-meeting/programregistration/

Website: http://www.iamevents.com.au/qh/passionate aboutpractice

First International Critical Dietetics Conference

10th Asia Pacific Congress of Endoscopic Surgery

Venue: Toronto, Ontario, Canada

Venue: Suntec Singapore International Convention and Exhibition Centre, Singapore

August 11-13, 2011

August 19-20, 2011 Website: http://www.criticaldietetics.org

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

CAse report

Organophosphate-induced Delayed Spastic Paraplegia and Distal Motor Neuropathy Ibraheem Khan*, Chandra Kant**, Alok Goyal*

AbstrACt Cases of organophosphate compound (OPC) poisoning with suicidal intent are common in Indian hospitals. We present the case of a 24-year-old male who consumed OPC and recovered on endotracheal intubation for two days and developed delayed spastic paraplegia and distal motor neuropathy with sphincter involvement later on. Key words: Organophosphate, suicidal intent, spastic paraplegia

rganophosphate (OP) poisoning is worldwide. Three million cases are reported every year.1 According WHO one million cases require intensive are out of which 2,000 deaths occurs and two million cases are hospitalized for suicidal intent with pesticides.1 OP poisoning is the most common poisoning in India accounting for almost half of the hospital admissions due to poisoning.2 Central nervous system manifestations of OP poisoning are the most important clinical entities. There are three distinct clinical phases which are described and summarized below on the basis of duration of occurrence and pathophysiology. Type 1 Paralysis or Acute Cholinergic Crisis This is secondary to persistent depolarization at neuromuscular junctions. Symptoms develop within 24-48 hours after blockade of acetylcholinesterase enzyme. Muscarinic feature are diarrhea, diaphoresis, urinary incontinence, meiosis, bronchorrhea, bronchospasm, bradycardia, blurred vision, emesis, lacrimation, salivation. The nicotinic features are fasciculation, twitching cramp, hypertension, tachycardia, mydriasis (rare), muscle weakness and paralysis. Respiratory muscles may also be involved *Postgraduate **Associate Professor Dept. of Medicine Jawaharlal Nehru Medical College, Ajmer Address for correspondence Dr Ibraheem Khan VPO: Samraya, Weir Dist.: Bharatpur, Rajasthan - 321 408 E-mail: imedicine2008@gmail.com

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

leading to acute respiratory failure in 33% patients requiring urgent ventilation.3 Type 2 Paralysis or Intermediate Syndrome Intermediate syndrome (IMS) was first described by Wadia et al in 1974, as type 2 paralysis.4 It was termed IMS in 1987 by Senanayake.5 The patients of IMS have paralysis of proximal limb muscle, neck flexors, cranial nerves and respiratory muscles, 24-96 hours after passing off a well-defined cholinergic phase in 8-49% patients.5 The pathogenesis is presumed to be dysfunction of neuromuscular junction caused by presynaptic and postsynaptic downregulation of nicotinic receptors due to release of excessive acetylcholine (Ach) and calcium (Ca2+), respectively.6 The paralytic symptoms remain upto 18 days depending upon severity of intoxication unless infections and cardiac arrhythmias complicate the course.4,6 Type 3 Paralysis or OP-induced Delayed Neuropathy Delayed neuropathy is a well-described and summarized complication of OP poisoning after ingestion of large doses of insecticides and pesticides. This generally occurs 2-3 weeks after exposure of certain OPCs. OPinduced delayed neuropathy (OPIDN) is a motorsensory distal axonopathy.4,7 Recovery is delayed upto 6-12 months. Case Presentation A 24-year-old male was brought in emergency room with complaints of nausea, vomiting and in stuporous 81

Case Report condition after ingestion of large doses of OP. There was no history of trauma or fall. Patient was alcoholic since two years. There was no history of smoking. General physical examination revealed bilateral constricted pupils and fasciculations in legs and arms. On auscultation, there were bilateral crackles in lung fields. After five days, we noticed the features of early IMS-like dysarthria, ptosis and fecal incontinence. Next day, the patient developed respiratory failure, which recovered after putting in an endotracheal tube for two days. Patient was discharged after two weeks in condition of performing routine activities without any help. Two weeks after discharge, he developed weakness in his right lower limb, which progressed to left lower limb in next 8-9 days to the extent that he could not walk without support. There was no weakness in upper limbs. He had urinary retention. On neurological examination, patient was conscious, cooperative, well-oriented to time, place, person with normal speech. Muscle tone was increased in lower limbs and power was Grade 2/5 in both lower limbs; knee reflexes were exaggerated with patellar clonus and ankle reflexes were absent. Other reflexes i.e., biceps, supinator and triceps were normal in both upper limbs. Plantars were bilaterally silent. There was no movement in both great toes. Cranial nerves were not involved and there was no sensory deficit. Other systems were essentially normal. His routine blood investigations were normal. X-ray spine did not show any evidence of compression or any other abnormality. Therefore, in view of the history of OP poisoning followed by (5-6 weeks later) signs of motor neuropathy and pyramidal tract with sphincter involvement, a diagnosis of OP-induced delayed spastic paraplegia and distal motor neuropathy with sphincter involvement was made (Table 1). Discussion OPIDN is an uncommon and rare cause of peripheral neuropathy. The cardinal feature is weakness which appears initially in distal leg muscles followed by small muscles of the hands and it may later extend proximally. Clinical involvement of the corticospinal 82

Table 1. Motor System Examination B/L upper

B/L lower limb

Bulk

Normal

Tone

Normal

Increased

Power

Normal

2/5

Deep reflexes

Normal

Knee-exaggerated, ankleabsent

Other reflexes

Normal

Plantars

Silent

tracts and the dorsal columns becomes apparent when the peripheral neuropathy improves.3 Our patient also showed pyramidal tract involvement in the form of increased knee reflexes and muscle tone. In the series by Senanayake,5 nearly 50% of patients had some evidence of pyramidal tract dysfunction, probably due to liposolubility of these substances. The prognosis in mild neuropathy is good but with severe neuropathy, partial recovery occurs in 6-12 months and patient is usually left with deficits i.e., claw hand, foot drop, ataxia.5 The pathogenesis of OPIDP is presumed to be due to phosphorylation and ageing of an enzyme in axons called neurotoxic esterase or neuropathic target esterase (NTE). Inhibition of NTE causes degeneration of predominantly long axons, with loss of myelin and macrophage accumulation in nerves leading to motor axonal neuropathy.4,5 The use of thiamine and high-dose methylprednisolone has been shown to be beneficial in experimental animals. However, Senanayake et al5 found that only physiotherapy was helpful. In India, there are very few case reports, which document dual neurotoxicity i.e., cholinergic crisis followed by delayed neuropathy and all these cases occurred following use of Dichlorovos. But our patient had all the three neurological phases and spastic paraplegia with sphincter involvement after ingesting large doses of insecticides. Spastic paraplegia is a rare neurological complication of OP poisoning. We report spastic paraplegia in this case in view of extended-spectrum of OP-induced delayed neurological complications. It is therefore recommended that, every patient of OP poisoning should be followed up for at least 2-3 months. Contâ&#x20AC;&#x2122;d on page 87... Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

CAse report

Steatocystoma Multiplex with Oligodontia: A Clinical Report Bharat Kumar PV*, Wilma Delphine Silvia CR**, Bhanu Prakash†, Santosh KV‡

AbstrACt Background: Steatocystoma multiplex (SM) with oligodontia is an extremely rare disorder that presents at puberty with multiple skin-colored nodules. It is associated with mutations in keratin 17 (K17). Objective: To arrive at a diagnosis of SM with oligodontia. Methods: Clinical examination and laboratory investigations were carried out. Results: Dermatological examination showed multiple, round, dry, nontender, nonscaly, yellowish and partly compressible, papules and nodules arranged discretely, cystic swellings in the anterior scrotal wall. Dental examination revealed oligodontia. Baseline hematobiochemical reports were within normal range. Biopsy of the excised cyst showed features consistent with SM. Conclusion: Family history, clinical examination and laboratory findings led to the diagnosis of SM with oligodontia. Further molecular studies are required to detect the type of K17 mutation. Recognition and genetic counseling of families affected by this autosomal dominant ectodermal dysplasia is important. Key words: Steatocystoma multiplex, cysts, keratin, oligodontia

teatocystoma multiplex (SM) is an uncommon disorder characterized by multiple widespread cutaneous, sebum-containing dermal cysts that have their origin in the pilosebaceous duct such as the trunk (especially the presternal area), neck, axilla, inguinal region, scalp and proximal extremities. The disease has been reported to be associated with pachyonychia congenita, acrokeratosis verruciformis, hypertophic lichen planus, etc.1 It is mostly thought to be inherited in an autosomal dominant pattern; however, many sporadic cases have also been reported. SM was demonstrated to be caused by mutations in the keratin 17 (K17) gene.2 We present a rare case report of SM with oligodontia, a psychologically and socially devastating disease, from an Indian family, which to the best of our knowledge has not been reported earlier. *Dept. of Biochemistry Vydehi Institute of Medical Sciences and Research Centre, Bangalore **Dept. of Biochemistry Sapthagiri Institute of Medical Sciences and Research Center, Bangalore †Dept. of Dermatology ‡Dept. of Pathology, Vydehi Institute of Medical Sciences and Research Centre, Bangalore Address for correspondence Dr Wilma Delphine Silvia CR Professor and Head Dept. of Biochemistry Sapthagiri Institute of Medical Sciences and Research Center #15, Hesaraghatta Main Road Chikkasandra, Bangalore - 560 090, Karnataka E-mail: widel@rediffmail.com, widel2008@gmail.com

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Case Report A 27-year-old healthy male visited the out patient department of Dermatology in May 2010 with chief complaints of progressively increasing, multiple, asymptomatic, dry, nonscaly swellings over the scrotum of four years duration. There was no history of similar lesions anywhere in the body. His personal and past histories were without any significance. He denied history of exposure or any genitourinary symptoms. Interestingly there was a history of similar lesions among many of his family members (Fig. 1). General physical examination showed no abnormalities except for the fact that the patient had 28 permanent teeth. Dental examination by a dentist, including radiological evidence confirmed the clinical finding without any other dental abnormalities (Fig. 2). Dermatological examination showed multiple, round, dry, nontender, nonscaly, yellowish and partly compressible, papules and nodules arranged discretely, the cystic swellings ranging in size from 0.5 to 2.5 cm in diameter, located on the anterior scrotal wall (Fig. 3). The remaining genital areas, skin and mucosal areas revealed no abnormalities. Scalp, hair and nails were normal. A clinical diagnosis of SM was made and the patient was subjected to investigations. 85

Case Report

III IV Filled symbols are affected member Indicates indexed patient

Figure 1. Patientâ&#x20AC;&#x2122;s pedigree.

Figure 4. The lining epithelium is a few layers thick without intercellular bridges.

Discussion

Figure 2. Oligodontia: A-Upper jaw, B-Lower jaw.

First described by Jamieson in 1873, and coined by Pringle in 1899, SM is a rare, benign, uncommon disorder of the pilosebaceous unit characterized by the development of numerous sebum-containing dermal cysts. Although it has historically been described as an autosomal dominant inherited disorder, most presenting cases are sporadic.3 It commonly presents in the second or third decade, over sebaceous-rich areas like the neck, chest, axillae, arms and groin. SM is associated with defects in K17.4 To date, 14 mutations have been described in patients with either SM or pachyonychia congenita type 2 (PC-2), all of which are localized to the helix initiation domain (1A domain) of the K17 gene.5 Two types of SM are recognized based on the presence or absence of natal teeth. K17 mutations have been identified in some patients with SM, as well as in patients with PC-2.6

Figure 3. Cystic swellings in the anterior scrotal wall.

On investigation, the baseline hemato-biochemical parameters were within normal ranges. Electrocautery excision of the lesions was done. Biopsy of the excised cyst showed features consistent with SM. The patient had no relapses of the lesions at three months postprocedure. 86

Lesions present as numerous, polysized, firm and yellow-colored dermal cysts. The lesions lack a central punctum. Cyst contents appear as an odorless creamy or oily fluid. In case of secondary bacterial infection, individual lesions of SM may become suppurative and have a foul-smelling discharge. Diagnosis is easily confirmed by the presence of dermal cysts. The cyst is located in the dermis and is lined by an epithelial layer consisting of stratified squamous cells lacking in intercellular bridges. The lining is a few cells thick and the luminal aspect is corrugated, rimmed by a narrow zone of hyalinized keratin (Fig. 4). The condition needs to be differentiated Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Case Report from other common conditions like acne vulgaris, acne conglobata, milia, sebaceous adenoma, epidermal inclusion cyst, sebaceous hyperplasia, eruptive vellus hair cysts, syringoma. The condition sometimes responds well to tetracycline group of antibiotics. Retinoids have not proven to be successful and are reported to cause flare-up of the lesions in some patients. Larger lesions and those refractory to medical management can be treated by surgical measures like cryotherapy and excision of the lesions. Carbon dioxide laser ablation has allowed treatment of multiple lesions during a single treatment session, with no anesthesia, a low percentage of recurrence and good esthetic results.7 Further molecular studies required to detect the type of K17 novel mutation. Acknowledgement Authors would like to thank Dr. Sandhya Belwadi, Principal, Vydehi Institute of Medical Sciences and Research Centre, Bangalore for having helped in Publishing this clinical report.

References 1. Moritz DL, Silverman RA. Steatocystoma multiplex treated with isotretinoin: a delayed response. Cutis 1988;42(5):437-9.

2. Covello SP, Smith FJ, Sillevis Smitt JH, Paller AS, Munro CS, Jonkman MF, et al. Keratin 17 mutations cause either steatocystoma multiplex or pachyonychia congenita type 2. Br J Dermatol 1998;139(3):475-80. 3. Cho S, Chang SE, Choi JH, Sung KJ, Moon KC, Koh JK. Clinical and histologic features of 64 cases of steatocystoma multiplex. J Dermatol 2002;29(3): 152-6. 4. Smith FJ, Corden LD, Rugg EL, Ratnavel R, Leigh IM, Moss C, et al. Missense mutations in keratin 17 cause either pachyonychia congenita type 2 or a phenotype resembling steatocystoma multiplex. J Invest Dermatol 1997;108(2):220-3. 5. Oh SW, Kim MY, Lee JS, Kim SC. Keratin 17 mutation in pachyonychia congenita type 2 patient with early onset steatocystoma multiplex and Hutchinson-like tooth deformity. J Dermatol 2006;33(3):161‑4. 6. Gass JK, Wilson NJ, Smith FJ, Lane EB, McLean WH, Rytina E, et al. Steatocystoma multiplex, oligodontia and partial persistent primary dentition associated with a novel keratin 17 mutation. Br J Dermatol 2009;161(6): 1396-8. 7. Rossi R, Cappugi P, Battini M, Mavilia L, Campolmi P. CO2 laser therapy in a case of steatocystoma multiplex with prominent nodules on the face and neck. Int J Dermatol 2003;42(4):302-4.

...Cont’d from page 82 References 1. Jeyaratnam J. Acute pesticide poisoning: a major global health problem. World Health Stat Q 1990;43(3):139‑44. 2. Lall SB, Peshin SS, Seth SD. Acute poisoning: a ten years retrospective hospital based study. Ann Natl Acad Med Sci (India)1994;30(1):35-44. 3. Tsao TC, Juang YC, Lan RS, Shieh WB, Lee CH. Respiratory failure of acute organophosphate and carbamate poisoning Chest 1990;98(3):631-6. 4. Wadia RS, Sadagopan C, Amin RB, Sardesai HV. Neurological manifestations of organophosphorus

insecticide poisoning. J Neurol Neurosurg Psychiatry 1974;37(7):841-7. 5. Senanayake N, Karalliedde L. Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome. N Engl J Med 1987;316(13):761-3. 6. Samuel J, Thomas K, Jeyaseelan L, Peter JV, Cherian AM. Incidence of intermediate syndrome in organophosphorus poisoning. J Assoc Physicians India 1995;43(5):321-3. 7. Morreto A, Lotti M. Poisoning by organophosphorus insecticides and sensory neuropathy. J Neurol Neurosurg Psychiatry 1998;64(4):463-8.

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

prACtiCe GuiDelines

AAP Revises Policy Statement on the Use of Postnatal Corticosteroids for Bronchopulmonary Dysplasia

ronchopulmonary dysplasia (BPD) is a major morbidity in very preterm infants that negatively affects neurodevelopmental outcomes and is resistant to therapeutic interventions. A 2002 American Academy of Pediatrics (AAP) policy statement determined that the routine use of dexamethasone to prevent or treat chronic lung disease in preterm infants could not be recommended. Although the incidence of BPD has not decreased, the postnatal use of dexamethasone for treatment and prevention has. This revised statement evaluates the information published since 2002 and updates recommendations for the use of corticosteroids in infants with BPD. Recommendations The use of high-dose dexamethasone for BPD cannot be recommended if no randomized controlled trials showing improved outcomes exist. High-dose dexamethasone (approximately 0.5 mg per kg per day) has been shown to reduce the incidence of BPD; however, it also has been associated with adverse outcomes. Currently, there are no data to support the idea that high daily doses provide additional benefit compared with lower doses. To optimize therapy and improve outcomes, additional randomized controlled trials of postnatal glucocorticoids are needed. Persons or groups who perform such trials should try to minimize the use of open-label glucocorticoids, because it has confounded the analysis of some previous trials. They should also evaluate longterm pulmonary and neurodevelopmental outcomes. There is insufficient evidence to make a recommendation about treatment with low-dose dexamethasone. Low-dose

dexamethasone (less than 0.2 mg per kg per day) may help with extubation and may decrease the incidence of adverse effects that occur with higher doses. Additional randomized controlled trials are needed. Although early hydrocortisone treatment may benefit certain patients, there is insufficient evidence to recommend its use in all infants at risk of BPD. Lowdose hydrocortisone (1 mg per kg per day) for the first two weeks of life may increase survival rates without BPD, especially in infants with prenatal inflammation. It will not adversely affect neurodevelopmental outcomes; however, there is a possibility of increased risk of isolated intestinal perforation associated with early concomitant treatment with prostaglandin synthesis inhibitors. More randomized controlled trials are needed. There is insufficient evidence to make a recommendation about treatment with high-dose hydrocortisone. Highdose hydrocortisone (3 to 6 mg per kg per day) started after the first week of postnatal age has not been shown to improve survival rates in infants without BPD. Additional randomized controlled trials are needed. Practice Implications Physicians should use clinical judgment when balancing the adverse effects of BPD with the possible adverse effects of treatment. Very low-birth-weight infants on mechanical ventilation for longer than one to two weeks after birth are at very high risk of BPD. When treating these infants, physicians who are considering corticosteroid therapy could determine that the risks of a short course of glucocorticoids are warranted. These decisions should be made with the infantâ&#x20AC;&#x2122;s parents. n

Source: Adapted from Am Fam Physician. 2011;83(12):1501.

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

photo quiz

Rapidly Growing Mass in the Chest Wall

49-year-old man presented with a growth in the middle of his chest that appeared about one year earlier. He became concerned when it started growing more rapidly over the previous six to eight months. It caused some discomfort, but was not acutely painful or pruritic. He did not recall any signs of inflammation, such as redness, warmth, or drainage, and stated that there were no other such lesions on his body. The patient history was unremarkable except for smoking one pack of cigarettes per day and drinking a six-pack of beer on the weekends. He was not taking any medications and had no allergies.

Figure 1.

Physical examination revealed a 3.1-in (7.9-cm) lesion located in the upper epigastrium. It had neovascularization on the surface, was soft (but not fluctuant), was flesh colored, and was not movable (Figs. 1 and 2). Question Based on the patientâ&#x20AC;&#x2122;s history and physical examination, which one of the following is the most likely diagnosis? A. Lipoma. B. Neurofibroma. C. Sarcoma. D. Sebaceous cyst. E. Skin metastasis. Discussion The correct answer is D: sebaceous cyst. Ultrasonography showed a solid mass with well-defined borders and interspersed areas of echogenicity, limited blood flow within the mass, and possible neoplasia. The lesion was surgically removed, and pathology confirmed it to be a large sebaceous cyst.

Source: Adapted from Am Fam Physician. 2011;83(12):1471-1472.

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Figure 2.

Sebaceous cysts are closed sacs in the epidermis that form when keratin blocks a sebaceous gland.1-3 Sebum buildup leads to a yellowish material that resembles cottage cheese and can have a foul odor when expressed. Sebaceous cysts can occur on any part of the body, most commonly on hairy areas. They can be caused by trauma, swollen hair follicles, or high testosterone levels, but are most often idiopathic. Some persons seem to be predisposed to them. The cyst begins as a soft nodule in the skin, which can enlarge over time. Many of these cysts resolve without treatment, but some become infected and need treatment such as medication, incision and drainage, excision, and heat. They can recur after surgical removal. 89

photo quiz Lipomas are common, benign, fatty tumors that can appear on virtually any body surface.2,4 They typically occur in middle-aged adults. Lipomas are soft, fleshcolored, usually slow growing, rarely painful, and easily removed. They usually do not undergo malignant transformation to liposarcomas. Surgical excision is the treatment, and most lipomas will not recur after removal. Neurofibromas are relatively uncommon and slowgrowing tumors that arise from peripheral nerve sheaths.1,2,5 They most often occur in patients with neurofibromatosis, an inherited disorder usually heralded by café au lait spots. However, neurofibromas can occur sporadically in persons who do not have neurofibromatosis. As they enlarge, they may cause electric shock-like sensations. The treatment is surgical excision, which is often risky because of nerve involvement. Sarcomas are uncommon, malignant, soft tissue tumors that originate from fat, muscle, subcutaneous or connective tissue, or bone.4,6 They can appear anywhere on the body, but most often on the arms and legs. Liposarcomas (malignant fatty tumors) often occur on the thigh, behind the knee, and on the retroperitoneum. Sarcomas are most common in persons between 50 and 65 years of age. They are resistant to chemotherapy. Treatment is surgical excision and sometimes radiation. Skin metastases can occur from almost any type of primary tumor, but most commonly from melanoma and cancers of the breast, lung, colon, ovary, nasal sinus, and oropharynx.1,7 Metastases typically appear suddenly and are painful. They are firm, rubbery, and sometimes discolored. The chest is a common location, especially if the primary tumor is located in the lung. Treatment is of the primary cancer, but skin metastases can be diminished by laser, liquid nitrogen, excision, or intralesional chemotherapy. References 1. Rook A. Rook’s Textbook of Dermatology. 4th ed. Boston, Mass.: Blackwell Scientific; 1986.

Summary Table Condition

Characteristics

Lipomas

Common, benign, fatty tumors on virtually any body surface; soft, flesh-colored, slow growing, and easily removed; rarely undergo malignant transformation to liposarcomas

Neurofibromas Uncommon, slow-growing tumors that arise from peripheral nerve sheaths; most common in persons with neurofibromatosis Sarcomas

Malignant, soft tissue tumors originating from subcutaneous or connective tissue, fat, muscle, or bone; most common on the arms and legs; resistant to chemotherapy

Sebaceous cysts

Closed, keratin-filled sacs in the epidermis that arise from sebaceous glands; cysts enlarge over time and can become infected; most common on hairy areas of the skin; can develop after trauma, although most occur spontaneously; can also be caused by swollen hair follicles or high testosterone levels

Soft tissue metastases

Can arise from any primary tumor, but most commonly from melanoma and cancers of the breast, colon, lung, ovary, nasal sinus, and oropharynx; sudden onset and painful; chest wall is a fairly common location, especially if primary tumor is in the lung

2. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 4th ed. New York, NY: Mosby; 2004. 3. Handa U, Chhabra S, Mohan H. Epidermal inclusion cyst: cytomorphological features and differential diagnosis. Diagn Cytopathol. 2008;36(12):861-863. 4. Weiss SW, Goldblum JR, Enzinger FM. Enzinger and Weiss’s Soft Tissue Tumors. 4th ed. St. Louis, Mo.: Mosby; 2001. 5. Karaoğlanoğlu N, Kürkçüoğlu IC, Eroğlu A. Giant neurofibroma of the chest wall. Ann Thorac Surg. 2004;78(2):718. 6. American Cancer Society. Sarcoma-adult soft tissue cancer. http://www.cancer.org/cancer/sarcoma-adultsoft tissuecancer/index. Accessed May 11, 2011. 7. Ngan V; New Zealand Dermatological Society Incorporated. Skin metastasis. DermNet NZ. http:// www.dermnet.org.nz/lesions/metastasis.html. Accessed May 11, 2011.

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

CliniCAl AlGorithm

An Approach to the Treatment of Peptic Ulcer Disease Patient presents with dyspepsia

Alarm symptoms* or age older than 55 years?

Yes

EGD (or barium studies if EGD not feasible)

Ulcer present?

Yes Eradicate Helicobacter pylori Administer antisecretory therapy for 4-8 weeks Treat bleeding or other complications Biopsy gastric ulcer

Detect and treat H. pylori infection Advise discontinuation of NSAIDs, smoking, alcohol and drug abuse Administer antisecretory therapy (with PPI such as esomeprazole preferably, or an H2-blocker) for 4 weeks

No Consider trial of antisecretory therapy (with PPI such as esomeprazole preferably, or a histamine H2-blocker) and follow clinically

Good clinical response

Persistent symptoms

Observe: Consider long-term maintenance with H2-blocker or PPI such as esomeprazole, if symptoms recur Consider EGD if red flags or more severe symptoms

Continue H2-blocker or PPI such as esomeprazole for 4-8 weeks

Response? Yes

Observe or consider maintenance therapy with H2-blocker or PPI such as esomeprazole

Consider EGD Recheck and treat H. pylori, if persistent Check for noncompliance Consider hyper-secretory states

*Alarm symptoms include evidence of bleeding (e.g. anemia, heme-positive stool, melena), perforation (e.g. severe pain), obstruction (e.g. vomiting) and malignancy (e.g. weight loss, anorexia). EGD: Esophagogastroduodenoscopy; PPI: Proton pump inhibitor; NSAID: Nonsteroidal anti-inflammatory drug.

Source: IJCPâ&#x20AC;&#x2122;s Algorithms in Gastroenterology.

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

liGhter reADinG

Lighter Reading

Mind Teaser sailing

Dr. Good and Dr. Bad

ccccccc

SITUATION: A patient with Mediclaim of 2 lakhs of

You will have to pay ` 20,000 from your pocket

You can claim cumulative bonus

Answer: Sailing over the seven seas Did you Know  Drinking water after eating reduces the acid in your mouth by 61%.  The song, Auld Lang Syne, is sung at the stroke of midnight in almost every English-speaking country in the world to bring in the new year.  Zero is the only number that cannot be represented by Roman numerals.

seven years duration needed a claim of ` 2.2 lakhs.

SMS of the Day A crust eaten in peace is better than a banquet partaken in anxiety. Quote “Healthy discontent is the prelude to progress.”

LESSON: Sum insured under the policy shall be progressively increased by 5% for each claim-free year of insured subject to maximum accumulation of 10 claim-free years of insurance. Dr KK Aggarwal

An Inspirational Story Realize before Its Too Late

Dante Gabriel Rossetti, the famous 19th-century poet and artist, was once approached by an elderly man. The old fellow had some sketches and drawings that he wanted Rossetti to look at and tell him if they were any good, or if they at least showed potential talent. Rossetti looked them over carefully. After the first few, he knew that they were worthless, showing not the least sign of artistic talent. But Rossetti was a kind man, and he told the elderly man as gently as possible that the pictures were without much value and showed little talent. He was sorry, but he could not lie to the man. The visitor was disappointed, but seemed to expect Rossetti’s judgment. He then apologized for taking up Rossetti’s time, but would he just look at a few more drawings - these done by a young art student? Rossetti looked over the second batch of sketches and immediately became enthusiastic over the talent they revealed. “These,” he said, “oh, these are good. This young student has great talent. He should be given every help and encouragement in his career as an artist. He has a great future if he will work hard and stick to it.” Rossetti could see that the old fellow was deeply moved. “Who is this fine young artist?” he asked. “Your son?” “No,” said the old man sadly. “It is me - 40 years ago. If only I had heard your praise then! For you see, I got discouraged and gave up - too soon.”

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

emeDinews seCtion

From eMedinewS

Ranthambore to have Biosphere Reserve for Tigers

Chronic Itching as Debilitating as Chronic Pain

About 11,500 squares kilometer area around the Ranthambore National Park would be made a biosphere reserve to accommodate the increasing number of tigers in this forest in Sawai Madhopur. This was announced by Union Environment and Forests Minister Jairam Ramesh on Friday after his meeting with Chief Minister Ashok Gehlot. Talking to the media, Ramesh said forest parts of Dhaulpur and Jhalawara would come under it and it would create kind of corridor between Ranthambore and these areas, to allow big cats to move around in bigger areas. He said that State Government has been asked to send the proposal for the clearance from his Ministry.

Everyone talks about chronic pain, but no one talks about chronic itching. And yet, researchers reported, chronic pruritus may have a similar effect on qualityof-life as chronic pain. In a convenience sample of patients with chronic pain or pruritus, those with itching were willing to forfeit 13% of their life span in order to live without the condition, according to Suephy Chen, MD, of Emory University School of Medicine in Atlanta, and colleagues. In contrast, those with chronic pain were willing for forfeit 27% of their life span to live in perfect health, Chen and colleagues reported online in Archives of Dermatology. (Source: Medpage Today)

Ramesh said that to save the reserve forests, the State Government would create eco-friendly zones around its 27 reserve forests that are facing the threat from illegal mining and mushrooming of hotels. He said a bypass road would be built, to divert the traffic from Sariska Tiger Reserve. The Center would bear 50% cost of this ‘20-crore project’. Ramesh said that he would visit Jaisalmer to have a first-hand idea about having a cheetah reserve there and also re-demarcate the Desert Sanctuary. (Source: The Pioneer, June 24, 2011) Minimally Invasive Colorectal Surgery Cuts VTE Risk Patients undergoing laparoscopic colorectal surgery had fewer clotting complications than were seen with open procedures, researchers found. Venous thromboembolism (VTE) occurred in 1.44% of patients who had open surgery but in only 0.83% of those having a colorectal resection laparoscopically (p < 0.001), Michael J Stamos, MD, of the University of California Irvine Medical Center, and colleagues reported in the June issue of Archives of Surgery. (Source: Medpage Today) Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Screen Time Driving Youth Obesity Epidemic Too much time parked in front of the television or computer screen is driving the epidemic of childhood obesity in the US, according to a new policy statement from the American Academy of Pediatrics. And it’s not just that many teens are couch potatoes, the academy argues in the July issue of Pediatrics: TV advertising drives sales of junk food, children and teens tend to snack while watching TV or online, and late-night use may interfere with sleep. (Source: Medpage Today) ADA: Older Diabetics better at Keeping Weight Off Weight loss among diabetic, overweight patients was most durable in those who lost >10% of their body weight in the first year and in those 65 and older, researchers said here. Compared with individuals who lost <5% of body weight in the first year of the trial, participants in the Look AHEAD (Action for Health in Diabetes) trial were nearly 10 times more likely to have maintained weight loss after four years (OR 9.8, 95% CI 6.99-13.74), said Donna Ryan, MD, of the Pennington Biomedical Research Center in Baton Rouge, La. “The strongest predictor of year four weight loss was year one weight loss,” Ryan said at the 95

emedinews Section annual meeting of the American Diabetes Association. (Source: Medpage Today) Level of Diastolic Function Predicts Death The presence of moderate or severe diastolic dysfunction in patients with preserved systolic function independently predicted mortality, a retrospective study determined. (Source: Medpage Today) ADA: Type 2 Diabetics can Alter Lifestyles A short-term lifestyle modification program for overweight diabetic patients seen in clinical practice showed long-term benefits for many of the participants, researchers reported here. In a study conducted at the Joslin Clinic in Boston, patients who had a mean glycated hemoglobin (HbA1C) of 7.6% at baseline were able to lower the HbA1C to 6.6% (p < 0.001) after 12 weeks of the intensive program and remained at 7% after three years, also a significant reduction from baseline (p < 0.01). (Source: Medpage Today) EUROPACE: Adding CRT to CABG Boosts HF Outcomes Implanting a cardiac resynchronization therapy (CRT) device at the time of coronary artery bypass grafting (CABG) in patients with ischemic heart failure improves outcomes over CABG alone, a small, randomized trial showed. The addition of CRT improved left ventricular systolic function, reduced signs of dyssynchrony and ultimately reduced mortality through 18 months of follow-up (p < 0.05 for all), according to Alexander Romanov, MD, of the Novosibirsk State Research Institute of Circulation Pathology in Russia. (Source: Medpage Today) Adverse Events Common with rhBMP-2 Device In stark contrast to published reports from manufacturer-sponsored studies of the Infuse spinal fusion device that incorporates a biologic bone-building drug, a new analysis of FDA documents and other data sources suggests that upto half of patients receiving the device may experience adverse events related to 96

the drug, researchers said. The Infuse device, which delivers recombinant human bone morphogenetic protein-2 (rhBMP-2) to speed vertebral fusion in patients with chronic back pain, has adverse event rates of 10-50% depending on the approach, according to Eugene Carragee, MD, of Stanford University’s outpatient clinic in Redwood City, Calif., and colleagues. (Source: Medpage Today) ACIP: Egg Allergy no Problem with Flu Vaccine Having an egg allergy is no longer a contraindication to influenza vaccination, according to new guidance for the upcoming flu season from the Advisory Committee on Immunization Practices (ACIP). Under the new recommendation - which was adopted with 14 Yes votes and one abstention at one of ACIP’s regular meetings at CDC headquarters in Atlanta - individuals with a history of allergic reactions to eating egg can receive the vaccine, with certain conditions. (Source: Medpage Today) Resident Work-hour Rule Falls Short, Group Says New rules that go into effect on July 1 to limit firstyear resident physicians from working more than 16 hours straight without sleep ‘stop considerably short’ of what’s necessary to prevent medical errors and improve patient safety, a group of experts said. The group - which includes physicians and health policy experts who have pushed for shorter hospital shifts published a white paper in the June 24 issue of the online journal Nature and Science of Sleep outlining recommendations to reduce fatigue among doctors and decrease medical errors. The recommendations are the product of a conference held at Harvard in the summer of 2010 which brought together 26 experts in medicine, physician training, sleep and workforce issues to discuss how to implement Institute of Medicine (IOM) recommendations from 2008. (Source: Medpage Today) Fitness Update Exercise, Inflammation and Type 2 Diabetes

It is well-known that physical activity reduces type 2 diabetes and cardiovascular disease. As a matter of fact, the American Heart Association lists becoming more Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

emedinews Section active as one of the top lifestyle changes necessary to prevent heart attacks. However, exactly how physical activity does this is still unknown, so researchers performed a study to find out whether a certain type of inflammation caused by C-reactive protein (which is lowered after physical activity) is related to mortality in type 2 diabetes patients. Researchers from the University of Turku in Finland followed 569 type 2 diabetic patients (ages 45-64) who were free of cardiovascular disease at the beginning of the study. They separated patients into groups according to the level of the protein in their blood and by the amount of physical activity they engaged in. During an 18-year follow-up, 356 patients died, 217 of whom died of cardiovascular disease-related complications. Those who were more physically active had significantly less coronary heart disease. However, researchers found that physical activity had nearly no effect on patients with a low level of inflammation, but that it significantly reduced total cardiovascular disease mortality in type 2 diabetic patients with elevated levels of inflammation. These results suggest that physical activity can have a protective effect against the risks associated with type 2 diabetes and high inflammation. â&#x2C6;&#x2019;Rajat Bhatnagar, International Sports & Fitness Distribution, LLC

Medicolegal Update What is accidental suffocation?

There have been numerous instances of accidental deaths as a result of children putting things into their mouths and swallowing them, which in turn blocks the airways. This is why it is imperative that small children are never left unattended and are not allowed to put anything in their mouths which may result in their choking. People also die of suffocation in the instance of a house fire where there is a lack of oxygen and they cannot breathe. The postmortem examination provides information whether or not the victim was conscious at the time of the fire starting or if indeed they had already been deceased. This process is measured by the amount of carbon dioxide in the deceasedâ&#x20AC;&#x2122;s system at the autopsy stage. Murder is comparatively rare; however, in some cases Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

the assailant has tried to cover his or her tracks by setting fire to the location where the deceased is finally found. This could be a house, an office, a workshop, anywhere. The autopsy surgeon must look for the telltale signs: The bloodshot eyes, the high levels of carbon dioxide in the blood and bruising around the nose and mouth and may even collect trace evidence such as hair and fiber from around the nose and mouth of the deceased. As accidental suffocation or smothering is relatively common; however, until proven otherwise by a forensic surgeon/doctor and subsequent inquest, all cases of suffocation or smothering are treated as potentially suspicious. â&#x20AC;&#x201C;Dr Sudhir Gupta, Additional Professor, Forensic Medicine & Toxicology, AIIMS

Spiritual Update Science Behind Hanuman Chalisa

Most spiritual powers can be explained by understanding the concept that soul and spirit are nothing but energized files of information that carry information of not only this birth but also of the past births. When Soul and Spirit are connected with each other, the transfer of data is just a formality. Vitamins - Open Secrets Revealed Vitamin B12 and Homocysteine Grain fortification with vitamin B12?

Since 1998, it has been mandatory to fortify grainbased foods with folic acid in the United States. Recent reports indicate that this measure has resulted in a 19% decrease in the incidence of neural tube defects. A similar fortification program is being considered in the UK. Irish researchers now suggest that the fortification protocol should include not only folic acid, but also vitamin B12. They point out that folic acid supplementation also lowers the level of homocysteine, a potent risk factor for heart and vascular disease. However, a recent trial carried out by the Dublin researchers clearly showed that as blood levels of folic acid increased through supplementation, blood levels of vitamin B12 became the limiting factor. In other words, additional folic acid as well as additional vitamin B12 is required in order to attain the maximum reduction in 97

emedinews Section homocysteine levels. Four to five hundred micrograms per day of folic acid were found to increase folic acid levels by 80-180% and lower homocysteine levels by about 30% in both men and women. Both folate and homocysteine levels tended to revert to their pre-supplementation levels after 10 weeks of no supplementation; this shows that continuous supplementation is necessary in order to keep homocysteine levels under control. (Ref: Quinlivan EP, McPartlin J, McNulty H, et al. Importance of both folic acid and vitamin B12 in reduction of risk of vascular disease. Lancet 2002;359(9302):227-8.) –Dr Jitendra Ingole, MD Internal Medicine

Pediatric Update What are the causes of vitamin a deficiency?

The risk of vitamin A deficiency is increased in patients suffering from fat malabsorption, cystic fibrosis, sprue, pancreatic insufficiency, IBD or cholestasis, as well as in persons who have undergone small-bowel

bypass surgery. The risk is also increased in vegans, refugees, recent immigrants, persons with alcoholism, and toddlers and preschool children living below the poverty line. These patients should be advised to consume vitamin A. –Dr Neelam Mohan, Director Pediatric Gastroenterology, Hepatology and Liver Transplantation, Medanta - The Medicity

GP Pearls According to a study, liraglutide was superior to sitagliptin for glycemic control in metformin-treated diabetic patients and resulted in greater reductions in body weight (Lancet 2010;375(9724):1447-56). But, the gastrointestinal tolerance profile is better with sitagliptin than with liraglutide, and one pill of sitagliptin daily might be judged as easier to administer than one subcutaneous injection of liraglutide daily. The increased cost of liraglutide should be compared with the benefit provided by (its) improved glucose control and weight reduction (Lancet 2010;375(9724):1410‑2). –Dr Pawan Gupta

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Indian Journal of

Clinical Practice

Information for Authors Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767). Indian Journal of Clinical Practice strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so. The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript. Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper. Covering letter –

–

The covering letter should explain if there is any deviation from the standard IMRAD format (Introduction, Methods, Results and Discussion) and should outline the importance of the paper. Principal/Senior author must sign the covering letter indicating full responsibility for the paper submitted, preferably with signatures of all the authors. Articles must be accompanied by a declaration by all authors stating that the article has not been published in any other Journal/Book. Authors should mentioned complete designation and departments, etc. on the manuscript.

Manuscript – Three complete sets of the manuscript should be submitted and preferably with a CD; typed double spaced throughout (including references, tables and legends to figures). –

The manuscript should be arranged as follow: Covering letter, Checklist, Title page, Abstract, Keywords (for indexing, if required), Introduction, Methods, Results, Discussion, References, Tables, Legends to Figures and Figures.

–

All pages should be numbered consecutively beginning with the title page.

departments and institutions where the work was performed, name of the corresponding authors, acknowledgment of financial support and abbreviations used. – The title should be of no more than 80 characters and should represent the major theme of the manuscript. A subtitle can be added if necessary. – A short title of not more than 50 characters (including inter-word spaces) for use as a running head should be included. – The name, telephone and fax numbers, e-mail and postal addresses of the author to whom communications are to be sent should be typed in the lower right corner of the title page. – A list of abbreviations used in the paper should be included. In general, the use of abbreviations is discouraged unless they are essential for improving the readability of the text. Summary – The summary of not more than 200 words. It must convey the essential features of the paper. – It should not contain abbreviations, footnotes or references. Introduction – The introduction should state why the study was carried out and what were its specific aims/objectives. Methods – These should be described in sufficient detail to permit evaluation and duplication of the work by others. – Ethical guidelines followed by the investigations should be described. Statistics The following information should be given: – The statistical universe i.e., the population from which the sample for the study is selected. – Method of selecting the sample (cases, subjects, etc. from the statistical universe). – Method of allocating the subjects into different groups. – Statistical methods used for presentation and analysis of data i.e., in terms of mean and standard deviation values or percentages and statistical tests such as Student’s ‘t’ test, Chi-square test and analysis of variance or non-parametric tests and multivariate techniques.

Note: Please keep a copy of your manuscript as we are not responsible for its loss in the mail. Manuscripts will not be returned to authors.

–

Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the

–

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011

Confidence intervals for the measurements should be provided wherever appropriate.

Results These should be concise and include only the tables and figures necessary to enhance the understanding of the text.

101

Discussion –

This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g., practicality and cost.

References These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited (Sinha12 confirmed other reports13,14...). References cited only in tables or in legends to figures should be numbered in the text of the particular table or illustration. Include among the references papers accepted but not yet published; designate the journal and add ‘in press’ (in parentheses). Information from manuscripts submitted but not yet accepted should be cited in the text as ‘unpublished observations’ (in parentheses). At the end of the article the full list of references should include the names of all authors if there are fewer than seven or if there are more, the first six followed by et al., the full title of the journal article or book chapters; the title of journals abbreviated according to the style of the Index Medicus and the first and final page numbers of the article or chapter. The authors should check that the references are accurate. If they are not this may result in the rejection of an otherwise adequate contribution. Examples of common forms of references are: Articles

–

Do not use clips/staples on photographs and artwork.

–

Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in the text and abbreviated as “Fig.”.

Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected

Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes. Q. J. Expt. Physiol. 1955;40:89-111.

4. Number of figures ___________________________

Books

5. Special requests _____________________________

Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985.

6. Suggestions for reviewers (name and postal address)

Articles in Books

2.____________

2._ _______________

Strong MS. Recurrent respiratory papillomatosis. In: Scott Brown’s Otolaryngology. Paediatric Otolaryngology Evans JNG (Ed.), Butterworths, London 1987;6:466-470.

3.____________

3._ _______________

4.____________

4._ _______________

Tables –

These should be typed double spaced on separate sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.

Legends – These should be typed double spaces on a separate sheet and figure numbers (in Arabic numerals) corresponding with the order in which the figures are presented in the text. –

102

Figures – Two complete sets of glossy prints of high quality should be submitted. The labelling must be clear and neat. – All photomicrographs should indicate the magnification of the print. – Special features should be indicated by arrows or letters which contrast with the background. – The back of each illustration should bear the first author’s last name, figure number and an arrow indicating the top. This should be written lightly in pencil only. Please do not use a hard pencil, ball point or felt pen. – Color illustrations will be accepted if they make a contribution to the understanding of the article.

The legend must include enough information to permit interpretation of the figure without reference to the text.

summary, etc.)_______________________________ 2. Total number of pages ________________________ 3. Number of tables ____________________________

Indian 1.____________Foreign 1._ _______________

7. All authors’ signatures________________________ 8. Corresponding author’s name, current postal and e-mail address and telephone and fax numbers __________________________________________

Online Submission Also e- Issue @ www.ijcpgroup.com For Editorial Correspondence

Dr K.K. Aggarwal Group Editor-in-Chief Indian Journal of Clinical Practice E-219, Greater Kailash, Part-1 New Delhi - 110 048. Tel: 40587513 E-mail: editorial@ijcp.com Website: www.ijcpgroup.com

Indian Journal of Clinical Practice, Vol. 22, No. 2, July 2011