Manisha Dwivedi

Epidemiology and symptom profile of gastroesophageal reflux in the Indian population: report of the Indian Society of Gastroenterology Task Force.

BackgroundGastroesophageal reflux disease (GERD) and its complications are thought to be infrequent in India; there are no data from India on the prevalence of and risk factors for GERD. The Indian Society of Gastroenterology formed a task force aiming to study: (a) the frequency and profile of GERD in India, (b) factors including diet associated with GERD.MethodsIn this prospective, multi-center (12 centers) study, data were obtained using a questionnaire from 3224 subjects regarding the frequency, severity and duration of heartburn, regurgitation and other symptoms of GERD. Data were also obtained regarding their dietary habits, addictions, and lifestyle, and whether any of these were related or had been altered because of symptoms. Data were analyzed using univariate and multivariate methods.ResultsTwo hundred and forty-five (7.6%) of 3224 subjects had heartburn and/or regurgitation at least once a week. On univariate analysis, older age (OR 1.012; 95% CI 1.003–1.021), consumption of non-vegetarian and fried foods, aerated drinks, tea/coffee were associated with GERD. Frequency of smoking was similar among subjects with or without GERD. Body mass index (BMI) was similar in subjects with and without GERD. On multivariate analysis, consumption of non-vegetarian food was independently associated with GERD symptoms. Overlap with symptoms of irritable bowel syndrome was not uncommon; 21% reported difficulty in passage of stool and 9% had mucus in stools. About 25% of patients had consulted a doctor previously for their gastrointestinal symptoms.Conclusion7.6% of Indian subjects have significant GERD symptoms. Consumption of non-vegetarian foods was an independent predictor of GERD. BMI was comparable among subjects with or without GERD.

Colonic mucosa in patients with portal hypertension

Background and Aims: To do a histomorphometric study of vascular changes in colonic mucosa of patients with portal hypertension (PHT) and to find their association with clinical and upper and lower gastrointestinal endoscopic observations.

Gallbladder Dynamics in Patients with Irritable Bowel Syndrome and Essential Dyspepsia

To assess whether gallbladder motility is altered in patients with irritable bowel syndrome (IBS) or essential dyspepsia (ED), we studied gallbladder function in 25 healthy volunteers, 20 patients with IBS, and 22 with ED. By real time ultrasonography, we studied the following parameters: (a) fasting gallbladder volume, (b) maximum percent of gallbladder emptied, (c) time required for maximal contraction, (d) residual volume after maximal contraction, and (e) percent fasting volume at 2 h. All parameters, except fasting gallbladder volume, were measured after a high-fat meal. The fasting gallbladder volume, maximum percent of gallbladder emptied, time required for maximal contraction, residual volume after maximal contraction, and percent fasting volume at 2 h in controls and patients with IBS was 19.3 +/- 8.8 ml and 24.4 +/- 9.7 ml, 67.1 +/- 10.7% and 67.6 +/- 13.5%, 41 +/- 20.6 min and 49.7 +/- 25.3 min, 6.2 +/- 3.3 ml and 7.6 +/- 5.3 ml, and 38.1 +/- 12.2% and 40.7 +/- 14.5%, respectively. The differences between the two groups were statistically not significant. The corresponding values in patients with ED were 15.5 +/- 6.3 ml, 57.6 +/- 16.5%, 51.8 +/- 29.3 min, 6.1 +/- 3.2 ml, 44.1 +/- 17%, respectively. Compared with controls there was no statistically significant difference in these parameters, except the maximum percent of gallbladder emptied, which was significantly less than that in controls (57.6 +/- 16.5% vs. 67.1 +/- 10.7%; p less than 0.05). Therefore, we could not find that patients with IBS have any abnormality of gallbladder function; postprandially, patients with ED have submaximal contraction of the gallbladder.

Endoscopic sclerotherapy for portal hypertension due to extrahepatic obstruction: long-term follow-up

Between 1982 and 1987, 43 patients with variceal bleeding due to extrahepatic portal obstruction were treated by repeated endoscopic injection sclerotherapy using 1% polidocanol intravariceally. This decreased rebleeding, as evidenced by a decrease in bleeding risk factor (BRF), mean transfusion requirement, and mean number of transfusions per patient per month of follow-up. Differences between pre- and postsclerotherapy parameters were significant (p less than 0.001). The varices were eradicated in 86% of patients. The mean sclerotherapy sessions required were 7.68 +/- 2.39 (SD). Complications were infrequent. Forty-three patients were followed from 5 to 68 months: cumulative survival was 97.7% and varices recurred in 16%. Sclerotherapy avoided a second operation in 21 postsurgical patients. Sclerotherapy for managing variceal bleeding due to extrahepatic portal obstruction is a reasonable alternative to surgery.

Helicobacter pylori and gastric cancer: Indian enigma

Helicobacter pylori (H. pylori) is a gram negative microaerophilic bacterium which resides in the mucous linings of the stomach. It has been implicated in the causation of various gastric disorders including gastric cancer. The geographical distribution and etiology of gastric cancer differ widely in different geographical regions and H. pylori, despite being labeled as a grade I carcinogen, has not been found to be associated with gastric cancer in many areas. Studies in Asian countries such as Thailand, India, Bangladesh, Pakistan, Iran, Saudi Arabian countries, Israel and Malaysia, have reported a high frequency of H. pylori infection co-existing with a low incidence of gastric cancer. In India, a difference in the prevalence of H. pylori infection and gastric cancer has been noted even in different regions of the country leading to a puzzle when attempting to find the causes of these variations. This puzzle of H. pylori distribution and gastric cancer epidemiology is known as the Indian enigma. In this review we have attempted to explain the Indian enigma using evidence from various Indian studies and from around the globe. This review covers aspects of epidemiology, the various biological strains present in different parts of the country and within individuals, the status of different H. pylori-related diseases and the molecular pathogenesis of the bacterium.

Helicobacter pylori in areas of gastric metaplasia in the gallbladder and isolation of H. pylori DNA from gallstones

Aims: To assess if the areas of gastric metaplasia in the gallbladder are colonised by Helicobacter pylori and to conduct a molecular study of gallstones for presence of H. pylori DNA. Methods: Sections from 111 gallbladders with evidence of gastric metaplasia on H&E and Alcian blue–periodic acid‐Schiff (pH 2.5) stain were stained with Loefflers methylene blue and Warthin Starry stain for demonstration of H. pylori. Presence of H. pylori was confirmed by immunohistochemistry. Formalin fixed mucosal tissues and gallstones from 11 cases showing heavy colonisation were subjected to molecular analysis. Results: Helicobacter pylori was present in 50 of 111 (45%) sections with gastric metaplasia. Areas adjacent to gastric metaplasia in gallbladder showed acute inflammation (6%) and lymphoid follicle formation in 58% of cases with H. pylori that were significantly higher than those seen in sections without H. pylori. In molecular study, 8 of 11 gallstones showed 16S rDNA. Amplification of material from one stone showed positivity for atpA, efp, mutY, ppa, trpC, UreI and vacA genes. Phylogenetic affiliation study of the isolates indicated that H. pylori sequence from the gallstones clustered with Indian strains of H. pylori. No considerable difference was observed in phylogenetic affiliations of eight stones studied. Conclusion: H. pylori colonises areas of gastric metaplasia in gallbladder producing histological changes similar to those seen in gastric mucosa. Isolation of H. pylori DNA from gallstones further support its presence in the gallbladder.

A comparative evaluation of scoring systems for assessing necro-inflammatory activity and fibrosis in liver biopsies of patients with chronic viral hepatitis.

INTRODUCTION To compare the five scoring systems in assessing grading and staging of liver biopsies from patients with chronic viral hepatitis and their problems and pitfalls. MATERIALS AND METHODS Liver biopsies from 25 patients with chronic viral hepatitis were studied. Sections were stained with Haematoxylin and Eosin, Reticulin and Massons Trichrome stains. Van Gieson, Perls and Shikatas Orcein stains were used as and when required. Coded histological sections were scored independently by three histopathologists using the Knodell Histology Activity Index (HAI), the Scheuer scoring system, Ishaks system, Metavir system and Ishak modified HAI. RESULTS There were 15 males and 10 females. Their mean age was 51.24 years. On histological examination, hepatocytes showed degenerative changes with varying grades of necrosis (spotty and confluent). Widening of portal tracts with varying severity of mononuclear inflammatory infiltrate and interface hepatitis was observed. Fibrosis appeared as periportal, portal-portal and portal-central septa. A significant agreement was found by kappa statistics for both grading (p< 0.001) as well as staging (p < 0.001) among all the five scoring systems. Lobular activity was the only parameter that showed some discrepancy. No significant intra observer difference was observed. CONCLUSION It is concluded that all the scoring systems are equally good for grading and staging in the hands of an experienced hepatopathologists.

Comparative efficacy of emergency endoscopic sclerotherapy for active variceal bleeding due to cirrhosis of the liver, non-cirrhotic portal fibrosis and extrahepatic portal venous obstruction

Patients with continued variceal bleeding due to portal hypertension (n= 202) were treated by endoscopic injection sclerotherapy after resuscitation. Portal hypertension was due to hepatic cirrhosis in 123, non‐cirrhotic portal fibrosis (NCPF) in 49 and extrahepatic portal venous obstruction (EHO) in 30 patients. Polidocanol 1% was injected intravariceally. An adequate sclerotherapy was carried out in 97% of patients.

Aluminum Phosphide-induced Esophageal Strictures : A New Cause of Benign Esophageal Strictures

Abstract Fifteen consecutive patients presenting with dysphagia due to aluminum phosphide (AP)-induced esophageal strictures were studied retrospectively to elucidate the natural history of AP-induced esophageal strictures and to evaluate the efficacy of bougie dilation. The median time lag between consumption of AP and occurrence of dysphagia was 3 weeks. All patients had a single stricture and could be dilated using a bougie dilator. Thirteen patients were relieved of dysphagia on a mean (SD) follow-up of 18 (7.3) months. Two patients had recalcitrant strictures and needed needle-knife incision of the stricture followed by balloon dilation. The strictures opened up well in both the patients and they were relieved of dysphagia. AP-induced esophageal stricture is a new cause of benign esophageal stricture. Most patients present with dysphagia around 3 weeks after consumption of AP tablets. A single esophageal stricture is found in these patients. Most strictures respond very well to bougie dilation. However, some of the strictures may be recalcitrant and may require needle-knife incision and balloon dilation.

Hepatitis B and C co-infection in HIV patients

Editor: Chronic viral infections with the human immunodeficiency virus (HIV), hepatitis B virus (HBV) and hepatitis C virus (HCV) share similar routes of transmission, mainly through blood and blood products, sharing of needles to inject drugs, and sexual activity, enabling co-infection with these viruses [1–4]. HBV and HCV co-infections in HIV positive individuals are of clinical importance and have been shown to decrease the life expectancy of HIV infected patients [4]. We evaluated 100 HIV positive patients (ranging in age from 15 to 65 years) attending the HIV clinic, excluding those with a history of drug induced hepatitis and alcoholic hepatitis. Hepatitis B surface antigen (HBsAg) and hepatitis C virus antibody (anti-HCV) were detected using SD HBsAg kit and INSTACHK hepatitis C kit respectively. Ninety-eight patients had multiple sexual partners and unprotected sex as the major risk behavior, while two had possible transfusion related infection. None of them were intravenous drug users. Eight patients (8 %) were also positive for HBsAg and 2 (2 %) were positive for antiHCV. None of them were positive for both HBsAg and anti-HCV. The mean (SD) CD4 count of HBsAg reactive patients was 267 (180)/μL and that of anti-HCV reactive patients was 196 (94)/μL, compared to 276 (194)/μL in patients without HBV or HCV co-infection. None of these differences was statistically significant. The mean (SD) SGPT was 58 (40) IU/L in HBsAg reactive patients and 23 (6) IU/L in anti-HCV reactive patients (p0ns). The mean (SD) SGOT value in HBsAg reactive patients was 67 (79) IU/L and 28 (5) IU/L in anti-HCV reactive patients (p0 ns). The mean (SD) serum ALP value in HBsAg reactive patients was 234 (190) IU/L and 129 (24) IU/L in anti-HCV reactive patients. None of these differences was statistically significant. The prevalence of HBV co-infection in this study was 8.0 %. Various studies have shown prevalence from 2.19 % to 9 % [5–7]. In the present study the prevalence of HCV co-infection was 2 %. Other studies have shown prevalence from 1.61 % to 10.99 % [5–7]. In present study elevation of liver enzymes in patients who were co-infected with hepatitis B or hepatitis C was not statistically significant. In a study by Olanisun et al. [8], liver enzymes were elevated in all the patient groups, though there was no significant association. The mean level was highest for those co-infected with hepatitis B, followed by those co-infected with hepatitis C. Our study shows that the highest copositivity was seen in those patients having CD4 count <200/μL and HBeAg reactivity of 3 out of 8 HBsAg reactive patients indicated the need for change in highly active antiretroviral therapy regime in these patients. Since these viruses share common modes of transmission, we suggest that all HIV positive patients be investigated for hepatitis B and C co-infection so that appropriate management can be instituted.