Etiological spectrum of sporadic malabsorption syndrome in northern Indian adults at a tertiary hospital.

BACKGROUND: The etiology of malabsorption syndrome (MAS) may differ in different geographical regions. Limited data are available on the etiological spectrum of MAS among Indian adults. METHODS: Ninety-nine consecutive adult patients with MAS (urine d-xylose <1 g/5 g/5 h with or without increased fecal fat (> or =7 g/24 h) were evaluated for cause of MAS using standard criteria. Past medical records were examined to know the nature of treatment received. RESULTS: The etiology of MAS was: tropical sprue 39, celiac disease 9, Crohn's disease 9, giardiasis 8, small intestinal bacterial overgrowth in absence of another cause of MAS 8, panhypogammaglobulinemia 2 (one with strongyloidiasis), intestinal lymphangiectasia 1, intestinal tuberculosis 4, idiopathic 15, acquired immunodeficiency syndrome 2, and amyloidosis 2. Twenty-eight patients had received anti-tubercular treatment earlier. CONCLUSIONS: Tropical sprue, celiac disease and Crohn's disease are common causes of MAS in Indian adults. Inappropriate anti-tubercular treatment is common in them and needs to be discouraged.

Occult hepatitis B virus infection as a cause of cirrhosis of liver in a region with intermediate endemicity.

BACKGROUND: Serological tests may fail to identify hepatitis B virus (HBV) infection as a cause of liver cirrhosis in a proportion of patients. The frequency of such occult infection in regions with intermediate HBV endemicity is not known. Such cases may be diagnosed by incremental testing for IgG anti-HBc, serum HBV DNA, and HBV DNA in liver tissue. METHODS: We tested sera of 111 patients with cirrhosis, including 39 with history of significant alcohol ingestion, for HBsAg, anti-HBc and serum HBV DNA. In addition, in a subset of 14 patients, HBV DNA was looked for in liver tissue. RESULTS: On HBsAg and anti-HBc testing, 66 patients had HBV infection. Serum HBV DNA testing identified HBV infection in 13 additional cases. Of 18 patients labeled as 'cryptogenic' on serological testing, HBV DNA was detected in the serum in 7 patients. Of 14 patients in whom paired liver tissue and serum specimens were tested, 4 additional patients with HBV infection were detected after liver biopsy analysis. CONCLUSIONS: Serological tests for HBsAg and anti-HBc antibody are insensitive in identifying HBV infection in patients with liver cirrhosis. HBV DNA testing in serum and liver can help in establishing HBV infection as etiology, either alone or in addition to another cause.

Evidence for activation of cellular immune responses in patients with acute hepatitis E.

INTRODUCTION: Although acute hepatitis E virus (HEV) infection is known to induce IgM and IgG humoral host immune responses, little is known about occurrence of cellular responses in this infection. We looked for evidence of lymphocyte sensitization to HEV peptides in patients with acute HEV infection. METHODS: peripheral blood lymphocytes were obtained from patients with acute hepatitis E and healthy controls. Proliferation of these lymphocytes in the presence of each of seven peptides with amino acid sequences corresponding to open reading frames 2 and 3 proteins of HEV (3 and 4 peptides, respectively) were studied; no peptide was added to control wells. Proliferative responses with stimulation indices exceeding 3.0 were taken as positive. RESULTS: More patients showed reactivity to two or more HEV peptides than did controls (11/21 vs 5/22, p<0.05). Reactivity to one peptide corresponding to open reading frame 2 of HEV was more frequent in patients than in controls (7/21 vs 1/22, p<0.05). CONCLUSION: Our results show that lymphocytes of patients with acute hepatitis E show sensitization to HEV peptides. This may have significance in understanding the pathogenetic mechanisms of liver injury in this infection.