Banumathi Ramakrishna

Colonoscopic study of 50 patients with colonic tuberculosis.

Fifty patients with colonic tuberculosis are reported in whom a colonoscopic diagnosis confirmed by histological examination was possible in 40. Bacteriological studies did not increase the diagnostic yield. Abdominal pain was the most common symptom (90%) and an abdominal mass the most common abnormal physical finding (58%). A nodular mucosa with areas of ulceration was the usual colonoscopic finding. Ileocaecal disease was found in 16, ileocaecal and contiguous ascending colon disease in 14, segmental colonic tuberculosis in 13, ileocaecal disease and non-confluent involvement of another part of the colon in five, and pancolitis in two patients. This report emphasises that colonoscopy is a useful procedure for diagnosing colonic tuberculosis and that segmental colonic tuberculosis is not uncommon.

Endoscopic mucosal biopsies are useful in distinguishing granulomatous colitis due to Crohn's disease from tuberculosis

BACKGROUND Intestinal tuberculosis and Crohn’s disease are chronic granulomatous disorders that are difficult to differentiate histologically. AIMS To characterise distinctive diagnostic features of tuberculosis and Crohn’s disease in mucosal biopsy specimens obtained at colonoscopy. METHODS Selected histological parameters were evaluated retrospectively in a total of 61 biopsy sites from 20 patients with tuberculosis and 112 biopsy sites from 20 patients with Crohn’s disease. The patients were chosen on the basis of clinical history, colonoscopic findings, diagnostic histology, and response to treatment. RESULTS The histological parameters characteristic of tuberculosis were multiple (mean number of granulomas per section: 5.35), large (mean widest diameter: 193 μm), confluent granulomas often with caseating necrosis. Other features were ulcers lined by conglomerate epithelioid histiocytes and disproportionate submucosal inflammation. The features characteristic of Crohn’s disease were infrequent (mean number of granulomas per section: 0.75), small (mean widest diameter: 95 μm) granulomas, microgranulomas (defined as poorly organised collections of epithelioid histiocytes), focally enhanced colitis, and a high prevalence of chronic inflammation, even in endoscopically normal appearing areas. CONCLUSIONS The type and frequency of granulomas, presence or absence of ulcers lined by epithelioid histiocytes and microgranulomas, and the distribution of chronic inflammation have been identified as histological parameters that can be used to differentiate tuberculosis and Crohn’s disease in mucosal biopsy specimens obtained at colonoscopy.

Histopathological study of chronic hepatitis B and C: a comparison of two scoring systems

BACKGROUND/AIMS Several histological scoring systems are used to evaluate chronic viral hepatitis. This study was undertaken to determine the correlation between the Ishak system (modified histological activity index, HAI) and the METAVIR system, in Indian patients with chronic viral hepatitis. METHODS Liver biopsies from 127 patients with chronic viral hepatitis B or C were examined, and scored using the Ishak and METAVIR systems, and weighted kappa analysis of correlation was done. Correlation of necroinflammatory activity with serum transaminase levels was analyzed, and prevalence of specific histological features compared in hepatitis B virus (HBV) and HCV biopsies. RESULTS HBV infection accounted for 64.6% of cases, and HCV for 35.4%; 91.3% of patients had minimal or mild hepatitis. The necroinflammatory scores of the Ishak and METAVIR systems correlated moderately well (weighted kappa 0.627), while there was excellent correlation with regard to fibrosis (weighted kappa 0.998). Similar concordance was found when HBV and HCV cases were analyzed separately. HAI showed poor correlation with serum transaminases (weighted kappa 0.21). Micronodular cirrhosis, lymphoid aggregates, bile duct damage, bile ductular proliferation and steatosis were significantly more common in HCV biopsies compared to HBV. CONCLUSIONS Concordance between Ishak and METAVIR scoring systems is good for necroinflammatory change, and excellent for fibrotic change.

Segmental colonoscopic biopsies in the differentiation of ileocolic tuberculosis from Crohn's disease

Background and Aim:  The differentiation between Crohns disease (CD) and tuberculosis (TB) of the intestine can be difficult in areas where both diseases occur. The present study examined histological criteria that would enable the diagnosis in mucosal biopsies.

Does oxidative protein damage play a role in the pathogenesis of carbon tetrachloride-induced liver injury in the rat?

Free radicals have been implicated in the pathogenesis of alcohol-induced liver injury in humans and carbon tetrachloride (CCl4)-induced liver injury in rats. The most extensively studied aspect of free radical induced liver injury is lipid peroxidation. Recently it has been found that free radicals can cause oxidative damage to cellular proteins and alter cellular function. One such susceptible protein is the enzyme glutamine synthase (GS). The chemical effects of CCl4 on cell proteins and their biological consequences are not known. Hence, in our study, the effect of CCl4 on liver protein oxidation and GS activity were investigated and compared with lipid peroxidation. A significant increase in liver protein carbonyl content (2-3 fold) and a significant decrease in hepatic GS activity (44-57%) were observed. Damage to proteins was rapid in onset and increased with time. Acute exposure of rats to CCl4 resulted in an increase in hepatic protein carbonyl content and a decrease in hepatic GS within 1 h. In cirrhosis of the liver induced by CCl4, the decrease in hepatic GS activity was accompanied by a significant increase in plasma ammonia levels. We conclude that protein oxidation may play a role in the pathogenesis of CCl4 induced liver injury and that the accumulation of oxidised proteins may be an early indication of CCl4 induced liver damage.

Guideline for the management of acute diarrhea in adults

provide a complete document that would be applicable to the case management of diarrhea. However, some explanation and amplification is necessary to clarify the terms and phrases that have been used, as well as to explain the basis for certain decision pathways in the algorithm. Adult: The definition of ‘adult’ varies from one country to another. As applied in this guideline, the term ‘adult’ refers to someone who is of age 12 years or above. Acute diarrhea: This is defined as the passage of three or more than three loose or watery stool in 24 h, or passage of one or more bloody stool. Acute diarrhea refers to illness not lasting longer than 14 days. Other conditions that may present as acute diarrhea: ‘Acute diarrhea’ is a clinical syndrome that is commonly understood to refer to infective gastroenteritis. However, as defined, acute diarrhea may be a symptom of other intra-abdominal or systemic illnesses. These other clinical conditions may require particular investigations and management, and will need to be recognized and excluded at the outset. Careful history and physical examination is necessary to exclude these conditions from the commonly understood ‘acute diarrhea’. Special attention should be paid to exclude signs of peritonism or peritonitis, which will indicate serious illnesses that might require surgical care. Examples of these diverse clinical conditions are presented in Table 1. Specific conditions of acute diarrhea that require special consideration: Although the term ‘acute diarrhea’ commonly refers to infectious, toxin-induced and drug-induced diarrhea, there are specific acute diarrhea syndromes that may need a specifically tailored approach and management, and where the general algorithm may need to be modified. For example, during epidemic acute diarrhea such as cholera, it is important to quickly identify the organism in the first patients presenting with illness, and to initiate public health meaINTRODUCTION

Collagenous gastritis and collagenous colitis: a report with sequential histological and ultrastructural findings

The case is reported of a young adult man with collagenous gastritis, an extremely rare disorder with only three case reports in the English literature, who subsequently presented with collagenous colitis. Sequential gastric biopsies showed a notable increase in thickness of the subepithelial collagen band. Ultrastructural study of gastric and rectal mucosa showed the characteristic subepithelial band composed of haphazardly arranged collagen fibres, prominent degranulating eosinophils, and activated pericryptal fibroblasts.

Liver injury in acute fatty liver of pregnancy: Possible link to placental mitochondrial dysfunction and oxidative stress

Acute fatty liver of pregnancy (AFLP) is a rare disorder which is fatal if not recognized and treated early. Delivery of the feto‐placental unit results in dramatic improvement in maternal liver function, suggesting a role for the placenta. However, the mechanisms by which defects in the fetus or placenta lead to maternal liver damage are not well understood and form the focus of this study. Placenta and serum were obtained at delivery from patients with AFLP, and placental mitochondria and peroxisomes were isolated. Placental mitochondrial function, oxidative stress, and fatty acid composition as well as serum antioxidants, oxidative and nitrosative stress markers, and fatty acid analysis were carried out. Hepatocytes in culture were used to evaluate cell death, mitochondrial function, and lipid accumulation on exposure to fatty acids. Oxidative stress was evident in placental mitochondria and peroxisomes of patients with AFLP, accompanied by compromised mitochondrial function. Increased levels of arachidonic acid were also seen in AFLP placenta when compared to control. Patients with AFLP also had a significant increase in oxidative and nitrosative stress markers in serum, along with decreased antioxidant levels and elevated levels of arachidonic acid. These levels of arachidonic acid were capable of inducing oxidative stress in hepatocyte mitochondria accompanied by induction of apoptosis. Exposure to arachidonic acid also resulted in increased lipid deposition in hepatocytes. Conclusion: Oxidative stress in placental mitochondria and peroxisomes is accompanied by accumulation of toxic mediators such as arachidonic acid, which may play a causative role in maternal liver damage seen in AFLP. (HEPATOLOGY 2010;51:191–200.)

Oxidative damage to the hepatocellular proteins after chronic ethanol intake in the rat.

BACKGROUND Protein carbonyl content, a measure of oxidative damage to hepatocellular proteins, and the activities of some thiol-containing proteins were assayed in the liver and plasma, as thiol-containing protein, appear to be targets for free radicals. These may be important in the mechanism of ethanol-induced liver injury. METHODS Tap water containing ethanol at the concentration of 25% (v/v) and phenobarbital (500 mg/l) was the only source of drinking water for the experimental rats for 24 months. Another group of rats were administered 25% (v/v) ethanol alone in drinking water for 24 months. Control rats were administered either phenobarbital alone in drinking water or tap water for 24 months. At the end of 24 months, the rats were sacrificed. The protein carbonyl content, activities of glutamine synthase and biotinidase-sulfhydryl group containing enzymes were assayed in the liver along with alkaline protease, an enzyme that degrades oxidized proteins. The total thiol, albumin and the activity of biotinidase were measured in the plasma. RESULTS The protein carbonyl content of the liver was increased in the ethanol/phenobarbital-treated rats as well as in the ethanol-treated rats as compared with the controls. The activities of glutamine synthase and biotinidase were decreased significantly in the livers of ethanol/phenobarbital-treated rats as well as the ethanol-treated rats as compared with the controls. The activity of alkaline protease was increased significantly in both the ethanol-treated groups. In the plasma of ethanol/phenobarbital-treated rats as well as the ethanol-treated rats total thiol, albumin and the activity of biotinidase were decreased significantly as compared with the controls. The ethanol/phenobarbital-treated rats as well as the ethanol-treated rats developed fatty liver. CONCLUSIONS Damage to proteins occurs upon chronic ethanol intake in the rat, and it may play a role in the pathogenesis of alcohol-induced fatty liver.

Prevalence of Helicobacter pylori in southern Indian controls and patients with gastroduodenal disease

Abstract The spiral organism Helicobacter pylori has been casually implicated in the genesis of various gastroduodenal diseases. Since these diseases are common in southern India, this study was undertaken to determine the prevalence of H. pylori in the gastric mucosa of asymptomatic adults and patients with various gastroduodenal diseases. H. pylori was detected in the gastric mucosa of 25 of 30 (83.3%) normal volunteers. Prevalence rates in the disease groups were also high, and included 38 of 41 patients with duodenal ulcer (92.6%), 13/16 with gastric ulcer (81.3%), and 85/119 subjects (71.4%) with non‐ulcer dyspepsia. Light microscopic examination of the gastric mucosa provided the best method of detecting H. pylori. H. pylori colonization was significantly associated with histological abnormalities, mainly chronic atrophic gastritis (147) and superficial gastritis (11), while only three of 161 H. pylori positive patients had histologically normal antral mucosa. Ultrastructural examination revealed changes in the apical complex of the gastric mucosal cells in response to bacterial adhesion, with mucus depletion and cellular damage. Bacteria were also noted disrupting the tight junctions and entering the intercellular spaces. The high prevalence of H. pylori infection may explain the high incidence of gastritis, duodenal ulceration and gastric carcinoma in this population. However, in this population, the prevalence of infection in asymptomatic individuals was nearly as high as that in duodenal ulcer, underlining the need for further study to identify the differences in host response or bacterial pathogenicity that lead to the development of ulcer in only some individuals.