Obstructive jaundice caused by pancreatic carcinoma in the setting of a normal pancreatogram.
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Adenocarcinoma↗
Biomedical subjects
E P Variyam
Publications and source records attributed to E P Variyam.
Bile salts promote adherence-decreasing effect of colonic luminal hydrolases on Entamoeba histolytica.
E. histolytica trophozoites cultivated for > 7 h in the presence of glycosidases, produced by a subset of the colonic anaerobic bacteria of healthy humans, and pancreatic proteases show decreased adherence to Chinese hamster ovary epithelial cells. Since activities of the glycosidases are enhanced by bile salts we investigated whether bile salts would enhance the E. histolytica-CHO cell adherence decreasing effects of the luminal hydrolases (glycosidases plus proteases). CHO cell adherence of control trophozoites was 78.4 +/- 1.2% (mean +/- SEM). Incubations with the hydrolases alone for 4 h did not change adherence. Addition of 5.0 mM sodium taurocholate to the hydrolases for 4 h decreased trophozoite adherence to 30.5 +/- 3.2% of that of control trophozoites (p < 0.05). The effect of sodium taurocholate was dose dependent over 0.5-5.0 mM. Four hour incubation with the hydrolases and sodium taurodeoxycholate at 2.0 and 5.0 mM also decreased trophozoite adherence to 25.1 +/- 2.9% and 29.4 +/- 1.7%, respectively, of that of control trophozoites. These findings show that bile salts enhance the effects of luminal hydrolases on E. histolytica trophozoites, decreasing their ability to adhere to epithelial cells.
Animals↗
Nondysenteric intestinal amebiasis. Colonic morphology and search for Entamoeba histolytica adherence and invasion.
There is controversy regarding the presence of colonic mucosal abnormalities or mucosal invasion by Entamoeba histolytica in patients with "nondysenteric intestinal amebiasis." To determine the role of E. histolytica in causing symptoms and mucosal changes and to detect if mucosal invasion by E. histolytica is present in nondynsenteric intestinal amebiasis, we evaluated 24 E. histolytica-infected patients (stool microscopy positive for E. histolytica) and 12 noninfected controls who presented with chronic gastrointestinal symptoms, but without dysentery, to a clinic in Calcutta. The colonic mucosa was evaluated at colonoscopy, and mucosal biopsies obtained from the cecum, sigmoid colon, and rectum were evaluated by light microscopy, indirect immunofluorescence microscopy, and scanning electron microscopy. At colonoscopy mucosal ulcerations were absent in all the controls and all except one of the E. histolytica-infected patients. E. histolytica trophozoites or cysts were not seen in the lamina propria or on the luminal surface in any infected patient by light and immunofluorescence microscopy. On scanning electron microscopy, structures that resembled rounded E. histolytica trophozoites were seen on the luminal surface in two of 19 cecal specimens from the infected patients. Moderate or severe mucosal inflammation was frequent on light microscopy in both the E. histolytica-infected patients and the noninfected controls with the cecum involved in two thirds of both groups. Antibodies to E. histolytica were detected in serum of 25% of study patients and 58% of controls. Mucosal inflammation did not correlate with stool positivity for E. histolytica or seropositivity for ameba antibody.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Pericardial effusion and left ventricular function in patients with acute alcoholic pancreatitis.
Pericardial effusion as a complication of acute pancreatitis has been described in several isolated case reports. However, the prevalence of pericardial effusion in patients with acute pancreatitis has not been studied. Alcoholism and severe acute pancreatitis have been shown to cause left ventricular dysfunction. We studied 15 consecutive patients, hospitalized for the treatment of acute, alcohol-induced pancreatitis, and 28 control subjects by M-mode echocardiography to detect pericardial effusion and to assess left ventricular function. Seven patients (47%) with pancreatitis and three control subjects (11%) had pericardial effusion; the prevalence of pericardial effusion in patients with pancreatitis was significantly greater (Fisher's exact test) than in control subjects. There was no evidence of impairment of left ventricular function in the patients, all of whom had mild acute pancreatitis; the mean fractional systolic shortening of the left ventricle in patients was not significantly different from that of control subjects (38% +/- 8.5% vs 37% +/- 8.0%), and the mean velocity of left ventricular circumferential shortening in patients was significantly higher than in control subjects (1.58 +/- 0.34 circumferences per second vs 1.29 +/- 0.32 circumferences per second). We conclude that in patients with mild acute alcohol-induced pancreatitis, pericardial effusion occurs frequently and that left ventricular function is unimpaired.
Acute Disease↗
Effect of parenteral amino acids on human pancreatic exocrine secretion.
Parenteral administration of amino acids has been utilized for the nutritional support of patients with a variety of gastrointestinal disorders including protracted pancreatitis and pancreatic fistulae. However, the effect of parenteral amino acid administration alone on human pancreatic secretion has not been studied. We have studied the short-term effect of parenteral administration of amino acids on pancreatic exocrine secretion in seven healthy men. A double-lumen tube was placed in the duodenum and polyethylene glycol was perfused into the proximal duodenum at the rate of 10 ml/min. A second double-lumen tube was placed in the stomach and bromsulfthalein was perfused into the cardia. Samples of duodenal contents were aspirated and gastric contents recovered during one hour of intravenous saline infusion followed by two hours of an amino acid mixture infusion. Hourly outputs of protein and pancreatic enzymes were determined, correcting for duodenogastric reflux based on concentrations of both markers in the samples. Despite an average increase of 72% in the plasma concentration of the infused amino acids, the outputs of protein, trypsin and amylase did not change significantly during amino acid infusion; the output of lipase decreased significantly during amino acid infusion. Two subjects were given intravenous secretin and cholecystokinin following amino acids; this resulted in increased outputs of protein, trypsin, and amylase in both. We conclude that the parenteral administration of amino acids to healthy young men does not stimulate pancreatic enzyme secretion as measured by the method using duodenal marker perfusion at the rate of 10 ml/min.
Adult↗
In vitro degradation of gastric mucin. Carbohydrate side chains protect polypeptide core from pancreatic proteases.
The polypeptide core of mucin glycoprotein subunits resists cleavage by proteases. To determine if the carbohydrate side chains of these subunits protect the underlying polypeptide core from proteolytic cleavage, we compared the effect of pancreatic proteases on hog gastric mucin before and after cleavage of its carbohydrate moieties by bacterial glycosidases from an anaerobic human fecal culture supernate. Hog gastric mucin was resistant to pancreatic proteases: less than 10% of the mucin protein became soluble in 80% vol/vol ethanol after 24-h incubation with trypsin, alpha-chymotrypsin, and elastase, and its elution pattern from Sephadex G-200 remained unchanged after elastase treatment, with 90% eluting at the void volume. By contrast, after removal of 50% of its carbohydrates, mucin was susceptible to pancreatic proteases: 50% of mucin protein became soluble in 80% vol/vol ethanol after 24-h incubation with alpha-chymotrypsin and elastase, and 24% of mucin protein became soluble in 80% vol/vol ethanol after 24-h incubation with trypsin; after elastase treatment, its elution from Sephadex G-200 was markedly retarded. We conclude that the carbohydrate side chains of hog gastric mucin glycoprotein protect the underlying polypeptide core from proteolysis and that degradation of the carbohydrate side chains by glycosidases from fecal bacteria renders the polypeptide core susceptible to pancreatic proteases.
Animals↗
Central vein hyperalimentation in pancreatic ascites.
Central vein hyperalimentation completely relieved pancreatic ascites associated with rupture of the main pancreatic duct in a patient after unsuccessful peripheral vein alimentation therapy. In two patients with pancreatic ascites associated with pseudocysts, central vein hyperalimentation was associated with complete relief of ascites in one and marked reduction in the other. Endoscopic pancreatography and ultrasonographic or computerized scanning studies revealed lesions that were considered requiring operative treatment in all the three patients; these studies should therefore be done even in patients whose ascites is completely relieved during medical therapy.
Aged↗
Mucin degradation in human colon ecosystems. Degradation of hog gastric mucin by fecal extracts and fecal cultures.
The enteric flora of rats plays a major role in the degradation of their gut mucin glycoproteins, but the role of human enteric flora in degrading gut mucin glycoprotein has not been as well defined. We have studied the degradation of hog gastric mucin, which is structurally similar to human gastric mucin, in anaerobic human fecal cultures and by partially purified enzyme fractions from human fecal extracts and anaerobic culture supernates. Extensive degradation of the mucin carbohydrate moieties occurred in all systems, but the degradation of mucin protein was less. During a 48-h incubation, the average percent degradation of mucin carbohydrates and mucin protein were respectively 96% and 57% in eight fecal cultures, 66% and 15% by four fecal culture supernates, and 78% and 43% by three fecal extracts. Degradation of mucin protein was greater during bacterial growth in fecal cultures than during incubation with fecal culture supernates, suggesting that bacterial protease activity was predominantly cell bound. We conclude that, as in the rat, the human enteric microflora degrades mucin carbohydrate moieties extensively and the mucin protein to a lesser extent.
Adult↗
Hookworm disease: nutritional implications.
Iron-deficiency anemia resulting from intestinal blood loss is the major consequence of hookworm infection. Development of the anemia can be prevented, and it can be treated by administration of iron. Hypoproteinemia, often associated with hookworm infection, may be the result of either protein malnutrition or increased intestinal loss of protein. It is unlikely that the worms cause diffuse morphologic or functional alterations of the intestine. Fortification or supplementation with iron is a practical method to control hookworm disease in endemic areas.
Ancylostomiasis↗