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Biomedical subjects

D V Datta

Publications and source records attributed to D V Datta.

At least 73 records · Page 4Linked to original sources
PubMed1976

The role of small intestine and kidney in bromosulphthalein conjugation.

1. The roles of the kidney and the small intestine in the conjugation of bromosulphthalein have been compared with that of the liver. 2. Studies with homogenates indicated that the liver has a higher bromosulphthalein-glutathione-conjugating activity than the intestine and kidney. The reduced glutathione content of the liver is greater than that of the small intestine and kidneys, which contain comparable amounts. 3. Experiments in vitro with tissue slices confirmed that the three organ are able to extract significant amount of bromosulphthalein. In carbon tetrachloride-induced hepatic necrosis the uptake and conjugation of the dye by the liver were reduced but were increased in the kidney and unchanged in the small intestine. 4. After an intravenous injection of bromosulphthalein, the percentages conjugated in the liver, kidney and gut were similar.

Animals↗
PubMed1976

Amebic peritonitis.

A total of 18 patients with amebic peritonitis were studied. Fourteen of these cases were due to rupture of amebic liver abscess into the peritoneum and the remaining cases were due to perforation of amebic colitis. No initial suspicion of amebic etiology was made in more than half of the cases. In the group of ruptured liver abscesses, nearly half of the patients showed right lower lung syndrome. The diagnosis in 13 of 14 cases of rupture of liver abscess was confirmed on aspiration. Patients with ruptured amebic liver abcess were of two types: 1. Diffuse type with diffuse signs, shorter duration of illness and poor prognosis. 2. Localized type with longer duration of illness, marked signs of peritonitis and better prognosis. Once the diagnosis of peritonitis was made, the management was surgical. Conservative treatment was tried only in cases with signs of localization. The mortality rate had been 33% in amebic liver abscess rupturing into the peritoneum and 75% in perforation of the intestine. A high index of suspicion of amebiasis in patients with an acute abdomen and institution of early treatment are recommended to help in reducing this mortality. Amebic liver abscess and amebic dysentery should be treated energetically to avoid this fatal complication and surgical intervention whenever indicated should not be delayed.

Adult↗
PubMed1975

Estimation of hepatic bilirubin UDP-glucuronyl transferase in patients with noncirrhotic portal fibrosis and liver disease: Significance and limitations.

Using a micromethod, hepatic bilirubin UDP-glucuronyl transferase has been assayed in percutaneous needle biopsy samples obtained from patients with infectious hepatitis, postnecrotic cirrhosis, Gilbert's disease, noncirrhotic portal fibrosis (NCPF), granuloma of the liver, and extrahepatic portal vein obstruction. The results were compared with those obtained from 10 control subjects. Patients with cirrhosis and infectious hepatitis revealed normal bilirubin transferase levels, whereas those with Gilbert's disease showed significantly low enzyme levels. Many patients with NCPF, some with extrahepatic portal vein obstruction, and patients with granulomatous involvement of the liver demonstrated significantly low levels. This low hepatitic-enzyme activity was not associated with hyperbilirubinemia. The mechanism of such low values in NCPF and other disorders is not known. It is postulated that low heaptic-enzyme activity in noncirrhotic portal fibrosis is due to sparse smooth endoplasmic reticulum. This study also emphasizes that serum bilirubin may remain normal with very low hepatic-enzyme activity. Although induction of the microsomal enzyme bilirubin transferase was observed following phenobarbitone administration in noncirrhotic portal fibrosis, this was not apparent in patients with cirrhosis, possibly due to maximal enzyme induction having been achieved by endogenous substrate.

Adult↗
PubMed1975

Impaired hepatic release of triglycerides: a possible cause of acute alcoholic fatty liver in the Rhesus monkey.

1. The mechanism of development of acute alcoholic fatty liver in the Rhesus monkey was investigated by studying the effect of Triton WR-1339 on plasma triglycerides. 2. After ethanol infusion, the rise in plasma triglyceride produced by Triton was greatly reduced and there was an accumulation of triglyceride in the liver. 3. Thus findings suggest that acute alcoholic fatty liver in Rhesus monkeys is probably due to a defect in the release of triglyceride from the liver.

Alcoholism↗
PubMed1975

Portal hypertension in chronic leukaemia.

Portal haemodynamic studies were carried out in 11 subjects, seven with chronic myeloid leukaemia and four with chronic lymphatic leukaemia, and results compared with those obtained in five patients with 'idiopathic' splenomegaly and with control subjects. All 11 patients with chronic leukaemia had intrasplenic pressures above 11 mmHg and of these four had pressures above 20 mmHg. Portosystemic collaterals were seen on splenovenography in four of these patients. Hepatic vein wedge pressure was above 7 mmHg in nine patients and these high levels were a result of increased free hepatic vein pressure. The corrected sinusoidal pressure and post sinusoidal resistance were essentially normal in all patients. Evidence of increased pre-sinusoidal resistance was seen in six patients. Estimated hepatic blood flow above 1500 ml/min was seen in six patients and all had evidence of histological portal or sinusoidal infilatration. Patients with 'idiopathic' splenomegaly regardless of increased liver blood flow did not have a significant increase in intrasplenic pressure and no alteration in other haemodynamic parameters. It appears that increased liver blood flow alone in a normal liver can only minimally elevate intrasplenic pressure but can play a significant part in the pathogenesis of portal hypertension when liver structure is altered.

Chronic Disease↗
PubMed1974

Thoracic duct and hepatic lymph in idiopathic portal hypertension.

Lymph dynamics in idiopathic portal hypertension has been studied in two phases. In the first phase thoracic duct lymph transport was studied in 11 patients with idiopathic portal hypertension by cannulating the duct. This revealed altered lymph transport in the form of a distended thoracic duct, raised pressure in the duct, and haemorrhagic lymph with an increased flow rate. The lymph flow rate was analysed in relation to various hepatic haemodynamic and biochemical parameters. In the second phase of the study hepatic lymphatics were studied by percutaneous hepatography in 16 patients with idiopathic portal hypertension. By this technique hepatic lymphatics were opacified in patients with idiopathic portal hypertension and cirrhosis with equal frequency. The significance of this finding in relation to the altered hepatic haemodynamics and thoracic duct lymph transport is discussed.

Humans↗