Search PubMed⌕ Search

Biomedical subjects

D V Datta

Publications and source records attributed to D V Datta.

At least 37 records · Page 2Linked to original sources
PubMed1980

Role of porta systemic shunt and hepatocellular damage in the genesis of hepatic neuropathy.

A study was undertaken to evaluate the relative role of porta-systemic shunts and hepatocellular damage in the genesis of neuropathy in chronic liver disease. Two of the 14 patients with non-alcoholic cirrhosis showed clinical evidence of neuropathy, whereas none of the patients with idiopathic portal fibrosis had evidence of neuropathy clinically. Decreased motor conduction velocities were present in some cases of idiopathic portal fibrosis as well as non-alcoholic cirrhosis. Subclinical evidence of histopathological neuropathy in the form of segmental demyelination and remyelination as well as myelin fiber loss was seen in 10 out of 11 sural nerves studied in idiopathic portal fibrosis group and in all the 10 patients in the non-alcoholic cirrhosis group. No correlation was found between histological features and various parameters studied. It is postulated that the development of clinical or subclinical neuropathy in chronic liver disease depends on two factors, being collateral shunting and hepatocellular damage or both and probably related to abnormalities of nitrogen metabolism.

Adult↗
PubMed1980

Alveolar hydatid disease of the liver with Budd-Chiari syndrome.

Alveolar hydatid disease in man is the intermediate stage in the life cycle of the tapeworm Echinococcus multilocularis. This is a rare disease restricted to very few areas of the world. The occurrence of this disease in India is now described for (so far as the authors are aware) the first time. Some unusual features of the disease are highlighted in this patient. The hepatic lesion had infiltrated into the right atrial wall resembling an atrial tumour. The ostium of the inferior vena cava was occluded, causing Budd-Chiari syndrome. The radiological and haemodynamic study of the hepatic outflow tract in this disease are documented.

Adult↗
PubMed1980

Renal immune complexes in viral hepatitis.

Twenty-two patients dying of acute viral hepatitis were studied for the presence of renal immune complexes using direct immunofluorescence. A detailed light microscopic study of liver, kidney and other organs was also done and sera scanned for the presence of HBsAg. Results of light microscopy indicate that thirteen of twenty-two patients showed mild to moderate glomerular abnormalities. Immunofluorescence was positive in fifteen of twenty-two patients. IgA being positive in 28%. The incidence of HBsAg was low. It is suggested that both B and non-B type of hepatitis viruses are associated with a high incidence of renal immune complexes along with morphological alterations in the glomerulus.

Acute Disease↗
PubMed1980

Hydatid disease associated with hepatic outflow tract obstruction.

Three unusual cases of hydatid disease associated with hepatic outflow tract obstruction are presented. One had Echinococcus multilocularis infection with complete obstruction of the inferior vena cava and the other two had E. granulosus infection with complete obstruction of the hepatic vein. The initial two were unsuspected clinically. The cases suggest that both outflow obstruction and hydatid disease may often be unrecognized. A high index of suspicion and appropriate investigation are essential for diagnosis and proper management.

Adult↗
PubMed1979

Amebic liver abscess with hemobilia.

A patient with hemobilia complicating an amebic liver abscess is described. The diagnosis was based on selective arteriography. The hemobilia did not stop with antiamebic treatment or ligation of the right hepatic artery. Successful results followed right hemihepatectomy.

Adult↗
PubMed1979

Kala-azar in north-western India: a study of 24 patients.

Twenty-four sporadic cases of kala-azar diagnosed over an 11-year period in a referral medical centre in north-western India are reported. Most of the patients were residents of non-endemic areas or where endemicity was low. Certain unusual clinical and laboratory features were seen in some of the cases, namely, lymphadenopathy, nasopharyngeal growth, acute and chronic hepatic involvement and portal hypertension. Awareness of the occurrence of the disease and of its protean modes of presentation was found to be an important factor in early diagnosis.

Adolescent↗
PubMed1979

The pathology and pathogenesis of fatal hepatic amoebiasis--A study based on 79 autopsy cases.

The present study is based on a retrospective analysis of 79 autopsy cases of hepatic amoebiasis. An attempt has been made to reconstruct the sequence of events starting from intestinal infection to invasion and transport of amoebae along the radicles of the portal veins, the formation of early Zahn's infarct and the proliferation of amoebae in such foci leading to the formation of small abscesses. The coalescence of small abscesses gives rise to the apparently large abscesses. Apart from direct contiguity, more distant extension leading to a satellite abscess is due to involvement of the hepatic and/or portal venous radicles. It seems that obstruction of the hepatic vein contributes substantially towards the enlargement of the liver and its exaggerated nutmeg appearance. Signs and symptoms of hepatic vein obstruction sometimes overshadow the abscess pathology. Thrombosis or pressure of a neighbouring abscess over the portal vein obstruction sometimes overshadow the abscess pathology. Thrombosis or pressure of a neighbouring abscess over the portal vein and bile-duct lead to development of portal hypertension and jaundice. Both cell-mediated and humoral immunity are depressed in fatal cases of hepatic amoebiasis.

Budd-Chiari Syndrome↗
PubMed1979

Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India.

Estimates were made of the arsenic concentration in liver specimens from nine patients having idiopathic portal hypertension (IP), and in four livers these were found to be significantly higher than those in patients with cirrhosis and in control subjects. The splenovenogram revealed extensive portosystemic collateral circulation. Corrected sinusoidal pressure and blood flow studies showed higher levels in four patients than in normal subjects. Microscopic examination of liver tissues revealed periportal fibrosis. The higher hepatic arsenic levels that were found were due to the inadvertent drinking of water contaminated with arsenic, adulterated opium, and indigenous medicines. A history of opium intake was not forthcoming but two patients had drunk water contaminated with arsenic and two others had taken bhasams (Ayurvedic medicines prepared by repeated oxidation of ores). Though the aetiology of idiopathic portal hypertension is not known, it is possible that arsenic intake may be one of the factors.

Adolescent↗
PubMed1979

Canidida infection of the upper gastrointestinal tract superadded upon chemical injury with acids.

Two male patients, who presented with Candida albicans infection of the upper gastrointestinal tract, superadded over local mucosal injury due to corrosive chemical agents and chronic alcoholism have been described. Such an association of prior local injury with this type of fungal infection has not been hitherto documented. One of these patients had a gastric antral stricture due to ingestion of concentrated sulfuric acid and Candida esophagitis, whereas the other had severe erosive gastritis and Candida gastritis following ingestion of thiocyanates.

Adult↗