Budd-Chiari syndrome following pregnancy. Report of 16 cases, with roentgenologic, hemodynamic and histologic studies of the hepatic outflow tract.

Budd-Chiari syndrome following pregnancy is an extremely rare disease as reported in the literature. Reported here are 16 such cases in a total of 105 patients with Budd-Chiari syndrome seen at Postgraduate Institute of Medical Education and Research, Chandigarh, from 1963 to 1978. The clinical pointer to the diagnosis was sudden occurrence of abdominal pain and ascites following childbirth. Eleven patients had diuretic-resistant ascites. Percutaneous hepatography was valuable in detecting the site and the nature of the outflow block. The prognosis was uniformly bad, and eight patients died within one year from the onset of their illness. The various treatment schedules, including anticoagulant therapy, Rhodiascit ascitic fluid re-infusion and portasystemic shunt surgery, had no beneficial effect on the survival of these patients.

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.

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.

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.

Levels of arsenic in liver cirrhosis.

The present studies were conducted to determine the arsenic levels in liver specimens obtained at autopsy from human subjects suffering from liver cirrhosis. Arsenic content was determined using the neutron activation analysis technique. Increased levels of arsenic were found in cirrhotic liver samples including alcoholic cirrhosis. Various surveys were conducted in different places to find the cause for high arsenic in patients with alcoholic cirrhosis. It was found that patients were consuming 'home-made brew' which was contaminated with arsenic. The study suggests that elevated levels of arsenic may be associated with liver damage in cirrhotic patients.

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.

Extrahepatic portal hypertension: a review of 70 cases.

Among 70 children with extrahepatic portal hypertension, more than 350 episodes of bleeding occurred. Of the 32 children who were not operated upon, six (19%) died of bleeding. Twelve children in the nonoperated group are thriving and well, although six of them have rebled 1-2 times. The operated group of 38 children had a total of 43 procedures. Central splenorenal and cavomesenteric anastomosis prevented further bleeding in 10 of 12 cases in which follow-up is available. Operative mortality was 24%, the majority of which were in emergency procedures.

Impairment of hepatic drug metabolism in patients with acute viral hepatitis.

Hepatic drug metabolism in patients with acute viral hepatitis was investigated under different conditions: pregnancy, postpartum, non-pregnancy, and among males. Liver function tests were altered in all of these conditions. The relationship between in vivo and in vitro drug metabolism was studied in twenty-two patients using diagnostic liver needle biopsies by comparing the drug metabolising enzymes (aminopyrine-N-demethylase and bilirubin-UDP-glucuronyl transferase) in these biopsies with the elimination kinetics of antipyrine. Drug clearance tests were repeated in the patients who had recovered. All patients gave altered liver function tests results. Antipyrine half-life was significantly higher in females as compared to males. Among females, it was maximum in the pregnant group. Activities of drug metabolising enzymes were found to be significantly lower in liver biopsy material. The half-life of antipyrine showed a significant correlation with drug metabolising enzymes. After recovery patients showed a normal antipyrine half-life.