SUMMARY 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.Idiopathic portal hypertension (IP) has recently been recognised as a new entity (Ramalingaswami et al., 1962;Boyer et al., 1967;Basu Mallik et al., 1967;Sama et al., 1971;Datta, 1975;Datta, 1976a). In this condition haematemesis and splenic enlargement are common features, and solenovenographic studies reveal collaterals in 80% of cases. The aetiology of the syndrome is unknown and it has been suggested that there may be several causes (Datta, 1975;Mahajan and Datta, 1976 Received for publication 27 February 1979
Methods
SUBJECTSThe livers of nine patients with idiopathic portal hypertension (IP) and seven with cirrhosis were investigated for their content of arsenic. A piece of liver (about 2 g) was obtained by wedge biopsy at laparotomy in six patients and the same quantity from necropsy in three patients. The gross and microscopic examination of 18 patients who showed no evidence of hepatic disease and who died from non-hepatic causes served as controls in our studies.Nine liver tissues were obtained from newborn infants. In addition, 105 livers were obtained through
SUMMARY Clinical features of obstruction of the intrahepatic portion of the inferior vena cava were observed in five out of the 11 patients with the Budd-Chiari syndrome seen during the last four years. These patients apparently formed a distinct group from the remaining six and resembled in clinical course, biochemical features, haemodynamic findings, and radiological investigations the patients described as cases of membranous obliteration of the intrahepatic portion of the inferior vena cava. The present study reports five such patients diagnosed with the help of venous catheterization, percutaneous hepatography, and haemodynamic studies. The value of distinguishing these patients from those with obstruction due to hepatic vein occlusion is highlighted because of the difference in the prognosis and treatment.
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.
Summary
Six cases are described of veno-occlusive disease (VOD) after medicinal herb ingestion. The herb Heliotropium eichwaldii, taken by three patients, was found to contain the toxic pyrrolizidine alkaloid, heliotrine. Two patients presented with fulminant hepatic failure while the other four patients had a clinical picture suggestive of decompensated cirrhosis. The medical use of this herb may possibly be responsible for a significant proportion of acute and chronic liver disease in India, making it of public health importance.
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