Hepatic, renal and other system abnormalities in patients with lepromatous leprosy in Nigeria.
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Biomedical subjects
Publications and source records attributed to S R Bhusnurmath.
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An experimental model of hepatic amoebiasis in guinea-pigs, simulating the natural infection in man, induced by progesterone following intracaecal inoculation of Entamoeba histolytica has been developed. On Day 3 after infection, 60% of the animals developed amoebic liver abscess, but on Days 7, 11, 15, 20 and 35 after infection liver involvement was recorded in all the animals. No animal in the control group developed hepatic amoebiasis. Severity and frequency of caecal lesions was greater in the control groups than in the experimental group receiving progesterone injections. The antiamoebic antibody levels were slightly higher in the experimental group as compared to the control group.
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Four cases of E. histolytica infection of the brain among 80 cases of hepatic amebiasis collected over a period of 18 years are reported. The patients were males aged 2, 30, 40 and 50 years. Three cases presented with chest and neurological manifestations. Intestinal and hepatic lesions were present in all and lung lesions in three cases. The cases with neurological manifestations showed extensive, almost confluent lesions in the brain. It is proposed that the condition should be called "Secondary cerebral amebiasis".
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Morphological changes of the liver were studied in 24 autopsy cases of noncirrhotic portal hypertension of unknown etiology (idiopathic portal hypertension, IPH), and in 123 surgical biopsies from such patients. For comparison, 15 whole-cut liver slices from autopsy cases of noncirrhotic portal fibrosis (NCPF) from India were also studied. Liver pathology was very similar in IPH and NCPF, characterized by phlebosclerotic changes and perivascular fibrosis of the portal vein system, and parenchymal atrophy perhaps secondary to portal circulatory insufficiency. The distribution of lesions was uneven, and despite marked fibrosis and occasional surface nodularity, there was no diffuse pseudonodule formation in the parenchyma. Surgical specimens showed similar changes except for more frequent portal cellular infiltrates, but the changes seen in one biopsy specimen were limited and not always diagnostic. It seems that IPH of Japan and NCPF of India are the same disease, and perhaps hepatoportal sclerosis elsewhere is also the same disease.
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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.
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.
A wide spectrum of clinical and morphologic changes in 32 autopsy cases of noncirrhotic portal fibrosis have been described. The disease frequently occurs in younger patients with a long history of splenomegaly, usually with a history of hematemesis. Females are affected almost equally as often as males in contrast to cirrhosis. The patients tolerate the bleeding episodes well. Death is usually due to massive hemorrhage. The diagnosis is achieved through a process of exclusion. A critical analysis of hemodynamic data, a splenoportogram, liver function tests (particularly Bromsulphalein retention) and angiographic data is mandatory. Needle biopsy of the liver appears to have limited value in making the diagnosis. The gross anatomic findings vary from a nearly normal liver to gross nodularity, seen particularly on the posteroinferior surface. In some cases these nodules are seen to physically impede the portal blood flow and contribute to portal hypertension. Phlebosclerosis of the smaller radicles of the portal vein and irregular scarring are the outstanding morphologic features of the disease. These changes are usually associated with irregular dilatation of some of the larger intrahepatic branches of the portal vein as well as fibroelastosis with or without occluding or organizing thrombi in both intra- and extrahepatic branches of the portal vein. The changes in hepatic venous radicles are characterized by irregular sclerosis, which seems to contribute significantly toward postsinusoidal block in advanced cases. The probable mode of evolution is discussed.
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The occurrence of Echinococcus multilocularis is reported in India for the first time. The patient was a young man, various clinical diagnoses were made and he finally died after an attempted membranotomy for suspected membranous obstruction in the inferior vena cava. Autopsy revealed classical E. multilocularis infection of the liver with direct spread of the inferior vena cava, the right atrium and through the diaphragm into the base of the left lung. It also had caused an outflow tract obstruction to the hepatic venous flow by direct physical pressure distorting the proximal intrahepatic portion of the inferior vena cava. In addition the patient had multi-valvular lesions of rheumatic origin and a terminal infective endocarditis due to staphyloccal infection.
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A patient with documented typhoid fever had several uncommon manifestations. These included (1) haematemesis as the presenting feature, (2) hepatocellular jaundice with hepatic encephalopathy, (3) acute intravascular haemolysis and (4) probable disseminated intravascular coagulation. Haematemesis as the presenting feature in typhoid fever has not been reported previously.
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