Blood counts in portal hypertension of non-cirrhotic origin: correlation with splenic size and splenic pulp pressure.
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Biomedical subjects
Publications and source records attributed to D V Datta.
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An attempt has been made to investigate drug elimination in patients with liver disease. Antipyrine was chosen as a model drug. The patients were divided into three groups depending upon clinical, biochemical, radiologic and histologic findings; (1) mild (Idiopathic portal hypertension, extrahepatic portal vein obstruction and Gilbert's syndrome); (2) moderate (Budd-Chiari syndrome and amoebic liver abscess); (3) severe (acute hepatitis, chronic active hepatitis and cirrhosis). A prolongation in antipyrine half-life (t1/2) was observed in 108 patients with liver disease (24.59 +/- 1.72 h) as compared to 12 controls (11.63 +/- 0.86 h). Similarly, metabolic clearance rate was decreased in all liver disorders. Among liver function tests, antipyrine t1/2 showed a significant correlation with serum albumin and prothrombin time index. After phenobarbitone administration, antipyrine clearance studied in 37 patients showed a significant decrease in t1/2 and an increase in MCR. Antipyrine t1/2 in 26 patients after recovery was comparable to those of controls.
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.
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.
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.
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.
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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.
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In a series of 19 patients with Budd-Chiari syndrome, transhepatic venography and inferior vena cavography were used to localize the site of hepatic outflow obstruction. Classification into two types was made on the basis of the site of obstruction. Four cases were grouped as type I, in which obstruction was localized in the hepatic vein alone, and the inferior vena cava (IVC) was patent. Fifteen cases were of type II, in which there was a well-defined obstruction in the intrahepatic portion of the IVC or ostium of a hepatic vein. This study highlights the frequent occurrence of IVC obstruction as a cause of chronic Budd-Chiari syndrome in northern India and the utility of transhepatic venography in its diagnosis.
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.
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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