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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Light and electron microscopy study of fourteen liver biopsies in typhoid fever disclosed a mild hepatitis in which there is marked reticulo-endothelial hyperplasia, with many lymphoid cells in the hepatic sinusoids. The hepatic cell lesion was non specific, manifested by reticulum endoplasmic dilatation, mitochondrial alteration and biliary canaliculus injury. Such findings were particularly evident in the jaundiced patients. Jaundice was, in our series, a more frequent complication of acute typhoid fever than commonly reported. Usually it is of short duration and the serum bilirubin was not markedly elevated. However, there were instances when the jaundice was so accentuated as to lead the clinician to a first diagnosis of virus hepatitis or leptospirosis. The pathogenesis of the intrahepatic cholestasis in typhoid fever is still obscure, but apparently it is, as has been described in other infectious diseases, due to an injury of the bile secretory apparatus brought out by the bacillary endotoxin.
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PMID:Jaundice in typhoid hepatitis: a light and electron microscopy study based on liver biopsies. 60 18

In a series of 212 liver biopsies which had been subjected to ultrastructural examination, the picture of cholestasis was encountered in 60 cases. In 32 cases it was associated with subhepatal obtruction. The reminder included hepatitis, hepatic fibrosis and cirrhosis and other diseases. Experiments in rats showed that the main findings following the ligature of choledochus included oedema and disintegration of mucosal microvilli in the bile ducts. Such changes preceded those of the hepatocytes. Simple overload by parenteral bilirubin did not evoke comparable changes. Therefore the mechanical disturbance of the epithelial wall of the bile ducts has been regarded as the basic changes subjected to later secondary modifications.
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PMID:[Hepatic cholestasis]. 61 36

The concentration of individual bile acids in serum was measured in 18 neonates and infants with various cholestatic conditions (extrahepatic biliary atresia, neonatal hepatitis syndrome, chronic intrahepatic cholestasis and posthemolytic cholestasis). The cholate/chenodeoxycholate ratio in serum was smaller than one in all patients with neonatal hepatitis syndrome or extrahepatic biliary atresia, cholestatic conditions which were accompanied by signs of liver cell injury. It was greater than one in the patients with chronic intrahepatic cholestasis. Administration of cholestyramine to patients with patent extrahepatic bile ducts decreased the total concentration bile acids in serum and elevated the cholate/chenodeoxycholate ratio. Thus, cholestyramine administration may be of diagnostic value for evaluation of bile duct patency in cholestasis of infancy. Differences between the bile acid pattern in serum and bile were observed. Thus, the cholate/chenodeoxycholate ratio was always higher in bile than in serum. 3beta-hydroxy-5-cholenoic acid found in serum was not detectable in bile. This finding suggests that impairment of biliary excretion rather than increased hepatic synthesis is responsible for elevation of this monohydroxy bile acid in serum.
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PMID:Bile acids in serum and bile of infants with cholestatic syndromes. 61 61

85 women, 16-43 years of age, were studied for liver damage caused by oral contraceptive (o.c.) use. Laboratory tests were performed, and point biopsies were taken in 76 cases. SGPT levels were consistantly higher than SGOT levels. The transaminase levels were normalized after 14 days in 47 cases and after a longer period in 38 cases. Pathological serum bilirubin levels were observed in 15 women; in 5 cases the patients had experienced hepatosis during pregnancy. Non-cholestatic hepatosis was found in 52 patients and cholestatic hepatosis in 9; in most cases the diagnosis was confirmed by the liver biopsy. Hepatosis in conjunction with reactive hepatitis was more frequent among Ovosiston users. Hepatosis with sinusoid ectasia was more frequent among Non-Ovlon users. Fatty liver in conjunction with hepatosis was observed more often among Gravistat and Non-Ovlon users. Hepatosis with reactive hepatitis and non-cholestatic hepatosis with sinusoid ectasia or fatty liver were associated with elevated transaminase levels. After laboratory test levels were normalized, 50 patients were reintroduced to o.c. use with frequent control check-ups. In those cases where o.c. use could be continued, liver damage was found to have been caused mainly by o.c. use in conjunction with other medications, e.g. analgesics, sedatives, or laxatives. Patients with cholestatic hepatosis redeveloped cholestasis after reintroduction to o.c. use. Blood tests are best taken after reintroduction to o.c. use at the end of the pill-taking period. SGPT tests should be taken at the end of the 2nd cycle of o.c. use and twice a year therafter to determine the effect of o.c.s on the liver.
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PMID:[Liver lesions caused by oral contraceptives. I. Contraceptive-induced hepatosis in 85 women: recommendations for diagnosis and prophylaxis]. 66 3

Cholestasis has been previously described after long-term hyperalimentation in infants. The present case documents the development of cholestasis in an adult after a relatively short period of total parenteral nutrition (TPN), i.e., hyperalimentation. Other causes for cholestasis, such as exogenous or endogenous hepatotoxic agents or allergic type hepatitis, do not offer an adequate explanation for the changes observed in this patient. The changes observed are consistent with the hypothesis that a taurine deficiency would interfere with bile salt conjugation and form a block at the cellular level.
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PMID:Cholestasis in association with short-term parenteral alimentation. 83 73

An epidemic of jaundice probably due to toxic hepatitis occurred in three adjoining districts of Northwest India during the period November and December, 1974. The dogs of the villages were affected first, then the human beings. Detailed clinical features, appropriate laboratory tests, and liver biopsies were studied. A retrospective epidemiological survey was carried out. The disease had a subacute onset starting with high fever, followed by rapidly progressive jaundice. Ascites appeared simultaneously and soon became quite massive. Hepatomegaly was recorded when ascites decreased. Liver function tests suggested cholestatic jaundice. The mortality rate in the hospital was 10%. Clinical features in dogs were similar, but mortality was almost 100%. Liver histology was characterized by (1) edema and collagenization of the central veins, never with thrombosis, (2) cholangiolar proliferation, (3) moderate to severe ballooning of the hepatocytes, (4) perisinusoidal fibrosis, (5) cholestasis, and finally, (6) cirrhosis with reverse lobulation. Etiology of this epidemic of hepatitis could not be unequivocally established. Critical analysis of the data suggests that some food toxin may have been a factor in the outbreak of this unusual epidemic of toxic hepatitis.
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PMID:Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India. 83 97

Hepatocellular diseases, such as hepatitis, cirrhosis, or hepatic neoplasm, are associated with impaired metabolism of certain drugs, including aminopyrine, whereas cholestasis produced variable effects on aminopyrine metabolism. Reasons for the variable effects of cholestasis on hepatic aminopyrine metabolism were sought by performing in patients with hyperbilirubinemia the aminopyrine breath test (ABT), which consists of measurements of 14CO2 in breath 2 hr after oral administration of [14C]aminopyrine. Hyperbilirubinemia (total serum bilirubin less than 1.2 mg/100 ml) in these patients was due to hepatocellular disease or cholestasis. The ABT, defined as the percentage of the administered dose of 14C excreted in breath for 2 hr after [14C]aminopyrine administration, was 6.2 +/- 0.8% (mean +/- SD) in 107 control patients with normal total serum bilirubin. The ABT was severely abnormal (less than 3.1%) in 54 of 77 hyperbilirubinemic patients (70%) with hepatocellular disease and normal (greater than 4.5%) in only 5 of these patients (6%). In contrast, the ABT was severely abnormal in only 1 of 40 cases of cholestasis with hyperbilirubinemia and normal in 70% of these patients. Thus, aminopyrine metabolism is normal in most cases of hyperbilirubinemia due to cholestasis and is only rarely severely abnormal in these patients. On the other hand, severe abnormality in aminopyrine metabolism occurs in the majority of patients with hyperbilirubinemia due to hepatocellular disease. It therefore appears that the ABT may be useful in hyperbilirubinemia to distinguish patients with hyperbilirubinemia due to cholestasis form most patients with hyperbilirubinemia due to hepatocellular disease.
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PMID:Aminopyrine metabolism in the presence of hyperbilirubinemia due to cholestasis or hepatocellular disease. Combined use of laboratory tests to study disease-induced alterations in drug disposition. 87 Feb 74

Liver biopsy was done at the time of operation in 125 consecutive upper abdominal procedures to assess the incidence of unsuspected or undiagnosed hepatic abnormalities. Specifically excluded were hepatic lesions unexpectedly identified at laparotomy. Sixty-seven percent of the liver biopsy specimens were abnormal, the most frequent findings being fatty metamorphosis, cholestasis, triaditis, fibrosis, inflammatory infiltrate, cholangitis, cirrhosis, and hepatitis. The most frequent operation performed was cholecystectomy. In 63 patients with chronic cholecystitis, there was a 51% incidence of abnormal liver histology, while in nine patients with acute cholecystitis, the incidence was 78%. In 83% of all other operations, abnormal liver biopsy specimens were identified. Bile leakage, hemorrhage, and infection did not occur in this series, despite inclusion of patients with severe biliary obstruction, abnormal clotting factors, and intra-abdominal sepsis. New techniques of histochemical enzyme analysis and electron microscopy are expected to enhance the clinical correlation of occult hepatic lesions. We conclude that liver biopsy in a safe, informative adjunct to all upper abdominal procedures.
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PMID:'Routine' liver biopsy in upper abdominal surgery. 88 45

7 individual cases of hepatocellular damage caused by the use of oral hormonal contraceptives are examined. 3 different morphological patterns of damage were observed: reactive hepatitis, intrahepatic cholestasis, and subacute hepatitis. Discussion of the pathenogenesis of this damage revolves around the theory of competitive effect of sex hormones on the metabolism and transport of bilirubin, the theory of hypersensitivity, and theoretical toxic actions of contraceptive hormones. The reversibility of hepatocellular damage in 3 cases in the form of gestational hepatosis perhaps advocates the theory of hypersensitivity to endogenous and exogenous hormones. 1 case of subacute hepatitis had a lethal outcome, which suggests the possibility of direct toxic effects of hormonal contraceptives.
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PMID:[Types of hepatocellular damage caused by contraceptives]. 90 63

The object of the investigation was to study the capacity of the liver to metabolize drugs under diversified conditions (cirrhosis, hepatitis, cholestasis in alcoholics, in diabetics as well as in eplieptics treated with barbiturates) as well as the possibility of inducing this function. To accomplish this we determined the half-life of Butazolidin. Only in cirrhotics it was shown that the capacity to metabolize Butazolidin was reduced. Induction with barbiturates increased hepatic captation of the drug but did not modify the biotransformation of the same. This is attributed to the development of a "hypoactive hypertrophy" of the reticuloendothelium.
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PMID:[Metabolism of phenylbutazone in the liver (author's transl)]. 95 7


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