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

Parts of Western India have experienced an outbreak of hepatitis affecting man and dogs and characterised by jaundice, rapidly developing ascites, portal hypertension, and a high mortality-rate. The disease was associated with the consumption of maize contaminated heavily with Aspergillus flavus. Analysis of contaminated samples showed that affected people could have consumed between 2 and 6 mg. of aflatoxin daily over a period of a month. A specimen of liver obtained at necropsy showed bileduct proliferation and giant cells. The disease appears to be a result of aflatoxicosis.
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PMID:Hepatitis due to aflatoxicosis. An outbreak in Western India. 4 30

Over a period of 18 months the development of hepatitis after intake of oxyphenisatin, a laxative, was established in 14 patients by re-exposure to the drug. The characteristic feature was nonspecific upper abdominal pain up to colic-like pain, lact of appetite, nausea or vomiting, and pruritus. The biochemical changes were those of chronic hepatitis with varying severity of biliary stasis and abnormal immunofluorescence. On re-exposure there was a particularly remarkable rise in GLDH activity. The histological picture showed acute inflammatory changes in the biliary passages on re-exposure, while the liver cells were clearly involved only secondarily. At a latter point the histological picture became non-specific. At laparoscopy there were different stages of minor periportal hepatic fibrosis to marked postnecrotic liver scars with portal hypertension and decompensation. Early diagnosis is difficult but crucial to the patient's fate, because this form of hepatitis regresses completely after oxyphenisatin has been stopped. Laxatives containing this drug should be withdrawn from the market.
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PMID:[Oxyphenisatin-induced liver disease (author's transl)]. 12 99

This paper gives, in detail, the causes of either liver disease or hepatomegaly in 100 patients, mostly adults, admitted to the medical wards of Angau Memorial Hospital, Lae, during 1968 and 1969. The major findings included liver cell carcinoma, cirrhosis (often with chronic active hepatitis), tropical splenomegaly, pericholangitis and hepatitis. There were 27 with miscellaneous findings including ten with normal, or almost normal, livers despite the definite enlargement. Patients with liver cell carcinoma presented late in the course of their illness and had a poor prognosis. Others, with pericholangitis, had clinical features of portal hypertension indistinguishable from that complicated cirrhosis. There was an unexpected number with chronic active hepatitis and a liver biopsy is essential for such a diagnosis. Hepatic sinusoidal lymphocytosis is almost invariably found in patients with TS but may occasionally be found in those with a non-palpable spleen. Patients with right heart failure of chronic respiratory disease, and jaundice of acute pneumonia were excluded from the study.
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PMID:Liver disease in Papua New Guinea. 19 19

In many cases so called neonatal hepatitis of unknown origin nowadays is recognized as a manifestation of alpha1-antitrypsin deficiency. Out of 12 patients with Pi-type ZZ, 5 were diagnosed because of cholestatic jaundice, 2 because of hepato-splenomegaly in the first trimenon, and 3 by family examination. We believe that the affection may be due to a perinataly acquired cytomegalic inclusion disease in one case, in another to a congenital rubella infection. The latter child died at the age of one year because of an esophageal hemorrhage. Over a mean observation time of 3 years the other patients are doing well and show no signs of portal hypertension. The very different course of the hepatopathy is demonstrated. Common bacteria or toxins which do not usually lead to an illness may be realisation factors just as "classical" causes of hepatitis. Up to now it is not known how these factors influence the course of alpha-antitrypsin deficiency.
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PMID:[alpha1-antitrypsin deficiency. Clinical and morphological aspects during childhood (author's transl)]. 21 96

Portal hypertension and variceal hemorrhage may be found in the renal transplant patient with chronic liver disease. The development of portal hypertension was found to occur after long-term graft survival without significant rejection. The development of positive cytomegalic virus and negative hepatitis-associated antigen appeared to be common. Splenomegaly and prominent venous collateral were the most frequent physical findings, while ascites and hepatomegaly were less frequent. Portasystemic decompression can be performed successfully, however, the mortality and morbidity appear to be higher for this group than for other cirrhotic patients with comparable hepatic reserve.
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PMID:Portal hypertension following renal transplantation. 35 15

The course and possible risks of pregnancy in 7 women between the ages of 20 and 30 yr with chronic-persistent hepatitis (CPH) were evaluated. Ten pregnancies occurred in these women during the follow-up period which ranged from 3 to 8 yr. Four of the fetuses were aborted electively for nonmedical reasons. The other six pregnancies resulted in normal spontaneous vaginal deliveries at term. Each of the women experienced uneventful pre- and postnatal courses, and the neonates were all healthy and developmentally normal at birth. There was no biochemical or clinical evidence to suggest worsening liver disease during pregnancy. Normal menstrual patterns when not pregnant and normal biphasic basal body temperature patterns in 4 women suggested that ovulation and fertility were not impaired significantly. Pregnancy in women with CPH appears safe to both mother and fetus alike. This finding contrasts with the morbidity and mortality some authors have found to be associated with cirrhosis and with portal hypertension. We speculate that our findings may be relevant to women with other portal lesions resembling CPH such as resolving acute hepatitis and chronic active hepatitis in sustained remission.
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PMID:Chronic-persistent hepatitis and pregnancy. 45 47

Oral glucose tolerance tests (100 g glucose) and the intravenous tolbutamide test were carried out. The glucose tolerance was seen to be disordered even in acute infectious hepatitis, but returning to normal when cured. If chronic hepatitis develops, however, the proportion of manifest diabetes increases to 7.2% in chronic persistent hepatitis and to 16.3% in chronic progressive hepatitis, while 30% each have latent diabetes. The glucose tolerance is most impaired in fatty liver (stage III) and in active cirrhosis of the liver with portal hypertension, where more than half of all patients present manifest or latent diabetes. Conversely, glucose tolerance improves even in chronic hepatitis and in cirrhosis of the liver as the inflammatory activity subsides. The main cause for the development of "liver diabetes" is therefore likely to be the activity of the inflammatory process, the extent of portal hypertension, disorders of glucose regulation in the liver and the increased insulin inactivation in the cirrhotic liver.
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PMID:[Disorders of glucose tolerance in 2600 histologically confirmed acute and chronic liver patients (author's transl)]. 81 Jun 95

This review deals with the clinically important aspects of etiology and symptoms of cirrhosis. Apart from alcohol and hepatitis, which are the most frequent etiological factors, also rare causes of cirrhosis are described, because their knowledge is important for the differential diagnosis of cryptogenic cirrhosis. Portal hypertension is the root of most symptoms and complications in cirrhosis. Therefore, a description of the haemodynamic changes precedes the extrahepatic syndromes, of which renal failures, ascites and portal encephalopathy are discussed more in detail.
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PMID:[Etiology and clinical aspects of liver cirrhosis]. 85 88

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.
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PMID:[Therapy of hepatic insufficiency]. 91 52

Besides lymphodenopathy and splenomegaly, hepatomegaly may also be detected in 25-50% of children with juvenile rheumatoid arthritis. This is particularly evident in patients with complete Still's syndrome. The hepatomegaly increases during relapse situations and disappears during remissions. Transient icterus, elevation of aminotransferases and delayed bromsulfalein excretion have been reported, particularly in patients with complete Still's syndrome, and indicate impairment of liver function. Liver biopsies have been performed only rarely and show nonspecific infiltrations of portal fields with lymphocytes and, in a few cases, "autoimmune" hepatitis and even cirrhosis with portal hypertension. Plasma cell hepatitis with affection of joints can be readily differentiated from juvenile rheumatoid arthritis: the synovitis is merely transiet and disappears with institution of steroid therapy. As in the adult, severe liver dysfunction leads to remission of arthritis. Amyloidosis should be considered in every case of long-lasting hepatomegaly.
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PMID:[Liver pathology in juvenile chronic polyarthritis]. 91 83


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