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

Two patients who presented with an exudative ascites in the course of typical acute type B hepatitis are reported. In one of them, ascites was associated with an exudative pleural effusion. In both patients, the clinical course of the hepatitis was uneventful, and ascites and pleural effusion disappeared spontaneously. Portal hypertension and common causes of exudative ascites were excluded. It is suggested that the development of exudative ascites in these patients represent a hitherto unrecognized manifestation of the hepatitis itself.
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PMID:Exudative ascites in the course of acute type B hepatitis. 662 16

Previous reports have suggested that idiopathic portal hypertension, a condition quite distinct from tropical splenomegaly syndrome, occurs in Kenya. In the present study patients with oesophageal varices were allocated to diagnostic groups on the basis of liver histology and results of splenoportovenography , and these groups were then compared for prevalence of hepatitis B markers, immunoglobulin levels and results of enzyme-linked immunosorbant assay (ELISA) for S. mansoni infection. 85 patients with oesophageal varices were studied. 29.4% had histological evidence of Schistosoma mansoni infection, 20% had cirrhosis and in 25.9% liver histology was non-diagnostic and the portal vein was radiologically shown to be patent. A comparison of clinical findings, serological data and parasitological investigations suggested that this latter group was a distinct one, and did no result from failure of histological diagnosis of cirrhosis or schistosomiasis. It is likely that these patients had idiopathic portal hypertension. In 82 normal controls, the carrier rate of hepatitis B surface antigen (HBsAg) was 12.2%, 59.8% had antibody to HBsAg (anti-HBs) and 7.3% showed antibody to core antigen (anti-HBc) as the only viral marker. 58.3% of the cirrhotics and 26.7% of patients with probable idiopathic portal hypertension were HbsAg positive. The implications of these results, and limited data on hepatitis Be antigen and antibody are discussed.
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PMID:Portal hypertension in Nairobi, Kenya. 667 49

Magnetic resonance (MR) imaging distinguished hepatitis from fatty liver and cirrhosis in a woman with a history of alcohol abuse. Anatomic and physiologic manifestations of portal hypertension were also demonstrated by MR.
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PMID:Chronic liver disease: evaluation by magnetic resonance. 668 54

Patients with non-A, non-B post-transfusion hepatitis were followed from the onset of their disease until their blood tests normalized, until they died, or until the present time. Of 66 patients, 30 had a spontaneous resolution of their biochemical disease. Ten patients died or were begun on immunosuppressive therapy with transaminases still abnormal. The remaining 26 patients had abnormal transaminase levels when last seen. By actuarial analysis, only 54% of hepatitis patients are predicted to develop s spontaneous biochemical remission within 3 yr. No further resolutions have occurred after that time, Icteric and anicteric acute disease may be equally likely to progress to chronic disease. Initial and follow-up liver biopsy specimens have revealed both chronic persistent and chronic active hepatitis. Two patients showed histologic evidence of cirrhosis, and a third developed a hepatic coagulopathy and sphenomegaly. No other patient to date, however, has veveloped overt evidence of hepatocellular failure or portal hypertension. Thus, non-A, non-B post-transfusion hepatitis frequently results in biochemical evidence of chronic liver disease, and in a few patients cirrhosis may develop slowly and in a clinically inapparent fashion.
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PMID:The long-term course of non-A, non-B post-transfusion hepatitis. 677 6

Between 1975 and 1980, 10 children with acute and 8 children with chronic hepatitis type Non A, NON B (NANB) were seen in our hospital. Parenteral inoculation was probable in 10 cases. Hepatitis NANB was diagnosed in about 11% of all children with acute viral hepatitis who were admitted over this period. Children with parenterally acquired disease were more frequently anicteric and had less pronounced transaminase elevation than "sporadic" cases. An uncomplicated outcome was observed in only three of the ten children. Two patients died from acute liver failure, chronic hepatitis developed in three other children. The 9 children with chronic hepatitis NANB are representing 17% of all patients with chronic hepatitis who were seen in our clinic between 1975 and 1980. In six children with CPH a benign course was observed whereas three children with CAH were severely ill including portal hypertension. Immunosuppressive therapy was tried in two cases without success. In children as well as in adult patients, acute hepatitis NANB apparently has more frequently a prolonged course or progression to chronic liver disease than acute hepatitis of other etiology. It seems that CPH NANB shows a similarly benign course as chronic persistent hepatitis B. CAH NANB in our patients, however, had a poorer prognosis than CAH type B.
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PMID:[Non A, non B-hepatitis in children]. 681 83

Studies of 14 North American Indian children with a familial type of severe neonatal cholestasis are described. Jaundice occurred during the neonatal period in 9 children, but disappeared before the end of the 1st yr. Progressive liver damage was documented by the persistence of high levels of alkaline phosphatase, moderate elevation of transaminases, and severe pruritus. Serum bile acids were constantly elevated (3.0-119.5 microgram/ml). Early portal hypertension and variceal bleeding necessitated portal-systemic shunts in 7 children. By light microscopy, the early stage was characterized by hepatitis with giant-cell transformation and biliary stasis. Later on, portal fibrosis became evident and was followed by cirrhosis. By electron microscopy bile canaliculi appeared slightly dilated with preservation or only partial loss of microvilli. They were surrounded by a prominent pericanalicular filamentous web. Immunofluorescence studies indicated the presence of action-containing microfilaments. This group of children might represent a human model of microfilament dysfunction-induced cholestasis.
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PMID:Severe familial cholestasis in North American Indian children: a clinical model of microfilament dysfunction? 689 6

A renal transplant recipient presented with bleeding esophageal varices. Needle biopsy, later confirmed by operative wedge biopsy, showed slight periportal fibrosis but no cirrhosis or hepatitis. No etiology for his liver disease could be determined and he could not be differentiated from other reported patients with idiopathic noncirrhotic portal hypertension (IPH). His liver biopsy did show massive hepatic iron deposition. He had received about 115 units of blood while on hemodialysis and had taken oral iron supplementation for 8 years. IPH has been associated with toxin exposure, especially arsenic and vinyl chloride. This case suggests that excessive iron deposition may also lead to IPH and the indiscriminate use of iron supplementation in hemodialysis or renal transplant patients should be avoided.
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PMID:Hemosiderosis without cirrhosis: an unusual case of portal hypertension. 700 99

Patients with liver disease have increased morbidity and mortality following general anesthesia and surgery when compared with the general population. The increase in mortality appears to be directly related to the severity of hepatic parenchymal cell failure and to the magnitude and duration of the surgical procedure. The importance of preoperative detection of subclinical liver disease by use of a variety of blood tests has been emphasized. However, with the exception of hepatitis B and non-A non-B hepatitis, a precise diagnosis of the exact cause of liver disease is usually less important to the anesthesiologist than is a full characterization of the severity of hepatic dysfunction. Recognition and understanding of the central metabolic role played by the liver in maintaining carbohydrate, fat, and protein homeostasis can help in predicting and managing abnormalities which may complicate the preoperative, interoperative, and postoperative periods. Liver failure after anesthesia and surgery is treated by the same management principles used for liver failure with acute hepatitis. The incidence of postoperative renal failure may be increased in patients who have severe hyperbilirubinemia and its occurrence should be differentiated from the hepatorenal syndrome. It should be understood that complications of portal hypertension may develop in the absence of overt hepatic parenchymal cell failure and that liver failure may occur without gross evidence of portal hypertension. Either situation must be recognized and treated as far in advance of surgery as possible. In general, elective surgery in the patient with liver disease should be delayed until consequences of hepatic parenchymal cell dysfunction and portal hypertension are optimally corrected.
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PMID:Medical evaluation of the patient with liver disease prior to surgery. 701 90

Chronic liver disease has become a significant complication of the therapy of hemophilia disorders. We describe two patients with hemophilia A and hepatitis B virus hepatitis who progressed to cirrhosis with bleeding esophageal varices. Each underwent distal splenorenal shunt under plasma concentrate therapy without difficulty. One patient died 19 months after operation and unsuspected hepatocellular carcinoma was found at autopsy. These cases illustrate the potential severity of liver disease in hemophilia and the ability to safely perform surgery for portal hypertension if required.
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PMID:Cirrhosis, variceal bleeding, and distal splenorenal shunt in hemophilia A. 712 25

In spite of extensive precausions and antibiotic therapy, pylephlebitis was found in 11 of 200 dead newborns as complicat infection after umbilical vein catherization. All stages from local pylephlebitis to suppurative hepatitis were found. The clinical manifestations are not characteristic and therefore misinterpreted very often. Umbilical vein infection should be taken into account in every newborn child with or after umbilical vein catheterization, even when the umbilicus appears normal, when body temperature is rising, the general condition is turning to the worse, and icterus is increasing. Blood picture and transaminase values might be helpful parameters. Reviewing the literature and reporting a case of fatal portal hypertension, pylephlebitis after umbilical vein catheterization is shown as a possible cause of the pseudo-Banti-syndrome in children.
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PMID:[Pylephlebitis after umbilical vein catheterization (author's transl)]. 736 83


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