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

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.
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PMID:Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens. 21 88

The activities of urea-cycle enzymes were measured in liver biopsies of patients suffering from chronic-persistent hepatitis (CPH), chronic-active hepatitis (CAH) and liver cirrhosis. Most of the activities of urea-cycle enzymes did not differ in the case of CPH as compared to controls. Chronic-active hepatitis and liver cirrhosis are associated with a significant (p less than 0.05) decrease of enzyme activity as compared to normal persons. Most of the urea-cycle enzymes are significantly decreased in patients with CAH in comparison with CPH. No significant differences can be demonstrated in the case of CAH as compared to patients with complete cirrhosis. In conclusion, progression of chronic liver disease is associated with increasing alterations of enzyme activities catalyzing a liver specific metabolic pathway. The decrease of the activities of the key enzymes of the urea cycle (Carbamylphosphate-Synthetase and Arginino-succinate-Synthetase) is nearly identical both in CAH and liver cirhosis, although CAH may be a reversible disease. Therefore, marked alterations in the metabolic pathway of ammonia detoxification seem to preceed the histological manifestation of irreversible liver damage.
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PMID:Activities of urea-cycle enzymes in chronic liver disease. 22 5

Until now, the hepatitis B virus has been thought to play a minor role in the aetiology of chronic liver disease in Australia. This is a report of 21 patients with cirrhosis and/or primary hepatocellular carcinoma with hepatitis B antigenaemia. Primary hepatocellular carcinoma occurred in six patients, five of whom had underlying cirrhosis. The disease occurred mainly in non-Australian born males, and was not often associated with a previous history of hepatitis. The death of 16 patients within 12 months of presentation is in contrast to previous concepts of the benign nature of hepatitis B associated cirrhosis.
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PMID:Emerging patterns of hepatitis B chronic liver disease in Australia. 22 47

The incidence of post-transfusion hepatitis and liver dysfunction is presented in fifty-four patients with classical hemophilia who received episodic and/or prophylactic Factor VIII concentrate. 42.5% had persistent biochemical evidence of liver dysfunction with elevated SGOT and SGPT; 3.8% have persistent (HBs) antigenicity and 90% have (HBsAb) antibodies. The results are the same for those who were treated episodically and received an average of 753 units Factor VIII per week as those treated prophylactically who received an average of 686 Factor VIII units per week. The incidence of clinical and/or subclinical disease is unaffected by the transfusion regimen or the amount of concentrate used. The necessity for close follow is emphasized for determination of chronic liver disease and its further therapy.
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PMID:Liver dysfunction in patients with hemophilia. 26 1

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

Rubella antibody titers were determined pretransplant and then serially posttransplantation in 52 consecutive patients whose renal allografts survived at least three months. Group A patients (18) had antibody titers greater than or equal to 1:128 in the posttransplant period. Group B (24) had intermediate antibody titers that never rose higher than 1:64. Group C (10) consistently had antibody titers less than 1:8. Group A did not differ from groups B and C with respect to age, race, sex, type of transplant, underlying renal disease, or maximum complement fixation antibody titers posttransplant to cytomegalovirus or herpes simplex virus, type 1. Group A did differ from groups B and C in its frequency of hepatitis, chronic liver disease, episodes of late rejection (greater than or equal to 21 days after transplant), transplant nephrectomy required for rejection, infections whose defense involves intact cell-mediated immunity, and the number of late rejection episodes per patient. Mechanisms underlying these associations are not known but apparently are not related to HLA phenotype.
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PMID:Rubella antibodies and adverse events late after renal transplantation. 36 6

A solid-phase enzyme linked immunosorbent assay was developed for the detection of immunoglobulin M antibody to hepatitis A virus. The system was capable of detecting hepatitis A-specific immunoglobulin M in a single dilution of serum and appears to be a reliable and rapid means of establishing a diagnosis of hepatitis A infection. Specific immunoglobulin M was only detected in patients with serologically confirmed hepatitis A and not in patients with other forms of hepatitis, chronic liver disease, or autoimmune disease. In patients with hepatitis A, specific immunoglobulin M was usually detectable for 6 weeks after the onset of dark urine, and the longest period for which it was present in any patient was 115 days. This enzyme-linked immunosorbent assay is rapid, simple to perform, and does not require complicated equipment. Provided adequate supplies of purified reagents can be obtained, this enzyme-linked immunosorbent assay procedure is likely to simplify hepatitis A serology, because the same antibody-coated plates can be utilized to detect hepatitis A virus, anti-hepatitis A virus, and hepatitis A-specific immunoglobulin M.
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PMID:Solid-phase enzyme-linked immunosorbent assay for detection of hepatitis A-specific immunoglobulin M. 37 36

Two patients with histologically verified acute hepatitis but without any serological evidence of hepatitis A or hepatitis B infection are described. In both cases the acute attack of hepatitis type 'non-A, non-B' progressed histologically and clinically to chronic active hepatitis within a two-year period. One of the patients died from liver insufficiency a year later, while the other is still alive after eight years of follow-up. The two cases illustrate that a progression of acute hepatitis 'non-A, non-B' to chronic liver disease may occur just as has been reported for hepatitis B infection.
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PMID:Progression of hepatitis non-A, non-B to chronic active hepatitis: a histological follow-up of two cases. 44 68

Twenty-six of 388 patients (6.7%) followed prospectively after open-heart surgery developed non-A, non-B hepatitis. Of these 26, 12 had an elevated (often fluctuating) serum alanine aminotransferase (SGPT) for greater than 1 year. Liver biopsy, done in eight of 12, showed chronic active hepatitis in six and chronic persistent hepatitis in two; one patient with chronic active hepatitis had early cirrhosis. Anicteric patients with peak SGPT greater then 300 IU/L were at greatest risk of developing chronic hepatitis. Chronic non-A, non-B hepatitis was symptomatically mild and unaccompanied by physical signs or laboratory evidence of autoimmune disease or severe chronic liver disease. In all 12 patients there was spontaneous improvement in serum transaminase over a period of 1 to 3 years, and four patients had sustained normalization of SGPT. Thus chronic active hepatitis is a common sequela of acute non-A, non-B hepatitis but may have a better prognosis than chronic active hepatitis of other causes.
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PMID:The chronic sequelae of non-A, non-B hepatitis. 46 17

A 18 year old man with protoporphyria had discrete, sunlight-induced skin changes at the nose and the back of his hands, and liver disease. The transaminases ranged from 30 to 200 U/1, uro- and coproporphyrins in the urine were in the normal range. There was no evidence of a progression of the liver disease during 4 years. At peritoneoscopy the liver was yellow-brown with a granular surface. Microscopically fibrosis was present and globular pigment was distributed mostly in hepatocytes. These findings had been misinterpreted as "chronic active hepatitis with choletasis and fibrosis". This observation shows that liver disease in protoporphyria may be present with a normal urinary excretion of uro- and coproporphyrins and suggests that in cases of chronic liver disease of unknown origin the gastroenterologist ought to pay attention to sunlight intolerance and the pathologist to the yellow-brownish pigment of protoporphyrin.
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PMID:[The liver in a case of protoporphyria (author's transl)]. 49 14


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