Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Investigations were performed concerning the elimination of the risk of hepatitis B transmission of potentially infectious plasma derivatives by the addition of a low dose of hepatitis B immunoglobulin (HBIg). To this end, clotting factor VIII concentrate, prothrombin complex, C1 esterase inhibitor concentrate, plasminogen and antithrombin III were prepared from plasma strongly positive for hepatitis B surface antigen (HBsAg). To one half of every preparation, HBIg was added up to a final concentration of 0.4 IU anti-HBs/ml (test preparations), the other half was not treated (control preparations). Furthermore, to 10(-3) diluted infectious reference plasma (Bureau of Biologics, FDA, USA), an overdose HBIg was added to a final concentration of about 0.4 IU anti-HBs/ml. 6 chimpanzees, injected either with the control plasma derivatives or with the untreated infectious reference plasma, were infected with hepatitis B virus, whereas 5 chimpanzees, injected either with the test plasma derivatives or the infectious reference plasma to which the HBIg had been added, did not show any evidence of hepatitis B infection during the follow-up of 1 year. Addition of a low dose of HBIg to potentially infectious plasma derivatives appears to be a reliable measure to eliminate the hepatitis B transmission and is preferred to other methods for labile plasma derivatives.
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PMID:Contributions to the optimal use of human blood. IX. Elimination of hepatitis B transmission by (potentially) infectious plasma derivatives. 662 9

560 patients with hepatic coma were treated during the years 1958 to 1982 in Homburg and Bad Kissingen . 82 patients had an endogeneous and 478 an exogeneous hepatic coma. Endogeneous hepatic coma was caused most frequently by fulminant virus hepatitis, intoxication, and hepatorenal syndrome accompanying serum hepatitis. Exogeneous hepatic coma in patients with cirrhosis of the liver was caused in most cases by gastrointestinal bleeding, by a diet too high in protein, or by excessive diuresis. Early clinical symptoms are changes in writing tests and ability to concentrate, whereas hepatic foetor occurs in coma stage III and IV. Clinical chemistry findings pointing to imminent hepatic coma are increase of arterial ammonia in exogeneous hepatic coma, and increase of free phenols in endogeneous hepatic coma. The increase of prothrombin time is prognostic for imminent hepatic coma in both types. Prognosis of endogeneous hepatic coma is still rather bad; 87% of the patients suffering from it died; in exogeneous hepatic coma prognosis has improved for stage I and II in the last 23 years, whereas however the total prognosis for all 4 stages is still unchanged, letality being 55%.
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PMID:[Causes and diagnostic criteria of hepatic coma--an analysis of 560 cases]. 667 13

The risk of hepatitis from prothrombin complex (pooled human clotting preparation) was retrospectively analysed. Of 39 patients who had undergone cardiac surgery, 22 (56%) developed hepatitis, while in those had not received pooled preparations the rate was only 5%. Although the proportion of multiple transfusions was significantly higher among the recipients of clotting preparations, it was found that the decisive hepatitis-inducing factor was the pooled preparation, not the transfusion blood. Contrary to earlier results, all cases were of the non-A, non-B type. The frequency of carriers of the causative virus is apparently not different from that with B virus. Thus both virus types must have occurred at similar frequency in earlier pooled clotting preparations. Since, furthermore, there seems to be no difference in their infectivity and their penetration in the population at large is likely to be similarly low, unrecognised double-infections in recipients of pooled clotting preparations were probably frequent before the introduction of recent methods of demonstrating hepatitis B.
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PMID:[Risk of hepatitis from conventional pooled PPSB preparations]. 681 65

A retrospective was designed to analyse the mode of presentation, clinical signs and haematological and biochemical abnormalities in 225 consecutive Black (Zulu) patients who were admitted to a general medical ward between the years 1970 and 1981 and in whom cirrhosis was later diagnosed. The most common presenting complaint was swelling of the body (60% of the patients), followed by abdominal pain (32%) and episodes of bleeding, mainly from the gastrointestinal tract (19%). On examination, hepatomegaly was encountered in 66% of the patients, with moderate to massive enlargement in 40%. Ascites was detected in 56%, with tense abdominal distension in 34%. Jaundice was present in 38% and emaciation, mental disturbance and splenomegaly in over 25%. Spider naevi (found in 2 patients) and Dupuytren's contracture (found in 1) were very rare. Thrombocytopenia and a high ESR were common. Over 90% of patients had low albumin and high globulin concentrations (albumin less than 20 g/dl and globulin greater than 60 g/dl in 25%). Bilirubin and alkaline phosphatase levels and the prothrombin index were found to be within normal limits in 32%, 24% and 52% of cases respectively. Histologically the lesion was most commonly micronodular (73%) with variable deposits of fat and iron. Peritoneoscopy was the most useful special investigation in the diagnosis of cirrhosis, leading to a correct diagnosis in 77% of cases. In conclusion, the clinical signs, biochemical abnormalities and histological features suggest that the factors causing cirrhosis in the community studied are mixed; it may result from the combined effects of alcohol abuse, malnutrition and chronic viral (e.g. hepatitis B) infections.
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PMID:Clinical presentation and biochemical abnormalities in black (Zulu) patients with cirrhosis in Durban. 707 88

A 22-year-old male Taiwanese was admitted to the hospital for acute hepatitis B associated with fulminant hepatic failure. After receiving supportive treatment, the patient's clinical condition improved and the results of liver function tests (including prothrombin time) gradually improved. However, in spite of seroconversion from hepatitis B surface antigen to antibody, hepatitis relapsed and serum alanine aminotransferase levels were persistently abnormal during the 3-year follow-up period. Liver biopsy performed 2 years after the onset of illness revealed chronic hepatitis. A retrospective review of the patient's serological test results revealed hepatitis C virus (HCV) RNA and the development of antibodies to HCV during the acute phase of illness as well as the persistence of HCV RNA during follow-up. Thus, we serologically and virologically proved that our patient had simultaneous acute infections with hepatitis B and C viruses and that these infections led to fulminant hepatic failure, relapse of hepatitis, and chronic hepatitis C.
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PMID:Simultaneous acute hepatitis B virus and hepatitis C virus infection leading to fulminant hepatitis and subsequent chronic hepatitis C. 775

To document the number of individuals who might qualify for interferon therapy and what impact the costs of treatment will have on the health care system, the serologic and biochemical profiles of 140 hepatitis B surface antigen (HBsAg) positive individuals of Asian descent (72 Vietnamese, 69 Chinese) were evaluated with respect to their hepatitis B e antigen (HBeAg) status and biochemical parameters (ALT, bilirubin, and prothrombin time). The mean +/- SD age of the study population was 33.5 +/- 13.4 y. Eighty-six (61%) were male. The HBeAg was positive in 64 (46%) of cases (41% of Vietnamese and 51% of Chinese) with no apparent sexual predilection. The ALT values exceeded 1.5 x normal in 23/64 (36%) cases. Mean serum bilirubin and prothrombin times were within normal limits. The results of this study demonstrate that approximately 50% of HBsAg positive immigrants from Southeast Asia are also HBeAg positive, and 36% of these individuals have elevated ALT values (> 1.5 x normal). Thus, according to estimated carrier rates and present guidelines for treatment, approximately 1-2% of the total Southeast Asian immigrant population are candidates for interferon therapy. With an immigrant population of approximately 900,000 and a cost of $6,500/patient, the total cost to the Canadian health care system will approach $100 million, or 1.3% of the present health care budget. These results underscore the need for a reappraisal of present treatment guidelines and implementation of universal vaccination in this country.
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PMID:A cross-sectional seroepidemiologic survey of chronic hepatitis B virus infections in Southeast Asian immigrants residing in a Canadian urban centre. 786 49

The preliminary results of a prospective double-blind controlled trial of colchicine in 100 patients with hepatitis B virus-related cirrhosis are reported. The patients, 94 males and 6 females, aged 32-80, were assigned to receive either 1 mg of colchicine or an identical placebo orally on a daily basis. The duration of the follow up ranged from 15 to 51 months (median 26 months). Seventy percent had histological proof of cirrhosis. On entry, 80 patients were in Child-Pugh class A, 19 were in class B, and one was in class C. Compared to the placebo group, there was no improvement in the colchicine group after a 24-month follow up in any of the biochemistry data, for example, serum albumin, alkaline phosphatase, alanine and aspartate aminotransferase, bilirubin, and prothrombin time. The difference in the cumulative survival rates at 51 months did not reach statistical significance (p = 0.8) in either group. There was no histological improvement in 30 patients who were willing to undergo repeated liver biopsies. No trend toward improvement of the hepatic pressure gradient was observed in these patients. The serum levels of aminopropeptide of type III procollagen increased significantly in patients in both groups after 24 months of therapy (1.07 +/- 0.06 vs. 1.36 +/- 0.06 U/ml in the colchicine group, 0.93 +/- 0.09 vs. 1.25 +/- 0.07 U/ml in the placebo group; p < 0.05). In addition, neither the clinical deterioration of cirrhosis nor death was prevented in patients receiving colchicine therapy. This report indicates that colchicine has no effect in the treatment of HBV-related postnecrotic cirrhosis.
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PMID:A double-blind randomized controlled trial of colchicine in patients with hepatitis B virus-related postnecrotic cirrhosis. 789 Sep 5

A 45-year-old hepatitis B surface antigen carrier had an allograft kidney transplantation and maintenance immunosuppression with cyclosporin A and prednisolone. Six months later, she experienced a rapidly progressive hepatic failure manifested by elevation of serum bilirubin level, prolongation of prothrombin time, and mild to modest increase of serum aminotransferase levels. She died in 6 weeks. Postmortem liver histology showed canalicular and cellular cholestasis and ground-glass appearance and ballooning of most hepatocytes, but only mild inflammatory cell infiltration. Immunohistochemical staining showed massive loads of hepatitis B surface and core antigens in the hepatocytes and extensive periportal fibrosis. The whole picture was compatible with fibrosing cholestatic hepatitis described in hepatitis B virus-infected liver transplant. Sequencing of the hepatitis B virus genome amplified from the patient's serum indicated a precore mutant but few mutations in the core, pre-S, and S genes. Little inflammatory reaction was observed histologically despite HLA compatibility, a situation differing from that in liver transplant. This observation indicates that fibrosing cholestatic hepatitis may also occur in non-liver transplant setting.
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PMID:Fibrosing cholestatic hepatitis in a hepatitis B surface antigen carrier after renal transplantation. 792 15

Recent advances in the medical and surgical treatment of chronic hepatitis and cirrhosis have made it increasingly important to develop noninvasive tests of liver function. Our study has evaluated the hepatic conversion of lidocaine to its primary metabolite monoethylglycinexylodide and compared this with liver histological findings in 225 patients with chronic hepatitis (161 with hepatitis C, 23 with hepatitis B, 21 with autoimmune hepatitis and 20 with cryptogenic hepatitis). One hundred seven (47.7%) patients had cirrhosis at the time of evaluation. A decline in monoethylglycinexylodide production was observed with worsening liver histological conditions from a mean of 81.5 +/- 7.0 ng/ml in patients with chronic persistent hepatitis to 61.2 +/- 5.5 ng/ml for chronic active hepatitis and 20.9 +/- 1.5 ng/ml in patients with cirrhosis (p < 0.05). A further stepwise decline in monoethylglycine xylodide production was observed with worsening Child class: from 25.5 +/- 2.2 ng/ml for class A patients to 8.9 +/- 1.4 ng/ml for patients with Child class C disease (p < 0.05). All patients with monoethylglycinexylodide production less than 20 ng/ml had cirrhosis confirmed on histological examination. In contrast, no relationship was observed between liver histological status and serum transaminases (AST or ALT), bilirubin, albumin and prothrombin time. Thirty-five patients underwent repeat histological evaluation and monoethylglycinexylodide testing after receiving at least 6 mo treatment for chronic hepatitis (interferon for hepatitis B and C and corticosteroids for autoimmune hepatitis). The change in monoethylglycinexylodide production observed in these patients was a linear function of the change in Knodell histological index (r = 0.73, p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic lidocaine metabolism and liver histology in patients with chronic hepatitis and cirrhosis. 776 26

To determine the risk of death at an early stage of fulminant viral hepatitis, we created severity indexes drawn from clinical data on the day of development of encephalopathy in 128 patients with fulminant hepatitis B and 103 with fulminant hepatitis non-A, non-B. In fulminant hepatitis B, the risk score was 2.75 x BL + 2.75 x BR + 2.7 x AG + 2.3 x WB + 1.67 x CD + 1.56 x AL - 0.098 x PR - 0.88, where BL is 1 if total bilirubin is higher than 20 mg/dl, BR is 1 if the ratio of total to direct bilirubin exceeds 2.2, AG is 1 if age is above 40 yr, WB is 1 if white blood cell count is less than 4,000 cells/mm3 or more than 18,000 cells/mm3, CD is 1 if a hazardous disease coexists and AL is 1 if ALT is less than 100 times the upper limit of normal (otherwise all are 0), and PR is prothrombin time (percentage of normal value). Using a cutoff score of 0, we found the positive predictive value, negative predictive value and predictive accuracy to be 0.90, 0.86 and 0.89, respectively. Sensitivity and specificity were 0.94 and 0.77, respectively. In fulminant non-A, non-B hepatitis, the risk score was 2.66 x BR + 2.25 x BL + 2.24 x DI + 2.05 x AL +/- 1.38 x AG + 0.00021 x WB - 6.33.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A multicenter study on the prognosis of fulminant viral hepatitis: early prediction for liver transplantation. 817 27


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