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Biomedical subjects

A G Redeker

Publications and source records attributed to A G Redeker.

At least 55 records · Page 3Linked to original sources
PubMed1988

A single antigenomic open reading frame of the hepatitis delta virus encodes the epitope(s) of both hepatitis delta antigen polypeptides p24 delta and p27 delta.

On the basis of the complete nucleotide sequence of the single-stranded, covalently closed circular hepatitis delta virus RNA genome (K.-S. Wang, Q.-L. Choo, A. J. Weiner, J.-H. Ou, R. C. Najarian, R. M. Thayer, G. T. Mullenbach, K. J. Denniston, J. L. Gerin, and M. Houghton, Nature [London] 323:508-514, 1986 [Author's correction, 328:456, 1987]), five long open reading frames (ORFs) encoding polypeptides containing a methionine proximal to the amino terminus were expressed in bacteria. Only polypeptides encoded by the antigenomic ORF5 cross-reacted with antisera obtained from patients with hepatitis delta virus infections. Immunological analysis of viral extracts and the recombinant ORF5 polypeptides synthesized in bacteria and yeast cells revealed that ORF5 encodes the immunogenic epitope(s) shared by both hepatitis delta viral polypeptides p27 delta and p24 delta and probably represents the complete structural gene for p27 delta and p24 delta. We also present evidence that ORF5 encodes the hepatitis delta antigen, an antigen originally found in the nuclei of hepatocytes of infected individuals (M. Rizzetto, M. G. Canese, S. Arico, O. Crivelli, F. Bonino, C. G. Trepo, and G. Verme, Gut 18:997-1003, 1977). A comparison of the primary structure of the predicted hepatitis delta antigen polypeptides with that of the core antigen of the hepatitis B virus shows that these polypeptides are very dissimilar.

Amino Acid Sequence↗
PubMed1988

Prevalence of hepatitis delta (delta) virus infection. A seroepidemiologic study.

In assessing the prevalence of hepatitis delta (delta) virus (HDV) infection in 358 patients with acute hepatitis B seen in Los Angeles between 1983 and 1985 and in 196 patients with chronic hepatitis B followed between 1980 and 1985, we found that 23% of patients with chronic and 5% of patients with acute hepatitis B were infected with HDV. Among patients with chronic hepatitis B, the prevalence of HDV infection was 73% in intravenous drug users and 14% in homosexual men. Acute coinfection with the hepatitis B virus was also more frequent in drug users (8%) than in other groups. delta-Hepatitis is a common infection in hepatitis B virus carriers in Los Angeles, particularly in drug addicts, but also in homosexual men who do not abuse drugs intravenously.

California↗
PubMed1987

Epidemic non-A, non-B hepatitis in patients from Pakistan.

Epidemic non-A, non-B hepatitis was diagnosed in three young Pakistani men during a 10-month period at the Los Angeles County-University of Southern California Medical Center. All three patients had recently visited or lived in Karachi, Pakistan. None had serologic markers of hepatitis B virus infection or IgM antibody (acute-phase) to hepatitis A virus. A liver biopsy from one patient showed marked cholestasis and cholangiolar transformation of hepatocytes, a pattern previously described in patients with epidemic non-A, non-B hepatitis. Immune electron microscopy of a stool specimen obtained from this patient 10 days after the onset of symptoms showed virus-like particles, 27 nm in diameter, that were specifically aggregated by antibody contained in acute-phase sera from the three Pakistani patients, from patients with non-A, non-B hepatitis in Burma and Nepal, and from an experimentally infected marmoset. Recognition of three separate cases of probable epidemic-type non-A, non-B hepatitis in patients at one institution during such a short time suggests that Pakistan is endemic for this infection and that the disease may be more commonly spread to the United States than is now presumed.

Adult↗
PubMed1986

HBsAg clearance in chronic active hepatitis B. A possible cause of cryptogenic cirrhosis.

Three patients with chronic hepatitis B infection, two with chronic active hepatitis and cirrhosis, and the third with quiescent cirrhosis, cleared HBsAg from their serum and eventually developed anti-HBs. All three were asymptomatic and had nearly normal serum aminotransferases following loss of HBsAg. Liver biopsy revealed cirrhosis in each patient. With the development of anti-HBs, these patients became serologically indistinguishable from patients with a cryptogenic cirrhosis who had prior unrelated exposure to hepatitis B. Remote chronic hepatitis B infection may be a more common cause of cryptogenic cirrhosis than is commonly appreciated.

Adult↗
PubMed1986

Results of a randomized trial of end-to-side portacaval shunt and distal splenorenal shunt in alcoholic liver disease and variceal bleeding.

Since 1976, we have compared the end-to-side portacaval shunt (PCS) with the distal splenorenal shunt (DSRS) in patients with alcoholic liver disease and recurrent variceal bleeding. Fifty-four patients were randomly assigned to receive either shunt procedure. There were 27 patients in each group and both groups were highly comparable in clinical and laboratory characteristics. Median follow-up was 31 mo in each group. Postoperative complications and operative mortality (7% after PCS, 12% after DSRS) were comparable. Spontaneous portasystemic encephalopathy developed in 32% of the patients at risk after PCS and in 39% after DSRS. Rebleeding from varices occurred in 4% of the patients after PCS and in 27% after DSRS. Cumulative survival was not significantly different between groups (5-yr survival: 31% after PCS, 43% after DSRS). We have failed to demonstrate superiority of DSRS in our patients with alcoholic liver disease with respect to postoperative encephalopathy or survival, and have experienced an unusually high rate of variceal rebleeding after DSRS.

Adult↗
PubMed1986

Delta hepatitis in the Los Angeles area: a report of 126 cases.

We describe the clinical course in 126 patients with delta hepatitis who have been evaluated in Los Angeles since 1967. In approximately two thirds of all patients, delta infection was associated with chronic hepatitis B. Most patients were members of two major risk groups: 65.9% were intravenous drug abusers, 11.9% were male homosexuals, and another 9.5% were both intravenous drug users and male homosexuals. The overall case fatality rate was 23%; fulminant hepatitis caused 17 of 29 (59%) deaths. Advanced liver disease occurred significantly more frequently in patients who had established chronic delta infections than in hepatitis B virus carriers with recent delta superinfections. Nonfatal infections with both hepatitis B virus and delta hepatitis virus resulted in clearance of both agents, whereas superinfection in carriers of chronic hepatitis B virus usually led to chronic delta hepatitis. Spontaneous loss of chronic delta infection was not observed. Delta hepatitis, a longstanding infection seen in patients in the Los Angeles area, has caused fulminant hepatitis and progressive liver disease in both intravenous drug users and male homosexuals.

Acute Disease↗
PubMed1985

Acute delta hepatitis without circulating HBsAg.

Infection with the delta agent can only occur in the context of coexistent hepatitis B virus infection. We describe a patient in whom the clinical features of acute delta hepatitis developed when seroconversion from hepatitis B surface antigen to antibody had already occurred and diagnosis of recent acute hepatitis B was based on high titre IgM antibody to hepatitis B core antigen. We discuss the significance of such a serological profile, not previously described.

Acute Disease↗
PubMed1985

Delta agent superinfection. Rapidly progressive liver disease in a hepatitis B virus carrier.

We report a case of rapidly progressive chronic active hepatitis (CAH) following acute delta infection in a previously asymptomatic hepatitis B virus carrier. Serologic evidence of delta superinfection coincided with an acute icteric hepatitis, and was followed by the development of clinically evident chronic liver disease. The liver biopsy specimens documented the acute hepatitis and subsequent progression of severe CAH. This case illustrates the clinical and pathologic changes that may follow acute delta infection in chronic hepatitis B carriers.

Adult↗
PubMed1984

Fulminant delta hepatitis in chronic hepatitis B infection.

Two male homosexual patients, one an intravenous (IV) drug abuser, had hepatitis B surface antigen-positive fulminant hepatitis. On the basis of tests for IgM antibody to hepatitis B core antigen (HBcAg) and for IgM and IgG antibodies to delta agent, acute delta hepatitis in chronic hepatitis B infection was diagnosed. The delta agent appeared to have a role in producing fulminant hepatic failure. Accurate diagnosis of fulminant hepatitis may be impossible without recourse to tests for IgM antibody to HBcAg and antibodies to delta agent. Although delta hepatitis in the United States primarily affects IV drug abusers, this infection can also occur in male homosexuals.

Acute Disease↗
PubMed1984

Fulminant hepatic and renal failure complicating Wilson's disease.

We report a case of fatal fulminant liver failure complicating Wilson's disease that is unique in several respects. The illness supervened after several years of medical noncompliance in a patient who had been previously diagnosed and successfully treated with penicillamine. Re-institution of penicillamine therapy 2 weeks prior to the fulminant decompensation failed to prevent it. Renal failure in this patient was apparently secondary to rhabdomyolysis. Addition of penicillamine to a peritoneal dialysis solution allowed chelation and removal of over 14 mg per day of copper but without apparent benefit. Exchange transfusion and high dose dexamethasone therapy (24 mg/day) were equally ineffective in reversing the liver failure. Other reported cases have also been fatal. The best treatment for fulminant Wilson's disease is prevention by diagnosis in a pre-symptomatic stage and institution of carefully supervised life-long therapy with penicillamine.

Acute Kidney Injury↗
PubMed1984

Direct transhepatic assessment of hepatic vein pressure and direction of flow using a thin needle in patients with cirrhosis and Budd-Chiari syndrome. An effective alternative to hepatic vein catheterization.

Portal pressure can be accurately measured transhepatically with a Chiba needle. Since 1980, we have used transhepatic hepatic vein pressures as our zero reference for transhepatic portal pressure measurements. To validate the latter technique, we performed hepatic vein catheterization and transhepatic hepatic vein puncture in 11 patients undergoing portal pressure measurement. Transhepatic hepatic vein puncture was simple, providing pressures as reproducible as those obtained by hepatic vein and inferior vena cava catheterization. These pressures were minimally higher than simultaneous free hepatic vein and inferior vena caval pressures, possibly reflecting the more proximal location of the small hepatic vein radicles often entered by this technique. Transhepatic hepatic vein puncture is an accurate way to determine hepatic vein pressure and, combined with transhepatic portal vein pressure measurement, completely obviates the need for venous catheterization for portal pressure determination. Transhepatic hepatic vein pressure was also measured in 3 patients with Budd-Chiari syndrome. In these patients, transhepatic hepatic vein pressure was elevated and equaled or exceeded portal vein pressure. Abnormal venous collaterals were identified in all patients. Transhepatic portal pressure studies are also an appropriate way to evaluate patients suspected of having hepatic outflow obstruction.

Blood Pressure Determination↗