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Annals of Internal Medicine | 1990

The Prevalence of Hepatitis C Virus Antibodies among Hemodialysis Patients

Jerome B. Zeldis; Thomas A. Depner; I.K. Kuramoto; Robert G. Gish; Paul V. Holland

Excerpt The incidence of viral hepatitis in hemodialysis units has declined over the past 20 years with improved infection control strategies, including patient surveillance and segregation, plus i...


The American Journal of Medicine | 1983

Aplastic anemia and non-A, non-B hepatitis

Jerome B. Zeldis; Jules L. Dienstag; Robert Peter Gale

Severe aplastic anemia is a rare but important complication of hepatitis. The agent(s) responsible for the hepatitis in these cases have not been well defined. Sixteen patient with hepatitis-associated aplastic anemia were studied for evidence of recent infection with hepatitis A virus, hepatitis B virus, cytomegalovirus, Epstein-Barr virus, and Toxoplasma. Results were compared with data from 10 randomly selected patients with aplastic anemia unassociated with hepatitis. Of the 16 patients, recent acute hepatitis A infection could be excluded in at least 14 patients. Hepatitis B surface antigen (HBsAg) was present in only one patient. A diagnosis of recent hepatitis B infection could not be excluded with confidence in two others. Tests for cytomegalovirus, Epstein-Barr virus, and Toxoplasma gave negative results. No patient with aplasia unassociated with hepatitis had evidence of recent hepatitis A infection, and the frequency of hepatitis B antibodies in this group was indistinguishable from that in patients with hepatitis. These data indicate that most cases of hepatitis that preceded aplastic anemia were not caused by hepatitis A virus or hepatitis B virus; non-A, non-B agents were probably involved in at least 13 of the 16 cases studied.


Gastroenterology | 1988

Primary hepatocellular carcinoma in idiopathic hemochromatosis after reversal of cirrhosis

Richard S. Blumberg; Sanjiv Chopra; Roberto Ibrahim; James M. Crawford; Francis A. Farraye; Jerome B. Zeldis; Marvin D. Berman

Previous reports have emphasized the association of primary hepatocellular carcinoma in patients with idiopathic hemochromatosis with cirrhosis. In contrast, patients with idiopathic hemochromatosis without cirrhosis have no increased risk of hepatocellular carcinoma. Phlebotomy therapy, by preventing the accumulation of parenchymal iron and subsequent cirrhosis, is believed to prevent hepatocellular carcinoma in the precirrhotic stage of the disease. We report the case of a 67-yr-old man with a 32-yr history of idiopathic hemochromatosis complicated by cirrhosis, who had reversal of cirrhosis with phlebotomy therapy, yet developed hepatocellular carcinoma. There was no serologic or tissue evidence of hepatitis B infection.


Journal of Virological Methods | 1986

Correlation of HBV DNA and monoclonal reactivity to HBsAg in serum of patients with HBV infection

Jerome B. Zeldis; Edna Ben-Porath; Rafael Enat; Katarina Kirsch; Jack R. Wands

Hepatitis B virus (HBV) DNA hybridization assay, a monoclonal radioimmunoassay (M-RIA) for hepatitis B surface antigen (HBsAg) and conventional polyclonal immunoassays for HBV associated antigens were used to study sera from patients on dialysis and with acute hepatitis B. HBV DNA was detectable in hepatitis B e antigen (HBeAg) negative patients with acute hepatitis but not in HBsAg+ HBeAg- dialysis patients. In acute hepatitis, HBsAg immunoreactivity by M-RIA could still be detected even though a commercial immunoassay for HBsAg, the AUSRIA II, and the HBV DNA assay were no longer positive. Unlike in acute HBV infection, serum HBV DNA was detectable in dialysis patients who were AUSTRIA II negative but M-RIA positive. Serial determination of HBsAg by M-RIA and HBV DNA revealed episodes of HBV DNA positivity months after both the HBsAg was no longer positive by polyclonal immunoassay. Thus, the M-RIA for HBsAg and the molecular hybridization technique for HBV DNA are sensitive and specific assays for the identification of potentially infectious individuals who would not have been characterized as such based on the results of conventional polyclonal immunoassays.


The American Journal of Medicine | 1985

Hepatitis in an adult with rubella

Jerome B. Zeldis; James G. Miller; Jules L. Dienstag

Rubella accompanied by serum aminotransferase elevations occurred in a 24-year-old woman. Although not generally recognized, hepatic involvement in adult rubella was the probable cause of her liver function test abnormalities. Sporadic hepatitis labeled as non-A, non-B may result from infection by common viruses such as rubella.


Journal of Medical Virology | 1991

Prevalence of hepatitis C virus antibodies among patients infected with human immunodeficiency virus.

Paul H. Hayashi; Neil M. Flynn; Stephen A. McCurdy; I.K. Kuramoto; Paul V. Holland; Jerome B. Zeldis


Journal of Medical Virology | 1989

Inhibition of human hemopoiesis by non‐A, non‐B hepatitis virus

Jerome B. Zeldis; Piet J. Boender; Jan A. Hellings; Howard N. Steinberg


Hepatology | 1988

In vitro hepatitis B virus suppression of erythropoiesis is dependent on the multiplicity of infection and is reversible with anti-HBs antibodies.

Jerome B. Zeldis; Francis A. Farraye; Howard N. Steinberg


Gastroenterology | 1994

Hepatitis C virus pathogenicity: the corner pieces of the jigsaw puzzle are found.

Jerome B. Zeldis; Philip Jensen


Gastroenterology | 2000

Open labeled pilot study of thalidomide(thal) as a novel therapy for medically resistant ulcerative colitis (UC)

Lori Y. Kam; Eric A. Vasiliauskas; Maria T. Abreu; Philip V. Hassard; Jerome B. Zeldis; Stephan R. Targan

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Robert Peter Gale

Medical College of Wisconsin

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