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Previous Volume 331:1607-1611 December 15, 1994 Number 24 Next

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ABSTRACT

Background In Scandinavia many patients with primary hypogammaglobulinemia contracted non-A, non-B hepatitis after intravenous treatment with an immune globulin product that was later found to contain a non-A, non-B hepatitis virus.

Methods We studied the prevalence and clinical course of hepatitis C virus (HCV) infection in a group of 55 Norwegian patients with primary hypogammaglobulinemia and investigated its association with the use of contaminated immune globulin. We used the polymerase chain reaction to detect HCV RNA and performed HCV genotyping. We also analyzed the responses to treatment with interferon.

Results Of 20 patients who received the contaminated immune globulin, 17 were seropositive for HCV RNA. In addition, 1 of 35 patients not exposed to the contaminated immune globulin was HCV RNA-positive. HCV genotype V was found in all 12 patients for whom genotyping was performed, but 8 patients also had genotype II or III, or both. All HCV RNA-positive patients had abnormal results on biochemical liver tests. All liver-biopsy specimens (from 15 patients) were abnormal, with portal inflammation, bile-duct damage, and focal necrosis. In six patients there was cirrhosis. Two patients died of liver failure. In 4 of the 10 patients treated with interferon there were complete, though transient, biochemical responses, but the follow-up biopsy specimens showed evidence of histologic progression. The poorest responses to interferon were among the patients with multiple HCV genotypes. All but one patient remained positive for HCV RNA.

Conclusions In patients with primary hypogammaglobulinemia there was a high rate of HCV infection after treatment with contaminated immune globulin. In these immunocompromised patients HCV infection has a severe and rapidly progressive course, and responses to interferon are poor.

Source Information

From the Section of Clinical Immunology and Infectious Diseases (K.B., S.S.F.) and the Section of Hepatology and Gastroenterology (K.B.), Medical Department A, and the Department of Pathology (T.H.), National Hospital, Oslo, Norway; the Department of Virology, National Institute of Public Health, Oslo (H.H.S.); and the Institute for Clinical Virology, Karolinska Institute, Huddinge Hospital, Stockholm, Sweden (Z.Y.).

Address reprint requests to Dr. Bjoro at Medical Department A, National Hospital, 0027 Oslo, Norway.

Full Text of this Article

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Extract | Full Text  
N Engl J Med 1995; 332:1235-1237, May 4, 1995. Correspondence

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