Outbreak of hepatitis C virus infection in patients with hematologic disorders treated with intravenous immunoglobulins: different prognosis according to the immune status.
The influence of immunodeficiency on the course of hepatitis C virus (HCV) infection is still debated, although a worsening effect has been suggested. We compared the characteristics of hepatitis C in two groups of hematologic patients with different levels of immunocompetence who acquired the same virus strain after treatment with contaminated intravenous immunoglobulins (IVIG). Indications for IVIG therapy were idiopathic thrombocytopenic purpura (ITP) in six patients and hypogammaglobulinemia in 7 patients with various hematologic disorders, who were defined immunodeficient (ID). Infection rate was 100%. Five ID patients never developed HCV antibodies despite serum HCV-RNA positivity. The same HCV genotype was shown in 10 patients tested. Moreover, E1-E2 gene partial nucleotide sequencing, performed in four patients, showed identical or closely related amino acid sequences, thus strongly supporting the hypothesis of a common source of infection. Clinical acute infection did not differ significantly between the two groups, but subsequent liver failure developed in five of the seven ID patients and in none of the ITP patients (P = .04). Liver biopsy, performed in three cases, documented HCV as the only cause of liver damage. Six ID patients died, with liver disease being the primary cause of death in four cases and a contributory cause in two cases. Their median survival after IVIG was 12 months, significantly worse than that of ITP patients (P = .0028). We conclude that immunodeficiency markedly worsens the course of IVIG-acquired HCV infection in hematologic patients.
Rossi
G
G
III Divisione Medicina Generale, Spedali Civili, Brescia, Italy.
Tucci
A
A
Cariani
E
E
Ravaggi
A
A
Rossini
A
A
Radaeli
E
E
D000328:Adult; D000361:Agammaglobulinemia / Q000150:complications / Q000628:therapy; D000368:Aged; D000595:Amino Acid Sequence; D004196:Disease Outbreaks; D004340:Drug Contamination; D005260:Female; D005500:Follow-Up Studies; D006402:Hematologic Diseases / Q000150:complications* / Q000276:immunology / Q000628:therapy; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification; D006526:Hepatitis C / Q000150:complications / Q000453:epidemiology* / Q000276:immunology / Q000635:transmission / Q000821:virology; D018937:Hepatitis C Antibodies / Q000096:biosynthesis; D006801:Humans; D007121:Immunocompetence; D016867:Immunocompromised Host; D016756:Immunoglobulins, Intravenous / Q000009:adverse effects*; D007558:Italy / Q000453:epidemiology; D017093:Liver Failure / Q000209:etiology / Q000401:mortality; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D011379:Prognosis; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000150:complications / Q000628:therapy; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid; D016019:Survival Analysis
D018937:Hepatitis C Antibodies; D016756:Immunoglobulins, Intravenous