Sjögren's syndrome without mixed cryoglobulinemia is not associated with hepatitis C virus infection.

OBJECTIVES

Hepatitis C virus infection has been associated with the formation of autoantibodies. Furthermore, several autoimmune and immune-complex mediated disorders have been proposed to be associated with hepatitis C virus infection. The best documented of these associations is between hepatitis C virus infection and essential mixed cryoglobulinemia. Essential mixed cryoglobulinemia is itself frequently associated with Sjögren's syndrome, and hepatitis C virus infection has been reported to be accompanied by lymphocytic sialadenitis and by xerophthalmia. We therefore searched for hepatitis C virus RNA and antibodies in 48 patients with SS-A/SS-B autoantibodies.

METHODS

Patients with both SS-A and SS-B autoantibodies were included if stored serum samples and medical records were available. No patients had clinically apparent chronic liver disease, and no patients had cryoglobulinemia. Six patients (group 1) had abnormally high aminotransferase values on one or more occasion, a history of acute hepatitis, or blood product exposure through transfusion or intravenous drug use. In 18 cases (group 2) no liver disease could be established, but there was insufficient information to exclude it. The 24 remaining patients (group 3) had no risk factors for liver disease, no known history of acute or chronic liver disease, a normal physical examination for signs of chronic hepatitis, and repeatedly normal aminotransferase values. Antibody to hepatitis C virus was determined by RIBA-2 (Chiron Corp, Emeryville, CA). The samples were tested for hepatitis C virus RNA after polymerase chain reaction amplification.

RESULTS

No patient had detectable antibody to hepatitis C virus; 47 were negative, and one sample from group 1 was indeterminate. No patients were positive for hepatitis C virus RNA.

CONCLUSIONS

We conclude that our patients with Sjögren's syndrome, without cryoglobulinemia and with detectable SS-A/SS-B autoantibodies, do not have clinically apparent liver disease, hepatitis C viremia by polymerase chain reaction, or antibodies to hepatitis C virus by second-generation testing using RIBA-2.