A Case of Interferon-Induced Anti-Jo1 Positive Polymyositis with Pulmonary Fibrosis

Abstract

Purpose: Interferon therapy for hepatitis C is rarely complicated by the onset of autoimmune diseases. Thyroid disease, hemolytic anemia and TTP are better known autoimmune diseases complicating interferon therapy. We present a case of anti-Jo1 positive polymyositis with pulmonary fibrosis induced by interferon therapy. A 54-year old female with hepatitis C and biopsy consistent with mild activity and mild fibrosis was treated with pegylated interferon and ribavirin. After starting therapy, she complained of flu-like symptoms. Four weeks later, she complained of worsening flu-like symptoms, shortness of breath and weakness in her arms and legs prompting admission to the hospital. At admission, her blood pressure, pulse and temperature were normal. She was dyspneic with increased work of breathing. On exam, she had bilateral coarse breath sounds and weakness in the proximal muscle groups in all extremities. Labs at admission were ALT93, AST115, Alkp144, TB0.2, Alb2.8, CPK2637, Aldolase33.8, ANA < 1:40, dsDNA < 30, C4 < 8, C3 < 9, RF14, and ESR70. Anti Jo1 was positive. SSA, SSB, pANCA, anticardiolipin, ASMA, and AMA were negative. Chest x-ray showed bilateral interstitial infiltrates. The patient underwent bronchoscopy with biopsy demonstrating interstitial organizing pneumonitis and chronic bronchitis. Pulmonary function tests demonstrated moderate chest restriction with reduced DLCO to 30% of predicted. Clinical presentation suggested a diagnosis of anti-Jo1 positive acute polymyositis with interstitial pneumonitis. This constellation of clinical features comprises the antisynthetase syndrome. Interferon therapy was discontinued and the patient was treated with cyclophosphamide and prednisone. She had gradual improvement in her weakness and pulmonary function. The serum aldolase and creatine phosphokinase levels returned to normal. Interferon therapy is rarely complicated by the development of autoimmune diseases. There have been few reports of acute polymyositis with pulmonary fibrosis associated with interferon therapy. The presence of anti-Jo antibody in patients with acute polymyositis is associated with the development of pulmonary fibrosis. An association between Anti-Jo1 positive polymyositis and hepatitis C has been previously described in patients without exposure to interferon therapy. Because of the temporal relationship between interferon therapy and the development of symptoms of this rare disease, the patient presents with interferon-induced antisynthetase syndrome.