Rinsho Shinkeigaku (Clinical Neurology)

Brief Clinical Note

Hypothyroid myopathy caused by interferon-α therapy for chronic hepatitis C

Yuriko Nagane, M.D., Kimiaki Utsugisawa, M.D., Hideki Kizawa, M.D., Ryushi Kondoh, M.D. and Yasuo Terayama, M.D.

Department of Neurology, Iwate Medical University

We reported a rare case with hypothyroid myopathy after interferon-α (IFN-α) therapy. A 59-year-old man complained of his weakness in proximal part of upper and lower extremities which started at 1 month and progressed during 6 months after IFN-α therapy for chronic hepatitis C, but he did not complained of any other symptoms. Blood chemistry showed an elevated level of CK (1,843 IU/l; normal range 43-170 IU/l) and increased myoglobin (250 ng/ml; normal range<60 ng/ml). Thyroid function tests revealed an elevated level of TSH (148.7 μIU/ml; normal range, 0.4-4.1 μIU/ml), and decreased levels of free T3 (0.56 pg/ml; normal range, 2.27-3.90 pg/ml) and free T4 (0.24 ng/ml; normal range, 0.95-1.74 ng/ml). Blocking type TSH receptor antibody titer was elevated (75.4%; normal range<15%) while other types of antithyroid antibody were not detected in his serum. Muscle biopsy from his quadriceps femoris muscle showed non-specific mild myopathic changes. His weakness was completely ameliorated and serum CK levels were normalized by thyroid hormone administration alone, confirming the diagnosis of hypothyroid myopathy. However, even after total amelioration of his hypothyroidism, blocking type TSH receptor antibody titer remained elevated. These findings may suggest that IFN-α fostered an autoreactivity arising from HCV infection to cause the autoimmune thyroid disease.

(CLINICA NEUROL, 45: 441|444, 2005)
key words: hypothyroid myopathy, interferon-α, chronic hepatitis C, blocking type TSH receptor antibody

(Received: 6-Jul-04)