Aihara M, Takahashi R, Ohtake T, Komori T, Nagashima T, Tanabe H
Department of Neurology, Tokyo Metropolitan Neurological Hospital.
Rinsho Shinkeigaku. 1990 Jan;30(1):103-6.
A 72-year-old man suddenly developed severe muscle weakness following the treatment with pindolol (Calvisken) for three days. Neurological examination on admission disclosed marked proximal muscle weakness with absent deep tendon reflexes. Laboratory data showed significant increase of serum CK, aldolase and myoglobin. Electromyography revealed both neurogenic and myogenic changes in all muscle tested. Skeletal muscle CT showed patchy low density areas in muscles of thigh and leg, especially in the hamstrings. Femoral muscle biopsy demonstrated a granulomatous nodule with multinucleated giant cells in the degenerated muscle fibers showing small-grouped atrophy. By Mb-PAP staining, Mb-negative fibers were randomly distributed among normally stained ones. Leu 1, 3a, 4, HLA-DR positive cells were found adjacent to the granuloma by immunoperoxidase staining. After immediate withdrawal of pindolol and treatment with steroid, he recovered muscle strength and enzyme activities were normalized in a week. Beta blockers have been known to induce muscle cramps or pain and moderate elevation of serum muscle enzymes. However, severe muscle weakness with highly elevated enzyme activities leading to rhabdomyolysis as noticed in the present case was rarely reported in the literature. Underlying sarcoid myopathy might be suspected to exaggerate this unusual case of pindolol-induced rhabdomyolysis. A careful use of pindolol is emphasized.