Premium
Myopathy in HIV infection: the role of zidovudine and the significance of tubuloreticular inclusions
Author(s) -
Lane R. J. M.,
McLean K. A.,
Moss J.,
Woodrow D. F.
Publication year - 1993
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1993.tb00462.x
Subject(s) - myopathy , medicine , zidovudine , inflammatory myopathy , pathology , inflammation , human immunodeficiency virus (hiv) , immunology , viral disease
Muscle biopsies were obtained from 3 3 consecutive HIV‐infected patients with symptoms suggestive of muscle disorder. Twenty‐three patients had clinical evidence of myopathy; 18 of these had been taking zidovudine (AZT) for between 8 and 28 months, and were found to have a multifocal necrotizing myopathy with little or no inflammation. However, the remaining five clinically myopathic patients, who had never received AZT or had stopped treatment at least 5 months earlier, had either a necrotizing myopathy which appeared indistinguishable for that seen in patients taking the drug, or an inflammatory myopathy. The 10 clinically non‐myopathic patients showed no significant histological abnormalities. Tubuloreticular inclusions (TRI), in capillary endothelial cells, were found in all clinically myopathic cases but were not seen in five out often clinically non‐myopathic cases. We suggest that AZT causes a myopathy only when an underlying HIV‐related inflammatory myopathy is present. The drug appears to substantially reduce the inflammatory reaction in the muscle, but this may recur when the drug is stopped. The appearance of TRI may be the first manifestation of HIV activity in muscle.