CHICAGO—On a Saturday morning in Chicago, Chester V. Oddis, MD, director of the Myositis Center at the University of Pittsburgh, explained to a crowded room of about 500 rheumatologists attending the ACR’s State-of-the-Art Clinical Symposium in April how best to use myositis autoantibodies in clinical care.
Explore this issueJuly 2017
Also by this Author
He began with an overview of the different types of myositis and explained that patients with myositis are symmetrically weak and meet several diagnostic criteria. Specifically, they may have elevated serum enzymes, such as creatine kinase (CK), aldolase, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH). They also have myopathic electromyographic abnormalities, such as sharp waves, fibrillations and polyphasic motor units. Finally, they have muscle pathology that is characterized by myofiber degeneration/regeneration, mononuclear cell infiltrates and perifascicular atrophy.
Many patients with myositis also have rashes and are thus diagnosed with dermatomyositis (DM), which is a much easier diagnosis to make than polymyositis (PM), which represents a diagnostic challenge. This is because there are many mimics of PM and therefore a muscle biopsy is necessary for its diagnosis. In particular, PM has histologic features that distinguish it from dermatomyositis. Histology reveals that “from a histopathological perspective, PM and DM are almost like different diseases in their own rights,” noted Dr. Oddis. “If you look at the histology, even from a distance, they look different,” he explained, pointing to the two histological examples projected onto the large screens.