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NEUROLOGY 1998;50:46-53
© 1998 American Academy of Neurology

Acute myopathy after liver transplantation

J. V. Campellone, MD, D. Lacomis, MD, D. J. Kramer, MD, A. C. Van Cott, MD and M. J. Giuliani, MD

From the Departments of Neurology (Drs. Campellone, Lacomis, Van Cott, and Giuliani), Pathology, Division of Neuropathology (Dr. Lacomis), and Anesthesiology and Critical Care Medicine (Dr. Kramer), The University of Pittsburgh Medical Center, Pittsburgh, PA.

Address correspondence and reprint requests to Dr. Joseph V. Campellone, Department of Neurology, Cooper Hospital/University Medical Center, 3 Cooper Plaza, Suite 320, Camden, NJ 08103.

Acute myopathy is a cause of weakness and additional morbidity in a variety of critically ill patients, including transplant recipients. We report the incidence of and risk factors associated with acute myopathy after orthotopic liver transplantation (OLTx). One hundred consecutive adult patients were prospectively assessed for muscle weakness after OLTx. Electrodiagnostic studies and muscle biopsies were performed on consenting affected patients. Potential risk factors for myopathy were evaluated in patients with myopathy versus control subjects. Seven patients developed acute persistent weakness after OLTx. Electrodiagnostic studies were consistent with a necrotizing myopathy. Histopathologic evaluation in five revealed a necrotizing myopathy with loss of myosin thick filaments. A higher initial index of illness severity, dialysis requirement, and higher doses of glucocorticoids were associated with development of myopathy. Patients with myopathy subsequently remained in the intensive care unit (ICU) longer than unaffected patients. In conclusion, acute substantial weakness was a source of additional morbidity in 7% of patients after OLTx. Most had myopathy with loss of myosin thick filaments. Patients with greater severity of illnesses and renal failure requiring dialysis were more likely to be affected. The effect of reducing exposure to corticosteroids in high-risk patients warrants further investigation.


Presented at the 121st Annual Meeting of the American Neurological Association, Miami, Florida, October 1996.

Received January 10, 1997. Accepted in final form July 23, 1997.




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