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Myopathic Changes Associated With Severe Acute Respiratory Syndrome
A Postmortem Case Series
Thomas W. Leung, MD;
Ka Sing Wong, MD;
Andrew C. Hui, MD;
Ka Fai To, MD;
Sik To Lai, FRCP;
Wai Fu Ng, FRCPath;
Ho Keung Ng, MD
Arch Neurol. 2005;62:1113-1117.
Background The March 2003 outbreak of the severe acute respiratory syndrome (SARS) resulted in significant morbidity and mortality. Muscle weakness and elevated serum creatine kinase levels are commonly encountered in patients with SARS. However, the nature and cause of myopathy associated with a SARS infection are unknown because, to our knowledge, there has been no report of histological or postmortem examination of the skeletal muscle from SARS-infected patients.
Objective To determine the exact nature of the myopathy associated with SARS.
Method Postmortem skeletal muscles from 8 consecutive patients who died of SARS in March 2003 were studied under light and electron microscopy as well as immunohistochemistry.
Results Focal myofiber necrosis was identified in 4 of 8 cases. Macrophage infiltration and regenerative fiber were scanty. All 4 patients treated with a steroid had significant myofiber atrophy. In situ hybridization for coronavirus was negative in all subjects. Viral cultures for coronavirus and examination for viral particles under electron microscopy were performed in 2 patients. The viral culture yielded no organisms and there were no viral particles seen on electron microscopic examination.
Conclusions There is a spectrum of myopathic changes associated with a SARS infection. Focal myofiber necrosis is common and possibly is immune mediated. Critical illness myopathy and superimposed steroid myopathy may also play an important role in SARS.
Author Affiliations: Departments of Medicine and Therapeutics (Drs Leung, Wong, and Hui), and Anatomical Pathology (Drs To and H. K. Ng), Prince of Wales Hospital, Chinese University of Hong Kong, and Departments of Medicine and Geriatrics (Dr Lai) and Pathology (Dr W. F. Ng), Princess Margaret Hospital, Hong Kong.
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