Pathophysiology of the eosinophilia-myalgia syndrome

Significant morbidity and mortality occur during the acute phase of the eosinophilia-myalgia syndrome (EMS), and many patients still have chronic manifestations of the disease. Although the precise etiologic agent or agents within implicated batches of L-tryptophan remain uncertain, histopathologic studies support a role for a cell mediated immune response underlying the pathophysiology of EMS. The cellular immune response seems to lead to a microangiopathy and release of cytokines that can induce eosinophilia and fibrosis. Such responses are most marked within the dermis, subcutis, fascia, and connective tissue in and around muscles, nerves, and other tissues. The pathophysiology of the chronic symptoms is poorly understood but may involve ischemia, neuropathy, and metabolic abnormalities.