PATHOPHYSIOLOGY OF THE EOSINOPHILIA-MYALGIA-SYNDROME

Significant morbidity and mortality occur during the acute phase of th e eosinophilia-myalgia syndrome (EMS), and many patients still have ch ronic manifestations of the disease. Although the precise etiologic ag ent or agents within implicated batches of L-tryptophan remain uncerta in, histopathologic studies support a role for a cell mediated immune response underlying the pathophysiology of EMS. The cellular immune re sponse seems to lead to a microangiopathy and release of cytokines tha t can induce eosinophilia and fibrosis. Such responses are most marked within the dermis, subcutis, fascia, and connective tissue in and aro und muscles, nerves, and other tissues. The pathophysiology of the chr onic symptoms is poorly understood but may involve ischemia, neuropath y, and metabolic abnormalities.