Sternberg E M
National Institute of Mental Health, Bethesda, Maryland 20892, USA.
Adv Exp Med Biol. 1996;398:325-30. doi: 10.1007/978-1-4613-0381-7_50.
Taken together, these studies suggest that many different etiologic agents alone or together may initiate the common final pathways of tissue pathologic response resulting in the clinical syndrome of eosinophilia, myalgias and fasciitis. Tryptophan itself may contribute to some of the scarring features of the illness, while impure L-tryptophan, and one or more of the impurities cause the characteristic features of the illness. The altered tryptophan metabolism in EMS is secondary to inflammation.
综上所述,这些研究表明,许多不同的致病因素单独或共同作用,可能引发组织病理反应的共同最终途径,导致嗜酸性粒细胞增多、肌痛和筋膜炎的临床综合征。色氨酸本身可能导致该疾病的一些瘢痕形成特征,而不纯的L-色氨酸以及一种或多种杂质则导致该疾病的特征性表现。嗜酸性粒细胞增多性肌痛综合征中色氨酸代谢的改变继发于炎症。