Bell S, Brand K, Meurer M
W.M. Keck Autoimmune Disease Center, Department of Molecular and Experimental Medicine, Scripps Research Foundation, La Jolla, Kalifornien.
Hautarzt. 1992 Jun;43(6):339-43.
In 1981 epidemic poisoning with adulterated cooking oil occurred in Spain, affecting more than 20,000 people. The condition caused has since become known as the toxic oil syndrome (TOS). About 10-15% of the patients with acute symptoms developed a chronic disease with scleroderma-like skin manifestations, polyneuropathy and myositis. While the acute phase of the TOS was characterized by eosinophilia and elevated IgE, the chronic stage involved humoral autoimmune phenomena, such as antinuclear and antinucleolar antibodies, in many cases. In women with the chronic phase of TOS there was a possible prevalence of HLA-DR3 and HLA-DR4. The recently characterized eosinophilia-myalgia syndrome (EMS), which is thought to have been induced by contaminated L-tryptophan preparations, is similar to the TOS in some particulars. Understanding of the toxicological, immunological and genetic pathways leading to these diseases might give us some insight into the pathogenesis of spontaneously occurring autoimmune diseases, such as systemic scleroderma.
1981年,西班牙发生了掺假食用油导致的流行性中毒事件,超过2万人受到影响。此后,这种病症被称为有毒油综合征(TOS)。约10% - 15%出现急性症状的患者发展成了一种慢性病,伴有硬皮病样皮肤表现、多发性神经病和肌炎。TOS的急性期以嗜酸性粒细胞增多和IgE升高为特征,而慢性期在许多情况下涉及体液自身免疫现象,如抗核抗体和抗核仁抗体。处于TOS慢性期的女性中,HLA - DR3和HLA - DR4可能普遍存在。最近发现的嗜酸性粒细胞增多性肌痛综合征(EMS),被认为是由受污染的L - 色氨酸制剂引起的,在某些方面与TOS相似。了解导致这些疾病的毒理学、免疫学和遗传途径,可能会让我们对系统性硬皮病等自发性自身免疫性疾病的发病机制有所洞察。