Etiologic considerations in peripheral vascular diseases of the lower extremity with special reference to diabetes mellitus.

DURING the past several years the existence of thromboangiitis obliterans as a distinctive disease entity has been seriously questioned. This evidently began with the suggestion by Fisher' that the peripheral manifestations of so-called Buerger's disease might actually represent atherosclerosis of the large arterial trunks with distal thrombosis. A more comprehensive study by Wessler et al.2 appears to support Fisher's suggestion, although such a view has been contested by others.3-7 This controversy represents only one facet of a larger, and perhaps more important, problem. In recent years there has developed an ever increasing tendency to consider almost all occlusive disease of the major arterial trunks as atherosclerosis attributable to faulty lipid or lipoprotein metabolism. An alternate concept8 holds that sclerotic disease (including lipid deposition) of the large arterial trunks may represent the common endstage of pathologic changes produced by a variety of etiologic factors. This common endstage is considered to be due to limitations in the response capabilities of the various tissue components that constitute the structure of the artery wall. Thus the pathologic characteristics of the end-stage lesion may provide no clue as to etiology.