Pathogenesis of ulcerations in deficiency of prolidase. The role of angiopathy and of deposits of amyloid.
The structure of the skin and the pattern of alteration in chronic ulcerations associated with deficiency of prolidase have been studied superficially in the past. We examined histologically several biopsies taken from apparently normal skin and from ulcerations afflicting a young woman with such a syndrome. Deposits of amyloid were found within the walls of medium-sized vessels and occasionally occluding their lumens. Impaired cutaneous microcirculation resulting from statis, moderate vasculitis, and abnormal structure of the dermis may be responsible for the regional preponderance of deposits of amyloid and ulcerations in the legs.
D000328:Adult; D000682:Amyloid / Q000378:metabolism*; D001706:Biopsy; D001808:Blood Vessels / Q000473:pathology; D004150:Dipeptidases / Q000172:deficiency*; D005260:Female; D006801:Humans; D007871:Leg Ulcer / Q000209:etiology* / Q000473:pathology; D012867:Skin / Q000098:blood supply / Q000473:pathology*
D000682:Amyloid; D004150:Dipeptidases; C022449:proline dipeptidase