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Chonnam Med J. 1996 Jun;32(1):49-58. Korean. Original Article.
Cho DY , Won YH , Chun IK .
Department of Dermatology, Chonnam National University Medical School, Kwangju, Korea.
Abstract

BACKGROUND: Allergic purpura is a vasculitis characterized by leukocytolastic histopathological finding. It is associated with petechial spots or ecchmymosis on the lower extremities and is sometimes accompained by general symptoms such as arthralgia and abdominal pain. Although the vascular destruction by an inflammation has been suggested to be mediated by deposition on circulating immunecomplexes secondary to infections, food, drugs, autoimmune disease, etc., the pathomechanism of the allergic purpura is still unclear. METHOD: To determine the types of deposits of the immuneoreactants and to understand pathogeneic mechanism of allergic purpura, direct immunofluorescence tests (DIF) were performed as well as clinical and histopathological findings were evaluated. Ten patients with allergic purpura diagnosed by clinical and histopathological findings and examined by IF test were objected. RESULT: The purpuric skin lesions are located predominantly on the lower extremity. Arthralgia in 6 cases and abdominal pain in 4 were found. Leukocytosis, elevated ESR and ASO, hematuria, proteinuria and occult blood were revealed in laboratory examinations. The histopathological findings including RBC extravasation, fibrin deposition, nuclear dust and perivascular inflammatory cell infiltrations were limited mainly to the upper dermis. In early lesions less than 24 hr old, the cellular infiltration was consisted mainly of neutrophils. In late lesions older than 72 hr, however, the number of neutrophils decreased more and mononuclear cells predominated. In the DIF study, fibrin in 10, C3 in 6, lgA and C4 in 4, lgM in 1 of 10 patients were found to accumulate mainly on the blood vessels of the upper demis. Five cases of early lesions less than 24 hour-old were associated with the deposition of immunoglobulins 'particularly lgA' and complement, while 5 cases of late lesions more than 72 hour-old were with fibrin only except 1 case. CONCLUSION: This study supports that allergic purpura is caused by vascular destruction by leukocytic infiltration mediated by deposition of immunoglobulins 'particularly lgA' and complement It is also demonstrated that there are variations in immunoreactant and cellular changes observed by DIF test and H-E staining accounting to the duration of skin lesions.

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