A Abouzahir1, P Chaurin, G Coutant, J M Garcin. 1. Service de médecine interne, hôpital d'instruction des armées Bégin, 69, avenue de Paris, 94160 Saint-Mandé, France. a_abouzahir@yahoo.fr
Abstract
INTRODUCTION: The Gleich syndrome associates episodic angioedema, hypereosinophilia and elevation of immunoglobulin M. It's a rare cause of nonallergic angioedema and is characterised by no organ involvement. EXEGESIS: We report a case of a 27-years-old african women, with five years history of recurrent angioedema of face and extremities, associated with a major hypereosinophilia. Serum IgM elevation, elimination of other etiologies and spectacular response to corticoid treatment permitted to retain diagnosis. CONCLUSION: The majority of cases of Gleich syndrome were reported in USA, Europe and Japan. The nonepisodic angioedema, which is not accompanied by elevation of immunoglobulin M, was described in Japan. There are currently no case reported in Africa where parasites are the principal cause of hypereosinophilia. The immunohistochemical studies permit to explain cytochemical disturbances responsible for the release of disease whose initial mechanism is unknown.
INTRODUCTION: The Gleich syndrome associates episodic angioedema, hypereosinophilia and elevation of immunoglobulin M. It's a rare cause of nonallergic angioedema and is characterised by no organ involvement. EXEGESIS: We report a case of a 27-years-old african women, with five years history of recurrent angioedema of face and extremities, associated with a major hypereosinophilia. Serum IgM elevation, elimination of other etiologies and spectacular response to corticoid treatment permitted to retain diagnosis. CONCLUSION: The majority of cases of Gleich syndrome were reported in USA, Europe and Japan. The nonepisodic angioedema, which is not accompanied by elevation of immunoglobulin M, was described in Japan. There are currently no case reported in Africa where parasites are the principal cause of hypereosinophilia. The immunohistochemical studies permit to explain cytochemical disturbances responsible for the release of disease whose initial mechanism is unknown.