Publication date: Available online 17 April 2018
Source:Annales de Dermatologie et de Vénéréologie
Author(s): C. Jacquin-Porretaz, F. Castelain, E. Daguindau, E. Seilles, C. Nardin, F. Aubin, F. Pelletier
IntroductionL'angiœdème bradykinique par déficit en C1 Inhibiteur acquis (AOA) est une forme rare d'angiœdème bradykinique. Il se caractérise cliniquement par une survenue tardive après l'âge de 40 ans, l'absence d'antécédents familiaux d'angiœdème et une moindre fréquence des crises abdominales par rapport aux angiœdèmes héréditaires (AOH). Ses caractéristiques biologiques sont un dosage pondéral et une activité fonctionnelle de la protéine C1 inhibiteur (C1 Inh) abaissés ; il se distingue de l'AOH par une diminution du taux de C1q. Une majorité des cas d'AOA ont également des anticorps anti-C1 Inh. Le pronostic à long terme est déterminé par la présence d'une hémopathie sous-jacente, qui s'associe fréquemment aux AOA.ObservationsNous rapportons les cas de quatre patients atteints d'AOA, âgés de 60 à 77 ans, vus dans le centre de compétences du centre de référence des angiœdèmes du CHRU de Besançon. Les manifestations cliniques d'angiœdème étaient déclenchées chez trois patients par l'introduction d'un inhibiteur de l'enzyme de conversion (IEC) ou d'un sartan (ARA2). Trois patients sur quatre avaient des anticorps anti-C1 Inh. Le bilan étiologique a mis en évidence un lymphome indolent de la zone marginale chez un patient, une gammapathie monoclonale chez deux autres et enfin un patient avait une leucémie lymphoïde chronique connue.DiscussionL'apparition d'un angiœdème après introduction d'un IEC ou d'un ARA 2 peut révéler un AOA par déficit en C1 Inh. Ce mode de révélation ne doit pas faire porter à tort le diagnostic d'angiœdème aux IEC ou aux sartans ; un dosage du C1 Inh et du C1q est nécessaire dans cette situation. La recherche d'une hémopathie sous-jacente est systématique et détermine le pronostic à long terme.BackgroundAcquired C1-esterase inhibitor (C1-INH) deficiency angioedema (C1-INH-AAE) is a form of bradykinin-mediated angioedema. This rare disorder is due to acquired consumption of C1-INH, hyperactivation of the classic pathway of human complement, and potentially fatal recurrent angioedema symptoms. Clinical symptoms of C1-INH-AAE are very similar to those of hereditary angioedema (HAE) but usually appear after the fourth decade of life and induce abdominal pain less frequently. Laboratory tests are essential in establishing the diagnosis with low levels or abnormal structure and function of C1-INH. Most patients present C1-INH autoantibodies. Furthermore, C1q is reduced in AAE, contrary to HAE. The long-term prognosis is determined by associated hematologic malignancies.Patients and methodsWe report 4 cases of C1-INH-AAE associated with lymphoproliferative disorders referred to the Reference Centre for Angioedema of Besançon, France. The patients were aged between 60 and 77 years. C1 INH antibodies were found in three patients. Symptoms were triggered by angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) in 3 patients. Hematologic malignancy was present at diagnosis (one case of chronic lymphoid leukemia) or was diagnosed during follow-up (one case of indolent marginal zone non-Hodgkin lymphoma and two cases of monoclonal gammopathy).DiscussionC1-INH-AAE induced by ACE inhibitors or ARBs may be associated with hematologic malignancies. This form of revelation does not necessarily indicate a diagnosis of ACE or ARBs angioedema, and screening should therefore be performed for C1 Inh and C1q. An underlying hematologic malignancy should be routinely sought and the long-term prognosis determined.
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Παρασκευή 20 Απριλίου 2018
Angiœdème bradykinique par déficit en C1 Inhibiteur acquis : quatre cas
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