Myeloid and lymphoid neoplasm with eosinophilia and abnormalities of PDGFRB presenting as congestive heart failure and hypereosinophilia.
10.4168/aard.2017.5.4.232
- Author:
Jae Woo KWON
1
;
Ji Hyun KWON
;
Ae Young HER
Author Information
1. Department of Allergy and Clinical Immunology, Kangwon National University School of Medicine, Chuncheon, Korea. legent@hanmail.net
- Publication Type:Case Report
- Keywords:
Hypereosinophilic syndrome;
PDGFRB;
Imatinib;
Eosinophilia
- MeSH:
Adrenal Cortex Hormones;
Blood Platelets;
Bone Marrow Diseases;
Drug-Related Side Effects and Adverse Reactions;
Eosinophilia*;
Eosinophils;
Estrogens, Conjugated (USP)*;
Heart Failure*;
Heart Ventricles;
Helminths;
Humans;
Hypereosinophilic Syndrome;
Imatinib Mesylate;
Korea;
Receptor, Fibroblast Growth Factor, Type 1;
Receptor, Platelet-Derived Growth Factor beta*;
Thrombectomy
- From:Allergy, Asthma & Respiratory Disease
2017;5(4):232-236
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Hypereosinophilic syndrome (HES) is a heterogeneous disorder characterized by persistent hypereosinophilia with the evidence of organ dysfunction caused by eosinophilic involvement. HES can be induced by various secondary causes, including helminthic infections, adverse drug reactions, and allergic diseases. Primary/clonal bone marrow disease, including genetic mutations in platelet driven growth factor receptor alpha (PDGFRA), platelet driven growth factor receptor beta (PDGFRB), and fibroblast growth factor receptor 1 (FGFR1) could be its causes. Although corticosteroids are the mainstay of therapy in confirmed HES, imatinib is considered a definitive treatment for HES with these mutations. However, there have been few reports about HES with these genetic mutations in Korea. Here, we report a patient who presented with sudden onset of congestive heart failure and hypereosinophilia, proved to have PDGFRB rearrangement, and was controlled successfully with imatinib after left ventricle thrombectomy.
