title: Immunohistochemical differentiation of eosinophilic heart diseases using antibodies against eosinophil activation markers.
abstract: OBJECTIVE
  Eosinophilic heart syndromes are rare in Western countries and include endocarditis parietalis fibroplastica (EPF) and hypersensitivity myocarditis (HM). There are striking differences in natural history and morphological findings. Since diagnosis can be difficult when analysing small myocardial biopsies lacking the characteristic histological features, we studied a set of immunohistochemical markers in order to characterize the activation status of the infiltrating eosinophils to distinguish between these two entities.
  
  
  RESULTS
  This study is based on the investigation of seven explanted hearts and one left ventricular specimen collected during implantation of a left ventricular assist device from a total of seven patients with HM. Also investigated were three right and three left ventricular specimens from five patients with EPF. We used antibodies (Ab) against EG1, and EG2, CD44, and CD69 which have been described as markers to distinguish between resting and activated eosinophils. The EG1 to EG2 ratio of eosinophils and the immunoreactivity against CD44 showed no differences between the two entities. However, eosinophils in the EPF were completely negative for CD69, whereas eosinophils reacted positively within the HM group.
  
  
  CONCLUSIONS
  The immunohistochemical investigation of eosinophilic heart diseases using antibodies against CD69 can be a useful tool to distinguish between hypersensitivity myocarditis and endocarditis parietalis fibroplastica.
authors.affiliation: Institute of Pathology, University Hospital of Essen, Essen, Germany.
authors.forename: F
authors.initials: F
authors.lastname: Grabellus
authors.forename: G
authors.initials: G
authors.lastname: Mall
authors.forename: P A
authors.initials: PA
authors.lastname: Schnabel
authors.forename: H
authors.initials: H
authors.lastname: Wieneke
authors.forename: U
authors.initials: U
authors.lastname: Pfeifer
authors.forename: C
authors.initials: C
authors.lastname: Kersting
authors.forename: K J
authors.initials: KJ
authors.lastname: Schmitz
authors.forename: J
authors.initials: J
authors.lastname: Wohlschläger
authors.forename: H H
authors.initials: HH
authors.lastname: Sigusch
authors.forename: E
authors.initials: E
authors.lastname: Bierhoff
authors.forename: M
authors.initials: M
authors.lastname: Kamler
authors.forename: H-H
authors.initials: HH
authors.lastname: Scheld
authors.forename: H A
authors.initials: HA
authors.lastname: Baba
mesh_terms: D000368:Aged; D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology; D003937:Diagnosis, Differential; D004696:Endocarditis / Q000175:diagnosis / Q000276:immunology / Q000473:pathology; D004804:Eosinophils / Q000276:immunology* / Q000473:pathology; D005260:Female; D006331:Heart Diseases / Q000175:diagnosis / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D037181:Lectins, C-Type; D008297:Male; D051379:Mice; D008875:Middle Aged; D009205:Myocarditis / Q000175:diagnosis / Q000276:immunology / Q000473:pathology; D000099192:CD69 Antigens
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D037181:Lectins, C-Type; D000099192:CD69 Antigens