Der Hautarzt

, Volume 58, Issue 4, pp 347–360

Eosinophile Dermatosen

CME Weiterbildung • Zertifizierte Fortbildung

Zusammenfassung

Der eosinophile Granulozyt (e. G.) ist angesichts seiner morphologischen und funktionellen Eigenschaften in Abwehrmechanismen, immunologische Reaktionen und proentzündliche/neoplastische Prozesse eingebunden. Die zunehmende Identifikation pathophysiologischer Vorgänge in den e. G. auf molekularer Ebene gestattet heute weitaus häufiger die Abgrenzung zwischen reaktiver (sekundärer) und klonaler Eosinophilie einschließlich des idiopathischen Hypereosinophiliesyndroms. Es soll in diesem Beitrag auf das Spektrum dermatologischer Krankheitsbilder hingewiesen werden, die häufig mit einer Eosinophilie assoziiert sind. Zusätzlich werden dermatologische Erkrankungen mit persistierender Eosinophilie charakterisiert. Beide Gruppen sind den reaktiven Eosinophilieformen zuzuordnen. Im Hinblick auf die differenzialdiagnostische Bedeutung erfolgt eine Berücksichtigung des Hypereosinophiliesyndroms, zumal hier aktuell selektive Targets erkannt (z. B. IL-5, CD52) und durch monoklonale Antikörper wie Mepolizumab, Alemtuzumab oder SCH55700 genutzt werden können.

Schlüsselwörter

Eosinophilie Eosinophile Dermatosen Hypereosinophiliesyndrom Therapie Eosinophiler Granulozyt 

Abkürzungsverzeichnis

CCR3

CC-Chemokinrezeptor 3

ECP

Eosinophiles kationisches Protein

EDN

Eosinophil-derived neurotoxin

e. G.

Eosinophile(r) Granulozyt(en)

EMEA

European Medicines Evaluations Agency (europäische Zulassungsbehörde)

EPF

Eosinophile pustulöse Follikulitis

EPO

Eosinophile Peroxidase

FIP1-L1

FIP1-like-1(-Gen)

FISH

Interphase fluorescent in situ hybridization

GM-CSF

Granulocyte-macrophage colony-stimulating factor

HE

Hämatoxylin-Eosin

HES

Hypereosinophiliesyndrom

HIES

Hyperimmunglobulin-E-Syndrom

ICAM

Intercellular adhesion molecule

IL-5

Interleukin-5

IVIG

Intravenöse Immunglobuline

LTB4

Leukotrien B4

MBP

Major basic protein

PAF

Plättchenaktivierungsfaktor

PAS

Periodic acid-Schiff (Reagenz)

PDGFR α

Platelet-derived growth factor receptor α

PDGFR β

Platelet-derived growth factor receptor β

RANTES

Regulated and normal T cell expressed and secreted

RT-PCR

Reverse-transcription polymerase chain reaction

TCR

T-cell-Rezeptor

TGF β

Transforming growth factor β

Eosinophilic dermatoses

Abstract

Morphological and functional properties of the eosinophilic granulocyte (e. G.) feature this haematopoietic stem cell-derived cell type as an important cellular component of defense mechanisms, immunologic reactions and proinflammatory/neoplastic processes. Over the last decade significant advances of the molecular pathophysiology of eosinophilic disorders enable increasingly the distinction between the more common reactive (secondary) and clonal eosinophilia including the hypereosinophilic syndrome. This review features a comprehensive clinical summary of dermatological disorders that are frequently associated with transient or persistent eosinophilia belonging to the reactive eosinophilia. The hypereosinophilic syndrome is a subset of idiopathic eosinophilia frequently associated with major tissue targets as skin, heart and others. Therefore, the hypereosinophilic syndrome has to be considered as important differential diagnosis. Most recently, the identification of selective targets (e. g. IL-5, CD52) has translated into therapeutic approaches with monoclonal antibodies such as mepolizumab, alemtuzumab or SCH55700.

Keywords

Eosinophilia Eosinophilic dermatoses Hypereosinophilic syndrome Therapy Eosinophilic granulocyte 

Literatur

  1. 1.
    Antic M, Lautenschlager S, Itin PH (2006) Eosinophilic fasciitis 30 years after – What do we really know? Dermatology 213: 93–101CrossRefPubMedGoogle Scholar
  2. 2.
    Azouz EM, Saigal G, Rodriguez MM, Podda A (2005) Langerhans‘ cell histiocytosis: pathology, imaging and treatment of skeletal involvement. Pediatr Radiol 35: 103–115CrossRefPubMedGoogle Scholar
  3. 3.
    Boura P, Sarantopoulos A, Lefaki I et al. (2006) Eosinophilic cellulitis (Wells‘ syndrome) as a cutaneous reaction to the administration of adalimumab. Ann Rheum Dis 65: 839–840CrossRefPubMedGoogle Scholar
  4. 4.
    Chong WS, Thomas A, Goh CL (2006) Kimura’s disease and angiolymphoid hyperplasia with eosinophilia: two disease entities in the same patient. Case report and review of the literature. Int J Dermatol 45: 139–145CrossRefPubMedGoogle Scholar
  5. 5.
    Cools J, DeAngelo DJ, Gotlib J et al. (2003) A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes is a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 348: 1201–1214CrossRefPubMedGoogle Scholar
  6. 6.
    DeWitt CA, Bishop AB, Buescher LS, Stone SP (2006) Hyperimmunglobulin E syndrome: two cases and a review of the literature. J Am Acad Dermatol 54: 855–865CrossRefPubMedGoogle Scholar
  7. 7.
    Ellis E, Scheinfeld N (2004) Eosinophilic pustular folliculitis – a comprehensive review of treatment options. Am J Clin Dermatol 5: 189–197Google Scholar
  8. 8.
    Fletcher S, Bain B (2007) Diagnosis and treatment of hypereosinophilic syndromes. Curr Opin Hematol 14: 37–42PubMedGoogle Scholar
  9. 9.
    Gleich GJ, Adolphson CR, Leiferman KM (1992) Eosinophils. In: Gallin JI, Goldstein IM, Snyderman R (eds) Inflammation – basic principles and clinical correlates, 2nd edn. Raven Press, New York, pp 663–700Google Scholar
  10. 10.
    Gotlib J, Cools J, Malone JM et al. (2004) The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukaemia: implications for diagnosis, classification, and management. Blood 103: 2879–2891CrossRefPubMedGoogle Scholar
  11. 11.
    Gotlib J, Cross NCP, Gilliland DG (2006) Eosinophilic disorders: molecular pathogenesis, new classification, and modern therapy. Best Pract Res Clin Haematol 19: 535–569CrossRefPubMedGoogle Scholar
  12. 12.
    Grimbacher B, Holland SM, Puck JM (2005) Hyper-IgE syndromes. Immunol Rev 203: 244–250CrossRefPubMedGoogle Scholar
  13. 13.
    Imanka A, Tarutani M, Itoh H et al. (2004) Langerhans cell histiocytosis involving the skin of an elderly woman: a satisfactory remission with oral prednisolone alone. J Dermatol 31: 1023–1026PubMedGoogle Scholar
  14. 14.
    Klion AD, Law MA, Noel P et al. (2004) Safety and efficacy of the monoclonal anti-interleukin-5 antibody SCH55700 in the treatment of patients with hypereosinophilic syndrome. Blood 103: 2939–2941CrossRefPubMedGoogle Scholar
  15. 15.
    Liesveld JL, Abboud CN (1991) State of the art: hypereosinophilic syndromes. Blood 5: 29–37CrossRefGoogle Scholar
  16. 16.
    Moossavi M, Mehregan DR (2003) Wells‘ syndrome: a clinical and histopathologic review of seven cases. Int J Dermatol 42: 62–67CrossRefPubMedGoogle Scholar
  17. 17.
    Peters MS, Schroeter AL, Gleich GJ (1983) Immunofluorescence identification of eosinophil granule major basic protein in the flame figures of Wells‘ syndrome. Br J Dermatol 109: 141–148CrossRefPubMedGoogle Scholar
  18. 18.
    Sefcick A, Sowter D, DasGupta E et al. (2004) Alemtuzumab therapy for refractory hypereosinophilic syndrome. Br J Haematol 124: 558–559CrossRefPubMedGoogle Scholar
  19. 19.
    Simon D, Braathen LR, Simon HU (2005) Anti-interleukin-5 antibody therapy in eosinophilic diseases. Pathobiol 72: 287–292CrossRefGoogle Scholar
  20. 20.
    Szeimies RM, Meurer M (1993) Tryptophan-assoziiertes Eosinophilie-Myalgie-Syndrom. Dtsch Med Wochenschr 118: 213–220PubMedGoogle Scholar
  21. 21.
    Tefferi A (2005) Modern diagnosis and treatment of primary eosinophilia. Acta Haematol 114: 52–60CrossRefPubMedGoogle Scholar
  22. 22.
    Tefferi A, Patnaik M, Pardanani A (2006) Eosinophilia: secondary, clonal and idiopathic. Br J Haematol 133: 468–492CrossRefPubMedGoogle Scholar
  23. 23.
    Teixeira MM, Williams TJ, Hellewell PG (1995) Mechanisms and pharmacological manipulation of eosinophil accumulation in vivo. TiPS 16: 418–423PubMedGoogle Scholar
  24. 24.
    Wilkins HJ, Crane MM, Copeland K, Williams WV (2005) Hypereosinophilic syndrome: an update. Am J Haematol 80: 148–157CrossRefGoogle Scholar
  25. 25.
    Wozel G (1996) Dapson – Pharmakologie, Wirkmechanismus und klinischer Einsatz. Georg Thieme, Stuttgart New YorkGoogle Scholar
  26. 26.
    Ziemer M, Böer A (2005) Eosinophilic pustular folliculitis in infancy – not a distinctive inflammatory disease of the skin. Am J Dermatopathol 27: 443–455CrossRefPubMedGoogle Scholar

Copyright information

© Springer Medizin Verlag 2007

Authors and Affiliations

  1. 1.Klinik und Poliklinik für DermatologieUniversitätsklinikum Carl Gustav Carus Dresden an der Technischen Universität DresdenDresdenDeutschland

Personalised recommendations