Volume 81, Issue 1 pp. 27-32
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Epidermolysis bullosa acquisita induced by GM-CSF: a role for eosinophils in treatment-related toxicity

Jeffery C. Ward

Jeffery C. Ward

Department of Medicine, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

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Jeffrey B. Gitlin

Jeffrey B. Gitlin

Department of Medicine, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

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Daniel J. Garry

Daniel J. Garry

Department of Medicine, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

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Aminah Jatoi

Aminah Jatoi

Department of Medicine, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

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Sharon D. Luikart

Sharon D. Luikart

Department of Medicine, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

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Brian D. Zelickson

Brian D. Zelickson

Department of Dermatology, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

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Mark V. Dahl

Mark V. Dahl

Department of Dermatology, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

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Keith M. Skubitz

Corresponding Author

Keith M. Skubitz

Department of Medicine, University of Minnesota Medical School, and Masonic Cancer Center, Minneapolis, Minnesota

Dr K. M. Skubitz, Box 325 University Hospital, Minneapolis, MN 55455, U.S.A.Search for more papers by this author
First published: May 1992
Citations: 23

Abstract

A patient treated with granulocyte-macrophage colony-stimulating factor (GM-CSF) developed eosinophilia and epidermolysis bullosa acquisita. The bullae were subepi-dermal, and filled with an inflammatory infiltrate composed predominantly of eosinophils. Immunofluorescence studies disclosed linear deposition of IgG, IgA and C3 at the basement membrane zone and immunoelectron microscopy demonstrated antibody deposition in the lamina densa and sub-lamina densa region; however, the patient's serum did not contain circulating antibody to basement membrane zone antigens. Staining with monoclonal antibodies revealed dense deposits of both eosinophil peroxidase and eosinophil major basic protein at the dermal–epidermal junction. The eosinophilia and skin lesions resolved upon discontinuation of GM-CSF. This case provides evidence for two hypotheses: (1) GM-CSF induced proliferation and activation of eosinophils may contribute to some of the toxicities of GM-CSF treatment, and (2) activated granulocytes, including eosinophils, may mediate blister formation in epidermolysis bullosa acquisita.

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