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Epidermolysis bullosa acquisita induced by GM‐CSF: a role for eosinophils in treatment‐related toxicity
Author(s) -
Ward Jeffery C.,
Gitlin Jeffrey B.,
Garry Daniel J.,
Jatoi Aminah,
Luikart Sharon D.,
Zelickson Brian D.,
Dahl Mark V.,
Skubitz Keith M.
Publication year - 1992
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1992.tb08166.x
Subject(s) - epidermolysis bullosa acquisita , lamina densa , eosinophilia , eosinophil , basement membrane , pathology , eosinophil peroxidase , immunology , dermoepidermal junction , immunoelectron microscopy , lamina lucida , medicine , antibody , bullous pemphigoid , dermis , ultrastructure , asthma , basal lamina
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.