fibrin and Erythema-Multiforme

In a prospective study of erythema multiforme, forty-two cases were selected with the use of defined criteria. In thirty-three cases (79%), the erythema multiforme occurred following a lesion of recurrent herpes simplex; in four cases (10%), it was related to administration of a sulfonamide drug. Herpes-associated erythema multiforme (HEM) was largely recurrent erythema multiforme minor and was characterized histopathologically by inflammatory changes, such as spongiosis and exocytosis, and by focal liquefaction degeneration of the basal cell zone of the epidermis. Sulfa-associated erythema multiforme (SEM) was a nonrecurrent illness with widespread cutaneous and mucosal damage associated with prominent histologic necrosis of epidermal cells. The deposition of C3 and fibrin along the dermoepidermal junction and the deposition of IgM, C3, and fibrin around dermal blood vessels by immunofluorescence microscopy were similar in both groups. Although HEM and SEM may have somewhat different clinical and histologic features, there is significant overlap in the pattern of tissue damage.

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Complement C3; Epidermis; Erythema Multiforme; Female; Fibrin; Herpes Simplex; Humans; Immunoglobulin M; Male; Middle Aged; Necrosis; Prospective Studies; Recurrence; Sulfonamides

The immunologic parameters of 23 patients with erythema multiforme who were seen by us (17 patients) or who had biopsies sent for immunofluorescence testing (6 cases) are reviewed. Biopsy specimens were sectioned and tested with labeled antisera to human IgG, IgA, IgM, C3 and fibrin. Fourteen biopsies showed IgM deposits in the superficial blood vessels, 13 demonstrated C3, 15 showed fibrin deposition, and 1 biopsy showed IgA deposition. All biopsies were negative for IgG. Eight serum samples tested by indirect IF were negative for skin-reactive antibodies. In addition to IF testing, serum samples from 20 patients were tested for circulating immune complexes with a Clq binding radioassay and a monoclonal rheumatoid factor (mRF) inhibition assay. Immune complexes were not detected by the Clq binding assay, but 6 of 20 serum samples demonstrated low to moderate levels of immune complexes by the mRF inhibition assay. By sucrose density gradient ultracentrifugation in the mRF-reactive material in one serum sample sedimented in high molecular weight fractions and also demonstrated anticomplementary activity. These findings suggest that immune complex formation and subsequent deposition in the cutaneous microvasculature may play a role in the pathogenesis of erythema multiforme.

Topics: Antigen-Antibody Complex; Complement C3; Erythema Multiforme; Fibrin; Fluorescent Antibody Technique; Humans; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Skin

Topics: Aged; Biopsy; Diagnosis, Differential; Erythema Multiforme; Female; Fibrin; Fibrinogen; Humans; Leukoplakia; Lichen Planus; Male; Microscopy, Fluorescence; Microtomy; Mouth Diseases; Mouth Mucosa; Pemphigus; Staining and Labeling

Topics: Blister; Dapsone; Dermatitis Herpetiformis; Diagnosis, Differential; Erythema Multiforme; Fibrin; Fluorescent Antibody Technique; Humans; Pemphigus; Skin; Staining and Labeling