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subepidermal cleft

Differential Diagnosis:

Pathophysiology:

■ Erythema multiforme minor and major are thought to represent a cell-mediated immune response to complexes formed between exogenous antigens (e.g., viral antigens or from reactive metabolites of drugs) and host tissues.

■ It is thought that these host cell-antigen complexes lead to

■ release of soluble cytokines by cytotoxic T-lymphocytes (e.g., tumor necrosis factor-a and others), which cause keratinocyte necrosis, and

■ increased expression of keratinocyte Fas ligand (FasL), thereby activating the keratinocyte Fas-FasL pathway and culminating in massive keratinocyte apoptosis

References:

1. Fritsch PO, Sidoroff A. Drug-induced Stevens-Johnson syndrome/toxic epidermal necrolysis. Am J Clin Dermatol 2000; 1(6):349-360.

2. Finan MC, Schroeter AL. Cutaneous immunofluorescence study of erythema multiforme: correlation with light microscopic patterns and etiologic agents. J Am Acad Dermatol 1984; 10(3):497-506.

3. Paul C, Wolkenstein P, Adle H, et al. Apoptosis as a mechanism of keratinocyte death in toxic epidermal necrolysis. Br J Derma-tol 1996; 134(4):710-714.

ACUTE GRAFT-VS.-HOST REACTION Clinical Presentation:

■ Systemic syndrome with fever and cutaneous, gastrointestinal, and hepatic manifestations

■ Typically develops 7 to 21 days postprocedure as complication of allogeneic hematopoeitic stem-cell transplantation or, rarely, as a congenital disease as a result of maternal lymphocytes establishing themselves in fetal circulation and reacting against the host

■ Sudden onset of blanching, erythematous morbilliform eruption that begins acrally, with predilection for the palms, soles, cheeks, and ears

■ May eventually become generalized with bulla formation, desquamation and mucous membrane involvement

Histology:

■ Sparse lymphocytic infiltrate obscures dermoepidermal junction (Fig. 2A)

■ Exocytosis of mononuclear cells into epidermis associated with focal spongiosis (Figs. 2A and B). Classically divided into four histopathologic grades

■ Lerner Grade I: Vacuolar alteration of basal keratinocytes

■ Lerner Grade II: "Satellite cell necrosis"; individually necrotic keratinocytes within the epidermis with adjacent lymphocytes (Figs. 2A and B)

■ Lerner Grade III: Subepidermal cleft formation

■ Lerner Grade IV: Complete, full-thickness loss of epidermis

Immunofluorescence: Direct Immunofluorescence:

■ Granular staining for IgM along the dermoepidermal junction

Clinicopathologic Correlation:

Clinical Feature

Histopathologic Correlate

Epidermal desquamation

Confluent vacuolar alteration of basal keratinocytes resulting in subepidermal cleft

Differential Diagnosis:

Acute Graft-vs.-Host Reaction

Erythema Multiforme/Toxic Epidermal

Dyskeratosis of follicular keratinocytes

Follicular involvement less likely

Pathophysiology:

■ Donor-derived CD8+ T lymphocytes recognize host cell antigens as foreign

■ These T cells react directly to "foreign" antigens bound to major histocompatibility complex (MHC) molecules and, through mediation by a variety of cytokines, including interleukin-2 and interferon-gamma, effect target/host organ necrosis

References:

1. Lerner KG, Kao GF, Storb R, et al. Histopathology of graft-versus-host reaction (GvHR) in human recipients of marrow from HLA-matched sibling donors. Transplant Proc 1974; 6:367.

2. Tsoi MS, Storb R, Jones E, et al. Deposition of IgM and C at the dermoepidermal junction in acute and chronic cutaneous graft-versus-host disease in man. J Immunol 1978; 120:1485.

Erythema Multiforme/

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