A lichenoid infiltrate with vacuolar (liquefactive) degeneration of the basal keratinocytes is highly characteristic of acute GVHD. Note the presence of necrotic keratinocytes and pigment incontinence.
The lymphocytes may be adjacent to necrotic lymphocytes, so-called satellite cell necrosis. The inflammation obscures the dermal-epidermal junction. Other features that are typical include apoptosis at the base of epidermal rete pegs and dyskeratosis.
At the onset of acute GVHD, 81% of patients have skin involvement, 54% have GI involvement, and 50% have liver involvement (Martin).
Acutely, GVHD of the skin is one of the conditions exhibiting a "vacuolar interface dermatitis" pattern, characterized by intracytoplasmic vacuoles within the basal keratinocytes, along with a variable inflammatory infiltrate along the dermal-epidermal junction and pigment incontinence.
In the chronic form of GVHD, the dermis becomes diffusely fibrotic and there is no significant inflammation, mimicking scleroderma (Sternberg).
Graft versus host disease is common in bone marrow transplant patients. Scaly red patches or plaques are often seen on the acral skin, followed by other locations 10 to 21 days after tranplantation (Rapini).
The skin develops a pruitic maculopapular rash that can spread throughout the body, sparing the scalp. Severe cases may eventuate in skin blistering and even ulcerating.
Mild GVHD of the skin (Grade I) may be treated with topical steroids alone, but more severe skin GVHD and any degree of visceral GVHD involvement often requires high-dose systemic steroids.
Rapini RP.Practical Dermatopathology. Philadelphia, PA: Elsevier; 2005: 221-2.
Mills SE, ed. Sternberg's Diagnostic Surgical Pathology.4th Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004: 13.
Martin PJ, et al. A retrospective analysis of therapy for acute graft-versus-host disease: initial treatment. Blood. 1990 Oct 15;76(8):1464-72.