Dermatomal lichenoid graft‐versus‐host disease within herpes zoster scars

Case 1 A 23‐year‐old woman was diagnosed with chronic myelogenous leukemia in 1997. In 1999, she underwent allogeneic bone marrow transplantation (BMT) from a human leukocyte antigen (HLA)‐matched sibling donor after induction chemotherapy with cyclophosphamide and busulfan. At day 46 after BMT, she was discharged with a medication regimen which included cyclosporine, fluconazole, acyclovir, and trimethoprim/sulfamethoxazole. Five months later she developed clusters of vesicles and pain over the right inframammary and right infrascapular areas corresponding to the T5–T6 dermatomes. Herpes zoster infection was diagnosed clinically and acyclovir therapy (3 × 10 mg/kg/day) was started. All lesions healed within 2 weeks leaving atrophic cicatrices and postinflammatory hyperpigmentation. Eight months after BMT, she presented with erythematous and hyperpigmented macules on the malar areas. Follicular hyperkeratosis on the chest and interscapular area, reticulated white plaques on the buccal mucosa, and significant xerosis were also observed on dermatologic examination. Dermatopathologic examination of a biopsy specimen obtained from the lesions on the face was evaluated to be consistent with “atrophic folliculocentric lichen planus.” Two weeks later she was admitted again for new lesions on the trunk. Flat, violaceous, slightly scaly papules were located exactly on the dermatomes of the previous herpes zoster infection ( Fig. 1). A biopsy specimen of these lesions showed a dense, subepidermal, band‐like, lymphocytic inflammatory infiltrate, vacuolar degeneration of the basal cell layer, and scattered dyskeratotic cells in the epidermis, confirming the diagnosis of lichenoid graft‐versus‐host disease (GVHD) ( Fig. 2a and 2b). 1Lichenoid lesions on the dermatomes of a previous herpes zoster infection2(a) Dense, subepidermal, band‐like, lymphocytic infiltrate, vacuolar degeneration of the basal cell layer, and dyskeratotic cells in the epidermis (hematoxylin and eosin, ¥ 50). (b) Vacuolar degeneration of the basal cell layer,scattered dyskeratotic cells, and satellite cell necrosis (hematoxylin and eosin, ¥ 100)Case 2 A 47‐year‐old woman was diagnosed with chronic myelogenous leukemia in 1998. She underwent allogeneic BMT from an HLA‐matched sibling donor after a preoperative chemotherapy regimen with cyclophosphamide and busulfan in 1999. At day 20, she developed erythema and a burning sensation on her palms and soles and erythema, hyperpigmentation, and desquamation on her face and neck. The lesions increased gradually within 3 weeks. Dermatologic examination on day 40 revealed widespread violaceous, lichenoid papules and plaques on the face, neck, trunk, upper extremities, and genital region. There were also reticulated, white plaques on the buccal mucosa. A biopsy obtained from the lesions on the neck showed findings consistent with both acute and lichenoid GVHD. The skin lesions resolved within 1 month after prednisolone therapy leaving postinflammatory hyperpigmentation. Seven months later, she developed herpes zoster infection involving the right neck, shoulder, chest, and scapular area corresponding to the C3–C4 dermatomes. She was treated with famcyclovir for 10 days and the lesions healed completely. Three months after this infection, new, violaceous, lichenoid papular lesions were noted which remained confined to the dermatomes affected by the herpes zoster infection ( Fig. 3). Dermatopathologic examination revealed dyskeratotic cells, focal vacuolization in the basal cell layer, and a superficial band‐like lymphocytic infiltrate in the papillary dermis, consistent with lichenoid chronic GVHD. 3Lichenoid papules located on C3–C4 dermatomes