A clonal cutaneous CD30+ lymphoproliferative eruption in a patient with evidence of past exposure to hepatitis E

• Published in: International journal of dermatology 2000-07, Vol.39 (7), p.521-527
• Main Authors: Lemons-Estes, Freddye M., Capt, Hon Pak, Skelton, Henry, Smith, Kathleen J.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Diagnosis, Differential; Fingers; Gene Rearrangement, beta-Chain T-Cell Antigen Receptor; Hand Dermatoses - diagnosis; Hand Dermatoses - pathology; Hand Dermatoses - virology; Hepatitis E - complications; Human viral diseases; Humans; Immunohistochemistry; Infectious diseases; Lymphoma, Large-Cell, Anaplastic - diagnosis; Lymphoma, Large-Cell, Anaplastic - pathology; Lymphoma, Large-Cell, Anaplastic - virology; Male; Medical sciences; Microscopy, Electron; Middle Aged; Viral diseases; Viral hepatitis; Virion - ultrastructure
• ISSN: 0011-9059; 1365-4632
• DOI: 10.1046/j.1365-4362.2000.00986.x

The patient was a 52‐year‐old white man who had worked in remote areas of the world during the past 2 years, including an extended period in rural areas of Central Africa and in Central and South America. He had no acute illnesses during the 2‐year period except for rare, mild, upper respiratory tract infections. For approximately 1 year, however, he had developed recurrent, papular‐vesicular, slightly painful lesions on the fingers and palms, that spontaneously healed over weeks to months ( Fig. 1). The patient had no other concurrent illnesses and no abnormal laboratory findings, except for positive enzyme‐linked immunoabsorbent assay (ELISA) for immunoglobulin G (IgG) antibodies for hepatitis E virus (HEV) using a recombinant expressed HEV antigen (Genelabs Technologies, Inc., San Antonio). Prolonged treatment with minocycline did not appear to moderate the lesions. At approximately 2.5 years after the development of his first cutaneous lesion, however, the patient reported that he had had no new lesions for over 3 months. 1  Vesicular  lesion on the finger which regressed over a period of weeks A biopsy specimen showed an intraepidermal vesicle with prominent epidermal necrosis and reticular degeneration ( Fig. 2). Within the epidermis, there was a dense infiltrate of lymphoid cells. The majority of these cells were pleomorphic with prominent nucleoli and frequent mitotic figures ( Fig. 3). Sheets of atypical cells were found in the subjacent dermis. The infiltrate extended down into the reticular dermis. With extension into the dermis, the infiltrate became more polymorphous with more small lymphoid cells, large numbers of eosinophils, and some plasma cells located more deeply. 2 Intraepidermal  blister showing reticular degeneration and marked epidermotrophism of large atypical cells with extension into the dermis with a mixed infiltrate containing eosinophils and plasma cells (30×) 3 Intraepidermal  infiltrate of large atypical cells with extension into the dermis with a mixed infiltrate containing eosinophils and plasma cells (400×) Immunohistochemical stains for CD3 (DAKO), CD4 (Becton Dickinson), CD8 (Becton Dickinson), CD15 (LeuM1, Becton Dickinson), CD20 (L‐26, DAKO), CD30 (Ber‐H2, DAKO), CD45RO (UCHL1, DAKO), S‐100 protein (DAKO), T‐cell intracellular antigen (TIA) (Coulter), epithelial membrane antigen (EMA) (DAKO), KP‐1 (CD68, DAKO), MAC‐387 (DAKO), Epstein–Barr virus (EBV) latent membrane antigen‐1 (LMP‐1, DAKO), and EBV‐encoded nuclear ant