Lymphomatoid keratosis: an epidermotropic type of cutaneous lymphoid hyperplasia: clinicopathological, immunohistochemical, and molecular biological study of 6 cases.
OBJECTIVE
To provide evidence that lymphomatoid keratosis should be categorized as an epidermotropic subtype of cutaneous lymphoid hyperplasia.


METHODS
Clinicopathological, immunohistochemical, and molecular biological studies of epidermotropic and dermal bandlike infiltrates of lymphocytes without necrotic keratinocytes, Civatte bodies, or Max-Joseph spaces and solar lentigo or seborrheic keratosis adjacent to the lesion, but with epidermal hyperplastic change (clinically scaly plaque) in cases of lymphomatoid keratosis. Conventional histopathologic study as well as immunohistochemical examinations for CD1a, CD3, CD4, CD8, CD20, and CD79a and S100 protein and genotypic examinations were performed.


METHODS
University departments comprising 2 sections of dermatology and 1 section of pathology.


METHODS
Ratio of T to B cells and of CD4(+) to CD8(+) cells, and the phenotype of epidermotropic cells were evaluated. Gene rearrangement of the immunoglobulin heavy chain gene and T-cell receptor (TCR)-beta and TCRgamma genes was also investigated by the polymerase chain reaction method.


RESULTS
Immunohistochemically, epidermotropic CD20(+) and/or CD79a(+) cells were present. In the upper dermal lymphocytic infiltrates, the CD3(+)/CD79a(+) cell ratio ranged from 5:5 to 8:2. The CD4(+)/CD8(+) cell ratio was within normal limits. Rearrangements of the TCRgamma gene were demonstrated in 2 cases and of the TCRbeta gene in 1 case.


CONCLUSIONS
Our results indicate that lymphomatoid keratosis is a clinically benign keratotic lesion but histologically malignant, simulating mycosis fungoides. Immunohistochemical findings showed a reaction pattern in all cases, but genotypical examination showed some clonal dermatoses. Therefore, "lymphomatoid" keratosis should be classed as a pseudolymphoma, namely, a subtype of cutaneous lymphoid hyperplasia with epidermotropism.
Arai
Eiichi
E
Department of Pathology, Saitama Medical Center, Saitama Medical University, Saitama, Japan. e_arai@saitama-med.ac.jp
Shimizu
Michio
M
Tsuchida
Tetsuya
T
Izaki
Seiichi
S
Ogawa
Fumihiro
F
Hirose
Takanori
T
D000328:Adult; D000368:Aged; D018951:Antigens, CD20; D001402:B-Lymphocytes / Q000276:immunology; D016516:CD4-CD8 Ratio; D051925:CD79 Antigens; D003937:Diagnosis, Differential; D005260:Female; D015321:Gene Rearrangement; D019674:Genes, T-Cell Receptor beta; D019675:Genes, T-Cell Receptor gamma; D006801:Humans; D007150:Immunohistochemistry; D007564:Japan; D007642:Keratosis / Q000175:diagnosis / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D008297:Male; D008499:Medical Records; D008875:Middle Aged; D008967:Molecular Biology; D016133:Polymerase Chain Reaction; D019310:Pseudolymphoma / Q000175:diagnosis / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D012189:Retrospective Studies; D012878:Skin Neoplasms / Q000175:diagnosis / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D013601:T-Lymphocytes / Q000276:immunology
D018951:Antigens, CD20; D051925:CD79 Antigens