Hypopigmented Interface T-Cell Dyscrasia and Hypopigmented Mycosis Fungoides: A Comparative Study

Hypopigmented interface T-cell dyscrasia (HITCD) is a distinct form of lymphoid dyscrasia that may progress to hypopigmented mycosis fungoides (HMF). We compared both diseases as regards their CD4/CD8 phenotype and expression of granzyme B and tumor necrosis factor-alpha (TNF-α) and how these are affected by narrow-band UVB (nb-UVB). The study included 11 patients with HITCD and 9 patients with HMF. They received nb-UVB thrice weekly until complete repigmentation or a maximum of 48 sessions. Pretreatment and posttreatment biopsies were stained using anti CD4, CD8, TNF-α, and granzyme B monoclonal antibodies. Epidermal lymphocytes were CD8 predominant in 54.5% and 66.7% of HITCD and HMF cases, respectively, whereas dermal lymphocytes were CD4 predominant in 63.6% and 66.7%, respectively. Significantly, more dermal infiltrate was encountered in HMF (P = 0.041). In both diseases, granzyme B was only expressed in the dermis, whereas TNF-α was expressed both in the epidermis and dermis. No difference existed as regards the number of sessions needed to achieve repigmentation or cumulative nb-UVB dose reached at end of study. (P > 0.05). Narrow-band UVB significantly reduced only the epidermal lymphocytes in both diseases (P ≤ 0.05) with their complete disappearance in 8 (72.7%) HITCD and 6 (66.7%) HMF cases. In both diseases, nb-UVB did not affect granzyme B or TNF-α expression (P > 0.05). In conclusion, both diseases share the same phenotype, with HITCD being a milder form of T-cell dysfunction. In both diseases, epidermal lymphocytes are mainly CD8-exhausted cells lacking cytotoxicity, whereas dermal cells are mostly reactive cells exerting antitumor cytotoxicity. Tumor necrosis factor-alpha mediates hypopigmentation in both diseases and prevents disease progression. Repigmentation after nb-UVB in both diseases occurs before and independently from disappearance of the dermal infiltrate.