Examination of the patient’s bloodĭemonstrated a T-cell receptor gamma chain gene rearrangement, indicating evidence of a monoclonal population of T-cells.Ĭomputerized tomography of the chest, abdomen, and pelvis revealed bilateral axillary, inguinal, and iliac chain lymphadenopathy.Ī positron emission tomography scan showed bilateral axillary uptake and mild diffuse omental uptake.įigure 5. Antibody testsįor hepatitis A, B, and C and human T-lymphotropic virus types 1 and 2 were nonreactive. Beta-2-microglobulin level, erythrocyte sedimentation rate, and coagulation lab values were all normal. White bloodĬell count was 21,000/mm³ (normal 4,800 to 10,800/mm³) with 37 percent atypical lymphocytes the peripheral smear showed Sezary-likeĬells. AspartateĪminotransferase was 54 U/L (normal 0 to 37 U/L) and lactate dehydrogenase was 647 U/L (normal 105 to 233 U/L). No fluid was expressed from the tiny pustules on his palms. The plaques on his palms and soles were KOH negative. Pitted, thickened and dystrophic toenails Diffuse hyperkeratotis of the solesįigure 4. Also noted was marked xerosis over his trunk and extremities with some subtleįigure 3. Pitted, thickened, and dystrophic (Figure 4). Soles had coalescent hyperkeratotic plaques with a few small pustules on his hands (Figures 2 and 3). There was shotty cervical and impressive bilateral inguinal lymphadenopathy. His oropharynx showed violaceous discoloration On exam, the patient had large, soft confluent plaques on his scalp (Figure 1). Coalescent hyperkeratotic plaques with small pustules on the palms Large, soft confluent plaques of the scalpįigure 2. He had no family history of dermatologicįigure 1. Up to this point was a trial of a low potency topical corticosteroid to his hands. He denied a history of psoriasis or dyshidrosis. Review of systems and past medical history were negative. He also had an eight-month history of plaques on his scalp. Night sweats, fatigue, and episodes of fever and chills. Prior to presentation, generalized lymph node enlargement was noted on a routine physical exam, after which he began experiencing Thickness and roughness of the skin on the palms and soles, along with crumbling of his fingernails and toenails. Of acquired PPK as a potential harbinger to PTCL.Ī 27-year-old African-American male was referred to Wilford Hall Medical Center for evaluation of a 14-month history of increasing PPK that preceded the diagnosis of peripheral T-cell lymphoma (PTCL) by 14 months. The acquired form has been described as a paraneoplastic finding in a variety of malignancies or canĭevelop, as well as a result of direct involvement of the skin by cutaneous T-cell lymphoma (CTCL). Palmoplantar keratoderma (PPK) is an inherited or acquired condition characterized by diffuse or localized hyperkeratosis Skin Surgery Center, Winston-Salem, North Carolina AbstractĪ 27-year-old male with an acquired severe, diffuse palmoplantar keratoderma as the initial sign of peripheral T-cell lymphoma Wilford Hall Medical Center, San Antonio, Texas. Wendi E Wohltmann MD (Maj USAF MC FS) 1, Daniel M MacAlpine MD 2, Darryl Shaw Hodson MD 3 Dermatology Online Journal 16 (5): 3 1. Palmoplantar keratoderma as the initial sign in a peripheral T-cell lymphoma
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