[Show abstract][Hide abstract] ABSTRACT: Background:
Mycosis fungoides (MF) and the Sézary syndrome (SS) are non-Hodgkin's lymphomas that present with cutaneous lesions. Sézary syndrome is characterized by blood involvement, exfoliative eryrthroderma, lymphadenopathy, pruritus, keratoderma, and immunosuppression. This study was to estimate the prevalence of palmoplantar keratoderma and tinea pedis in Sézary syndrome and to analyze the effectiveness of anti-fungal treatment.
We conducted a retrospective review of 1562 prospectively collected patients at the MD Anderson Cancer Center Cutaneous Lymphoma Clinic over sixteen years. All patients' palms and soles were evaluated for clinical evidence of keratoderma (hyperkeratosis) and for dermatophytosis (tinea pedis or unguum) by examining scales under 10% potassium hydroxide by light microscopy for hyphae.
Of 138 Sézary syndrome patients (88 men, 50 women, median age at diagnosis 64 years), 85 (61.6%) had palmoplantar keratoderma; 45 of the 85 Sézary syndrome patients (52.9%) also had coexisting tinea pedis. Only 14 (10.1%) had tinea pedis without keratoderma. Treatment for tinea pedis resulted in microscopy cure of keratoderma in 12 of 45 (26.7%) patients and clinical improvement.
The prevalence of palmoplantar keratoderma in Sézary syndrome is 61.6%, with co-existing tinea pedis found in 52.9%. Palmoplantar keratoderma with tinea pedis showed clinical improvement with fungicidal therapy suggesting that tinea often contributes to the pathogenesis and severity of Sézary syndrome-related keratoderma.
Full-text · Article · Oct 2012 · International journal of dermatology
[Show abstract][Hide abstract] ABSTRACT: B-cell lymphoproliferative disorders are a continuum from benign cutaneous lymphoid hyperplasia (CLH) or "pseudolymphoma" to primary cutaneous B-cell lymphoma (PCBCL). Historically, CLH was treated with a combination of antibiotics, topical or intralesional corticosteroids, and/or localized radiotherapy. Rituximab, a monoclonal antibody that targets the CD20 marker on B cells, is an effective and well-reported treatment for PCBCL. We review the pathogenesis and current treatments of B-cell lymphoproliferative disorders and assess the role of rituximab for potential therapy in the setting of refractory CLH. We describe a case of CLH that was treated with intralesional rituximab. The patient had notable clinical improvement over the treatment period with rituximab. Because of some persistent and recurrent erythematous areas, topical tacrolimus was initiated, with significant clinical improvement. There were no reported side effects. Management of CLH with intralesional rituximab has been described. The treatment presented in this report substantiates rituximab as a reasonable therapeutic option for refractory CLH after failure of several other widely accepted treatments. Treatment with intralesional rituximab should be reserved for patients with documented CD20(+) lesions.