Gelling Your Dermatology Nursing Practice: A Practical Guide for Managing the Treatment of Mycosis Fungoides Cutaneous T-Cell Lymphoma With Mechlorethamine Gel.

Mycosis fungoides is the most common form of cutaneous T-cell lymphoma. Stage IA and IB mycosis fungoides cutaneous T-cell lymphoma can be effectively controlled by skin-directed therapies such as the mechlorethamine gel approved by the Food and Drug Administration. Dermatology nurses play a key role in promoting good patient compliance through patient education about mycosis fungoides cutaneous T-cell lymphoma disease, proper administration of mechlorethamine gel, and connecting patients with patient assistance programs or other supportive services. This article provides the dermatology nurse with a background about early-stage mycosis fungoides cutaneous T-cell lymphoma, skin-directed treatment options, questions that a patient may ask about mycosis fungoides cutaneous T-cell lymphoma and mechlorethamine gel, and patient education tools such as questions dermatology nurses may ask of their patients and a patient handout outlining mechlorethamine gel administration.

Optimizing Care and Compliance for the Treatment of Mycosis Fungoides Cutaneous T-Cell Lymphoma With Mechlorethamine Gel.

BACKGROUND: Mycosis fungoides is the most common form of cutaneous T-cell lymphoma (MF-CTCL). Quality nursing care is necessary for effective diagnosis and treatment of patients with MF-CTCL. Early-stage MF-CTCL (stages Ia and Ib) is most often managed in both dermatology and multidisciplinary settings. These stages can be effectively controlled by skin-directed therapies such as mechlorethamine gel (Valchlor®). Topical mechlorethamine has been used since the 1940s as an alkylating agent; however, compounded formulas have disadvantages that limit patient compliance. In contrast, newly approved mechlorethamine gel has demonstrated an efficacious and well-tolerated profile that has longer stability and is quicker to dry than its compounded counterpart. OBJECTIVES: This article aims to provide recommendations for optimal nursing care of patients who have been diagnosed with stage Ia or Ib MF-CTCL. METHODS: Four real-world patient cases are examined, along with practical considerations for the use of mechlorethamine gel to treat patients with MF-CTCL. FINDINGS: Nurses can promote patient adherence through specific interventions and strategies, such as education about mechlorethamine gel, its mechanism of action, and safety and efficacy, as well as connecting patients with patient assistance programs or other supportive services.

Skin effector memory T cells do not recirculate and provide immune protection in alemtuzumab-treated CTCL patients.

Cutaneous T cell lymphoma (CTCL) is a cancer of skin-homing T cells with variants that include leukemic CTCL (L-CTCL), a malignancy of central memory T cells (T(CM)), and mycosis fungoides (MF), a malignancy of skin resident effector memory T cells (T(EM)). We report that low-dose alemtuzumab (αCD52) effectively treated patients with refractory L-CTCL but not MF. Alemtuzumab depleted all T cells in blood and depleted both benign and malignant T(CM) from skin, but a diverse population of skin resident T(EM) remained in skin after therapy. T cell depletion with alemtuzumab required the presence of neutrophils, a cell type frequent in blood but rare in normal skin. These data suggest that T(CM) were depleted because they recirculate between the blood and the skin, whereas skin resident T(EM) were spared because they are sessile and non-recirculating. After alemtuzumab treatment, skin T cells produced lower amounts of interleukin-4 and higher amounts of interferon-γ. Moreover, there was a marked lack of infections in alemtuzumab-treated L-CTCL patients despite the complete absence of T cells in the blood, suggesting that skin resident T(EM) can protect the skin from pathogens even in the absence of T cell recruitment from the circulation. Together, these data suggest that alemtuzumab may treat refractory L-CTCL without severely compromising the immune response to infection by depleting circulating T(CM) but sparing the skin resident T(EM) that provide local immune protection of the skin.