Malignancy-associated pruritus can be the result of a neoplasm's local effect on tissue or due to the systemic reaction to malignancy. A systemic reaction to malignancy has been termed 'paraneoplastic itch' and can be the first sign of an underlying malignancy. Paraneoplastic itch is most commonly caused by lymphoproliferative malignancies, and severity of itch correlates with stage of disease in Hodgkin's lymphoma and polycythemia vera. Non-melanoma skin cancer is the most common type of malignancy-associated pruritus, and recent data indicate that pruritus is associated with more than one-third of non-melanoma skin cancers. Cutaneous T-cell lymphomas (CTCL), particularly more advanced stages, cause intractable pruritus and recent investigations into the pathophysiology of CTCL-associated itch have implicated cyotokine interleukin-31 as a putative mediator. Treatments that reduce itch in CTCL patients, such as histone deacetylase inhibitors (HDACi), Mogamulizumab, a novel monoclonal antibody against chemokine receptor type-4, and oral corticosteroids, have demonstrated a correlation between their anti-pruritic effect and reduced serum levels of interleukin-31.
Paraneoplastic itch occurs as the result of a systemic reaction to an underlying malignancy. Paraneoplastic itch is most commonly associated with lymphoproliferative malignancies and solid tumors that result in cholestasis. Paraneoplastic itch may occur in the absence of a primary rash or in association with dermatologic conditions such as erythroderma, acanthosis nigricans, dermatomyositis, Grover's disease, and eruptive seborrheic keratosis. Treatment of paraneoplastic itch is centered on targeting the underlying malignancy responsible for the systemic reaction. In cases of malignancy that are refractive to treatment, other therapies have been found to be effective for paraneoplastic itch, including selective serotonin reuptake inhibitors, mirtazapine, gabapentin, thalidomide, opioids, aprepitant, and histone deacetylase inhibitors.
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