RESUMEN
A 66-year-old female with a history of two renal transplants due to recurrent thrombotic thrombocytopenic purpura presented to clinic with multiple lesions identified to be non-metastatic cutaneous squamous cell carcinoma (CSCC). The patient previously underwent multiple Mohs procedures and radiation therapy treatment but continued to develop CSCC lesions with increasing frequency. After discussing multiple treatment options, it was elected to pursue treatment with Talimogene laherparepvec (T-VEC) given the systemic immune responses it can cause, with low theoretical risk of graft rejection. After starting intratumoral T-VEC injections, treated lesions began to decrease in size, and a reduction in the rate of new CSCC lesions was observed. Treatment was held due to unrelated renal complications during which time new CSCCs developed. Patient was restarted on T-VEC therapy with no recurrent renal issues. Upon reinitiating treatment, injected and non-injected lesions showed reduction in size, and the development of new lesions again ceased. One injected lesion was resected via Mohs micrographic surgery due to its size and discomfort. On sectioning, this demonstrated an exuberant lymphocytic perivascular infiltrate which was consistent with treatment response to T-VEC, with little active tumor. With high rates of non-melanoma skin cancer in renal transplant patients, their transplant status significantly limits treatment options, specifically with regards to anti-PD-1 therapy. This case suggests T-VEC can generate local and systemic immune responses in the setting of immunosuppression and that T-VEC may be a beneficial therapeutic option for transplant patients with CSCC.
RESUMEN
BACKGROUND: Experimental evidences have shown that tumor necrosis factor (TNF)-α may play a role in the pathogenesis of nonsegmental vitiligo, and successful cases of vitiligo treated with TNF-α inhibitors have been recently reported. MATERIALS AND METHODS: Two cases of refractory generalized vitiligo, which showed high tissue levels of TNF-α, were commenced anti-TNF-α antibody etanercept 50 mg weekly. A retrospective study, considering chart review and immunohistochemical staining for TNF-α, was then carried out on eight additional patients affected by untreated vitiligo. RESULTS: Etanercept achieved improvement of vitiligo in two patients at 6-month follow-up. Five out of eight specimens showed a strong cytoplasmic staining for TNF-α. Considering all 10 cases, patients with a strong TNF-α staining were characterized by a higher vitiligo disease activity score than patients with a weak staining. DISCUSSION: These findings, albeit limited in significance by the low number of cases and the retrospective nature of the study, confirm a probable role of TNF-α in the pathogenesis of vitiligo. The intensity of TNF-α staining in vitiligo lesions may be worth to be further studied as a biomarker for potentially successful anti-TNF-α treatment of nonsegmental vitiligo in cases refractory to conventional treatment.