Here, we report a patient with serum factor positive UVA-induced solar urticaria unresponsive to omalizumab. A 64-year-old Caucasian woman presented with a 28-year history of severe solar urticaria. Wheals developed within 3 min of exposure to sunlight, including through window glass. Sunlight exposure repeatedly provoked systemic symptoms with nausea and cardiovascular reactions. The relevant induction spectrum was found to lie between 340 and 400 nm (UVA1). The minimal dose was positive at 10 J/cm 2 and a profound urticarial response was elicited in all test fields. Intradermal skin test with UVAirradiated autologous serum was positive implicating the presence of a serum factor. FBC, ANA, liver and renal profiles were normal. Serum IgE was 12,6 kU/L. Treatment with sunscreens, antihistamines, including high-dose desloratadine 20 mg/die in combination with ranitidine 300 mg/die was ineffective. Light hardening with narrow band UVB over 6 months resulted in marginal, short-lived reduction in symptoms. Two grams of Mycophenolate mofetil daily showed no effect and nine cycles of plasmapheresis resulted in only very transient improvement in the severity of symptoms.Omalizumab was commenced at a dose of 150 mg every 4 weeks. Following three treatment cycles, she reported no improvement, in contrast she felt symptoms had worsened. On

Mycosis fungoides (MF) is the most common variant of primary cutaneous T‐cell lymphoma, and decreased forkhead box P3 (FoxP3) expression has been reported in MF late stages. Hypoxia‐inducible factor 1 alpha (HIF‐1α) may regulate FoxP3 expression; however, it is unknown whether HIF‐1α is expressed in the CD4+ T cells of MF patients and how it could affect the expression of FoxP3. Therefore, we evaluated the expression of HIF‐1α and FoxP3 in CD4+ T cells obtained from the skin lesions of MF patients. We found increased cell proliferation and an increase in CD4+ T cells with an aberrant phenotype among early stage MF patients. HIF‐1α was overexpressed in these CD4+ T cells. In addition, we found a decrease in the percentage of FoxP3+ cells both in the skin of MF patients, when compared with control skin samples, and with disease progression. In addition, a negative correlation was established between HIF‐1α and FoxP3 expression. Skin HIF‐1α expression in MF patients correlated with the extent of the affected area and increased with the disease progression. Finally, we showed that ex vivo inhibition of HIF‐1α degradation increases the percentage of FoxP3+ T cells in skin lesions. Our results suggest that overexpression of HIF‐1α affects the levels of FoxP3 in MF patients, which could have relevant implications in terms of disease outcome.

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Myxoid neurofibroma (MN) is a benign tumor of perineural cell origin, which is demonstrated with a positive immunohistochemical staining for S-100 protein. The most common locations of the MN are the face, shoulders, arms, periungual and in the feet. To our knowledge, this is the first time that a trunk location is reported. MN should be included in the differential diagnosis of tumors on this location.

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