tomography scan of the abdomen and bone marrow biopsy, which excluded systemic disease. As there were no remnants of lesion, radiotherapy was not performed. Mycophenolate mofetil and tacrolimus ANH were reduced to half the previous dosage. There was no recurrence at 12-month follow-up.Cutaneous CD30+ ALTCL is characterized by the expression of CD30 (an activation marker for B or T cells) in more than 75% of cells, and can be subdivided mainly into a primary cutaneous form, defined by skin-only involvement at presentation, or a systemic form, with secondary skin involvement from a node-based lymphoma, or following transformation of mycosis fungoides. 5-6 The localization of PTLs in the skin, as well as the CD30+ ALTCL type, are very uncommon. 2-4 To our knowledge, only five cases of CD30+ PT ALTCL have been reported to date: three in kidney recipients, one in a heart transplant and the other in a combined liver and heart transplantation recipient. 2-4 Whereas classical primary cutaneous CD30+ ALTCL usually carries a good prognosis, CD30+ PT ALTCLs seem to pursue an aggressive course: the previously reported cases were characterized by multiple lesions at presentation and ⁄or a rapid appearance of new nodules within a few months. 2-4 In our patient, there was a unique tumour at presentation, and no further lesions appeared within 12 months, although we think that a longer follow-up is necessary to evaluate the clinical behaviour more thoroughly. We think that the small size of the lesion was the most favourable prognostic factor in our case, as it allowed for a complete excision of tumour. We also found strong positivity for MUM1 ⁄IRF4, which is thought to be crucial for lymphoid development and has been found to be strongly expressed in various types of leukaemia, B-and T-cell lymphomas, including ALTCL. 7-9 MUM1 ⁄IRF4 expression is thought to be helpful for diagnostic purposes, whereas its prognostic role is controversial, probably depending on the type of leukaemia ⁄lymphoma considered. 7-9 MUM1 ⁄IRF4 was not investigated in the previously reported cases of CD30+ PT ALTCLs; it could be worthwhile to study its expression on a larger series of PTLs. The unusual clinical behaviour and histotype and the immunophenotype of our case may add knowledge to the spectrum of PTLs.
Diabetes mellitus is characterized by elevated plasma glucose and increased rates of skin infections. Altered immune responses have been suggested to contribute to this prevalent complication, which involves microbial invasion. In this study we explored the effects of a high-glucose environment on the innate immunity of keratinocytes by focusing on β defensin-3 (BD3) using in vivo and in vitro models. Our results demonstrated that the perilesional skins of diabetic rats failed to show enhanced BD3 expression after wounding. In addition, high-glucose treatment reduced human BD3 (hBD3) expression of cultured human keratinocytes. This pathogenic process involved inhibition of p38MAPK signaling, an event that resulted from increased formation of advanced glycation end products. On the other hand, toll-like receptor-2 expression and function of cultured keratinocytes were not significantly affected by high-glucose treatment. In summary, high-glucose conditions inhibited the BD3 expression of epidermal keratinocytes, which in turn contributed to the frequent occurrences of infection associated with diabetic wounding.
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