Dermatofibrossarcoma protuberante diagnosticado erroneamente como queloide e tratado com acetonido de triancinolona / Dermatofibrosarcoma protuberans misdiagnosed as keloid and treated with triamcinolone acetonide

INTRODUÇÃO: Dermatofibrossarcoma protuberante é um tumor de pele raro e de malignidade intermediária, com baixo potencial metastático, mas altas taxas de recorrência após tratamento cirúrgico. Por apresentar eventual semelhança clínica com cicatrizes hipertróficas e queloides, o diagnóstico correto mostra-se fundamental para o sucesso do tratamento. O objetivo do presente trabalho é fazer um alerta e relatar quatro casos de dermatofibrossarcoma protuberante erroneamente diagnosticados como queloide e tratados alhures com infiltração de acetonido de triancinolona. MÉTODO: Entre novembro de 1983 e janeiro de 2008, foram atendidos quatro pacientes com dermatofibrossarcoma protuberante que tinham sido submetidos alhures a infiltrações intralesionais de acetonido de triancinolona, em virtude de diagnóstico errôneo de queloide. Nos quatro casos, foram realizadas excisões cirúrgicas radicais, com remoção de 3 cm de tecido sadio nas margens laterais, incluindo-se, na margem profunda, uma estrutura anatômica não infiltrada pelo tumor. Os pacientes receberam avaliação médica periódica em longo prazo. RESULTADOS: Os pacientes foram acompanhados por uma média de 159 meses. Três pacientes (75%) permaneceram vivos, sem sinais de doença em atividade. Um paciente (25%) faleceu devido à doença, após tentativa de remover o avançado tumor recorrente, por meio de extensa cirurgia craniofacial. A recidiva ocorreu sete anos após a operação radical. CONCLUSÃO: Dermatofibrossarcoma protuberante deve ser considerado no diagnóstico diferencial dos queloides. A infiltração intralesional de acetonido de triancinolona só deverá ser realizada após diagnóstico de certeza, que pode demandar exame anatomopatológico prévio. Um exame clínico cuidadoso e o conhecimento da lesão favorecem um diagnóstico preciso e, portanto, um tratamento adequado.

INTRODUCTION: Dermatofibrosarcoma protuberans is a rare skin tumor with intermediate malignancy, low metastatic potential, and high recurrence rates after surgical treatment. Owing to a possible clinical resemblance with hypertrophic scars and keloids, the correct diagnosis is fundamental for treatment success. The objective of the present work is to report on four cases of dermatofibrosarcoma protuberans misdiagnosed as keloid and treated elsewhere with infiltration of triamcinolone acetonide. METHOD: Between November 1983 and January 2008, four patients with dermatofibrosarcoma protuberans who had undergone intralesional infiltration with triamcinolone acetonide elsewhere were treated because of an erroneous diagnosis of keloid. Radical surgical excision was performed, and 3 cm of healthy tissue was removed from the side margins, including the deep margin, an anatomical structure not infiltrated by the tumor. The patients underwent long-term periodic medical evaluations. RESULTS: The patients were followed-up for an average of 159 months. Three patients (75%) are still alive without signs of disease at the time of this report. One patient (25%) died of the disease after an attempt to remove the advanced recurrent tumor using extensive craniofacial surgery. Recurrence occurred 7 years after the radical operation. CONCLUSION: Dermatofibrosarcoma protuberans must be considered in the differential diagnosis of keloids. Intralesional infiltration with triamcinolone acetonide should only be performed after diagnostic confirmation , which may require pathological examination. A careful clinical examination and knowledge of the lesion favor a precise diagnosis and an appropriate treatment.

Triamcinolone Acetonide Prevents Enhancement of Hypoxia-induced Neuronal and Inducible Nitric Oxide Synthases in the Retinas of Rats with Oxygen-induced Retinopathy

PURPOSE: We investigated whether oxygen-induced retinopathy (OIR) results in changes in the protein expression of neuronal and inducible nitric oxide synthases (nNOS and iNOS, respectively) in rat model of OIR. In addition, we evaluated whether treatment of rats with triamcinolone acetonide (TA) prevents this response. METHODS: To promote OIR, Sprague-Dawley rats were exposed to hyperoxia from postnatal day 2 (P2) to P14. They were then returned to normoxia after P15. TA was injected into the right vitreous of P15 rats, while saline was injected into the left vitreous. At P18 the expression of nNOS and iNOS was determined using Western blotting and immunostaining techniques in retinas obtained from control rats. RESULTS: In P18 OIR rats, the abundance of nNOS and iNOS protein was significantly increased compared with controls. These increases were not observed in the retinas of rats treated with TA. The change in expression of nNOS and iNOS were specific to parvalbumin and glial fibrillary acidic protein-positive cells. Treatment with TA prevented the increased expression of nNOS and iNOS in all samples. CONCLUSIONS: Hypoxia upregulates expression of nNOS and iNOS in OIR rat retinas, which is can be prevented by treatment with TA.

Prophylactic anti-inflammation inhibits cigarette smoke-induced emphysema in guinea pigs / 华中科技大学学报（医学）（英德文版）

In this study, the effect of prophylactic anti-inflammation on the development of smoke-induced emphysema was investigated. Young male guinea-pigs aged 1.5-2 months (weighing 198.3+/-26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline-rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, i.m., every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air-space size, mean linear intercept (Lm): 120.6+/-16.0 microm in Group A; 89.8+/-9.2 microm in Group B and 102.4+/-17.7 microm in Group C. The average Lm in either group B or group C was shorter than that in Group A (ANOVA and Newman-Keuls test, F=8.80, P=0.0002) but comparable to that (94.8+/-13.2 microm) in group D (P>0.05). It is concluded that long-term prophylactic anti-inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.