Rhinophyma, the end stage in the development of acne rosacea, is characterized by sebaceous hyperplasia, fibrosis, follicular plugging, and telangiectasia. Although it is commonly considered a cosmetic problem, it can result in gross distortion of soft tissue and airway obstruction. Basal cell carcinoma (BCC) is a rare finding in patients with rhinophyma. The objective of this study is to review the literature of BCC in rhinophyma and report on a case. A 70-year-old male presented with long-standing rosacea that resulted in a gross nasal deformity. The patient suffered from chronic drainage and recurrent infections that failed conservative treatment with oral and topical antibiotics. The patient decided to proceed with surgical intervention and underwent tangential excision and dermabrasion in the operating room. Since 1955 there have been 11 cases reported in the literature. In our case, the pathology report noted that the specimen had an incidental finding of a completely resected BCC. The patient did well postoperatively and at follow-up remains tumor-free. Despite the uncommon occurrence of BCC in resection specimens for rhinophyma, we recommend that all specimens be reviewed by a pathologist. If BCC is detected, re-excision may be necessary and careful follow-up is mandatory. Larger studies would be needed to determine the correlation between the 2 conditions.
Background:Ischemia-reperfusion (IR) injury is seen in many settings such as free flap salvage and limb replantation/revascularization. The consequences—partial/total flap loss, functional muscle loss, or amputation—can be devastating. Of the treatment options available for IR injury, hyperbaric oxygen (HBO) is the most beneficial. HBO inhibits neutrophil-endothelial adhesion through interference of CD18 neutrophil polarization in IR, a process mediated by nitric oxide. The purposes of this study were to examine the involvement of vascular endothelial growth factor (VEGF) in the beneficial HBO effect on CD18 polarization and neutrophil adhesion and investigate the effect of plasmin on VEGF expression in skeletal muscle following IR injury.Methods:A rat gracilis muscle model of IR injury was used to evaluate the effect of VEGF in IR, with and without HBO, on neutrophil CD18 polarization and adhesion in vivo and ex vivo. Furthermore, we investigated the effects that plasmin has on VEGF expression in gracilis muscle and pulmonary tissue by blocking its activation with alpha-2-antiplasmin.Results:HBO treatment following IR injury significantly decreased neutrophil polarization and adhesion ex vivo compared with the IR group. Anti-VEGF reversed the beneficial HBO effect after IR with polarization and adhesion. In vivo adhesion was also increased by anti-VEGF. HBO treatment of IR significantly increased the VEGF protein in both gracilis and pulmonary vasculature. Alpha-2-antiplasmin significantly reversed the HBO-induced increase of VEGF in gracilis muscle.Conclusions:These results suggest that HBO inhibits CD18 polarization and neutrophil adhesion in IR injury through a VEGF-mediated pathway involving the extracellular matrix plasminogen system.
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