Abnormal Vessel Architecture Persists in the Microvasculature of the Massive Weight Loss Patient.

Plastic and reconstructive surgery(2016)

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摘要
BACKGROUND:Research demonstrates a link between obesity and increased circulating inflammatory cytokines, which lead to changes in the microvasculature. Massive weight loss patients often experience delayed wound healing after body-contouring procedures; however, no studies exist to explore the inflammatory response of massive weight loss on microvasculature. This study hypothesized that massive weight loss patients who undergo body-contouring procedures maintain persistently elevated inflammatory markers in the microvasculature that delay wound healing. METHODS:Superficial inferior epigastric artery vessels were harvested during abdominally based free flap surgery and abdominal contouring surgery for normal weight and massive weight loss patients, respectively. Vessels were histologically assessed using immunohistochemistry and trichome staining to assess and compare vessel architecture. Analysis was performed for intimal proliferation and luminal occlusion ratio. RESULTS:All patients (n = 23) were female. Quantitative analysis of immunohistochemistry stains revealed no difference between normal weight and massive weight loss patients. Trichrome staining demonstrated abnormal vessel architecture in the massive weight loss group. Intimal proliferation was 11.4 ± 4.8 percent for normal weight patients compared with 29.5 ± 4.9 percent for massive weight loss patients (p < 0.0001). Occlusion ratio for normal weight patients was 29.9 ± 3.9 percent compared with 46.2 ± 8.1 percent for massive weight loss patients (p < 0.0001) CONCLUSIONS:: Despite the return to normal levels of inflammatory markers after massive weight loss, trichrome staining demonstrated irregular composition in the tunica adventitia and tunica media and increased intimal proliferation and occlusion ratio. This suggests vasculopathy that could explain delayed wound healing in the massive weight loss population.
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