Lymphovenous Anastomosis Aids Wound Healing in Lymphedema: Relationship Between Lymphedema and Delayed Wound Healing from a View of Immune Mechanisms.
Lymphovenous Anastomosis Aids Wound Healing in Lymphedema: Relationship Between Lymphedema and Delayed Wound Healing from a View of Immune Mechanisms.
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淋巴静脉吻合术有助于淋巴水肿伤口愈合：从免疫机制的角度来看淋巴水肿与伤口愈合延迟之间的关系。
DOI：
10.1089/wound.2018.0871
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发表时间：
2019
期刊：
影响因子：
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通讯作者：
Yoshida Shuhei
中科院分区：
文献类型：
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作者：
Maeda Daisuke;Kubo Tateki;Kiya Koichiro;Kawai Kenichiro;Matsuzaki Shinsuke;Kobayashi Daichi;Fujiwara Toshihiro;Katayama Taiichi;Hosokawa Ko;前田大介;Hideyoshi Sato;Hideyoshi Sato;Yoshida S;Yoshida S;Yoshida S;Yoshida S;Yoshida S;Yoshida Shuhei;Yoshida Shuhei;Yoshida Shuhei;Yoshida Shuhei;Yoshida Shuhei;Yoshida Shuhei;Yoshida Shuhei
淋巴水肿的伤口愈合延迟被认为是由淋巴水肿的病理生理和免疫作用两个原因引起的。这篇综述的目的是建立受损淋巴如何改变伤口愈合病理生理和免疫，并提出治疗模式，可以促进伤口愈合淋巴水肿。淋巴小静脉吻合术（淋巴静脉吻合术[LVAs]）用于多次复发蜂窝织炎伴淋巴漏，并发严重溃疡，皮肤移植、皮瓣和保守治疗均难治的患者。4周后淋巴漏及溃疡愈合。此外，淋巴水肿在没有压迫治疗的情况下得到改善。淋巴水肿的病理生理特征是局部周围水肿，压迫微血管和淋巴血管，损害组织重塑。另一个被怀疑的机制是参与的免疫细胞分化的不平衡。对辅助性T细胞（Th）1的深度抑制可能会增加感染的风险，而Th2细胞的过度分化，包括M2巨噬细胞极化，可能会促进纤维化，从而破坏精心安排的伤口愈合过程。虽然负压伤口治疗对淋巴水肿的伤口延迟愈合是有用的，但lva可能是治疗淋巴水肿的根本问题所必需的。LVAs被认为是创建一个旁路到淋巴结的树突状细胞（dc）可以通过它将抗原信息传递给T细胞。lva被认为通过允许更多的dc返回循环来中和慢性炎症，从而改善伤口愈合。
Delayed wound healing in lymphedema is assumed to be caused by two reasons, pathophysiological and immunological effects of lymphedema. The aim of this review is to establish how impaired lymphatics alter wound healing pathophysiologically and immunologically, and to propose treatment modalities that can promote wound healing in lymphedema. Lymphaticovenular anastomoses (lymphovenous anastomoses [LVAs]) were performed on patients who had recurrent cellulitis several times with lymphorrhea and developed severe ulcers that were refractory to skin grafts, flaps, and conservative therapy. The lymphorrhea and the ulcer had healed by 4 weeks. Moreover, the lymphedema improved without compression therapy. Lymphedema is characterized pathophysiologically by localized peripheral edema that compresses the microvasculature and lymphatic vasculature and impairs tissue remodeling. Another suspected mechanism is an imbalance in the differentiation of participating immune cells. Profound suppression of T helper (Th)1 cells is likely to increase the risk of infection, and excessive differentiation of Th2 cells, including M2 macrophage polarization, may promote fibrosis, which disrupts the carefully orchestrated wound healing process. Although negative-pressure wound therapy is useful for the treatment of delayed wound healing in lymphedema, LVAs may be necessary to treat the fundamental problem of lymphedema. LVAs are considered to create a bypass to the lymph nodes through which dendritic cells (DCs) can transmit antigen information to T cells. LVAs are considered to neutralize chronic inflammation by allowing more DCs to return into the circulation, thereby improving wound healing.