Transforming Growth Factors

转化生长因子
  • 文章类型: Case Reports
    背景:肠道狭窄和梗阻是溃疡性结肠炎(UC)的罕见并发症。目前,关于治疗UC合并肠狭窄的研究很少,然而,尚无关于ustekinumab(UST)治疗UC合并良性肠狭窄的报道.
    方法:我院收治一名22岁女性,因3年反复出现便血黏液,过去一个月出现间歇性腹痛和腹胀。她是类固醇依赖性的,并且对英夫利昔单抗产生了继发性反应丧失。
    方法:诊断为UC合并狭窄所致不完全性肠梗阻。狭窄具有炎症和纤维化成分的混合模式,前者覆盖了肠道的较大部分。
    方法:患者接受UST治疗56周。
    结果:患者经UST治疗后症状消退。溃疡愈合了,狭窄减少。
    结论:UST对合并良性肠狭窄的UC有效。认为UST抑制转化生长因子-β和白细胞介素-17的产生,导致肌成纤维细胞增殖的抑制,最终缓解肠狭窄。
    BACKGROUND: Intestinal stricture and obstruction are rare complications of ulcerative colitis (UC). Currently, there are only a few studies on the treatment of UC with intestinal stenosis, however there are no reports on the treatment of UC with benign intestinal stenosis with ustekinumab (UST).
    METHODS: A 22-year-old woman was admitted to our hospital due to a 3-year history of recurrent bloody mucous in stool with intermittent abdominal pain and distension developed in the past month. She was steroid-dependent and had developed a secondary loss of response to infliximab.
    METHODS: She was diagnosed with UC combined with incomplete intestinal obstruction due to stenosis. The stricture had a mixed pattern with both inflammatory and fibrotic components, with the former covering a larger section of the intestine.
    METHODS: The patient was given UST for 56 weeks.
    RESULTS: The patient\'s symptoms subsided after treatment with UST. The ulcers healed, and the stenosis was reduced.
    CONCLUSIONS: UST is effective against UC with benign intestinal stenosis. It is thought that UST inhibits the production of transforming growth factor-β and interleukin-17, leading to the suppression of myofibroblast proliferation, ultimately alleviating intestinal stenosis.
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  • 文章类型: Journal Article
    杜氏肌营养不良症是一种严重的遗传性肌肉疾病,影响全球3500名男孩中的1名。炎症细胞对骨骼肌的浸润是疾病病理生理学的一个重要方面,并且与个体患者的疾病严重程度密切相关。在Duchenne肌肉的慢性炎症中,细胞因子和趋化因子被认为是炎症细胞的重要激活剂和招募者。此外,它们对肌纤维损伤控制和组织再生提供了潜在的有益效果。在这次审查中,列出了杜氏肌营养不良及其相关动物疾病模型中细胞因子和趋化因子表达的最新知识,并讨论了对未来治疗途径的影响。
    Duchenne muscular dystrophy is a severe inherited muscle disease that affects 1 in 3500 boys worldwide. Infiltration of skeletal muscle by inflammatory cells is an important facet of disease pathophysiology and is strongly associated with disease severity in the individual patient. In the chronic inflammation that characterizes Duchenne muscle, cytokines and chemokines are considered essential activators and recruiters of inflammatory cells. In addition, they provide potential beneficiary effects on muscle fiber damage control and tissue regeneration. In this review, current knowledge of cytokine and chemokine expression in Duchenne muscular dystrophy and its relevant animal disease models is listed, and implications for future therapeutic avenues are discussed.
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