Letter: enteral nutrition in advanced cirrhosis – a case of missing the boat?

Letter: enteral nutrition in advanced cirrhosis – a case of missing the boat?
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来信:晚期肝硬化的肠内营养——错失良机的案例?

DOI:
10.1111/j.1365-2036.2012.05132.x
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发表时间:
2012
影响因子:
7.6
通讯作者:
K. Goh
K. Goh
中科院分区:
医学1区
文献类型:
--
作者:
S. Mahadeva;K. Goh

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先生们,感谢您给我们机会回复 Raza 和 Shata 关于我们文章的来信。经过仔细考虑,我们认为信中讨论的数据和得出的结论有一些重要的注意事项。首先,作者使用 Harvey-Bradshaw 指数(克罗恩病活动指数的缩写形式)来评估克罗恩病 (CD) 和溃疡性结肠炎 (UC) 的临床症状。 Harvey-Bradshaw 指数包括一些参数,例如适用于 CD 的瘘管或腹部肿块,但不适用于 UC,而它不考虑直肠出血,而直肠出血是 UC 疾病严重程度的良好指标。更重要的是,Raza 和 Shata 假设抗 IL-17(或抗 IL-17R)疗法可能在 CD 中失败,因为根据他们的数据,这些患者缺乏 IL-17 的产生,而他们假设该疗法可能对 UC 有效。需要强调的是,活动性 UC 和 CD 患者中 IL-17 产生的增加已被多个小组(除我们之外)记录到,众所周知,UC(使用 Mayo 评分测量)和 CD 患者的临床和内镜活动都伴随着 IL-17 产生的增加。此外,抗 IL-17 治疗似乎会使一些患者的疾病恶化,这表明,正如在不同动物模型中所观察到的那样,IL-17 的缺乏可能会对肠道稳态产生有害影响。鉴于证据,我们认为,根据作者在信中提供的数据,抗 IL-17 可能对 UC 有益的假设是具有误导性的。
SIRS, Thank you for giving us the opportunity to respond to the letter from Raza and Shata concerning our article. After careful consideration, we believe that the data discussed in the letter and the conclusions made have some important caveats. First, the authors use the Harvey-Bradshaw index, an abbreviated form of the Crohn’s disease activity index, to evaluate both Crohn’s disease (CD) and ulcerative colitis (UC) clinical symptoms. The Harvey-Bradshaw index includes parameters, such as the presence of fistulae or abdominal mass that apply to CD, but not UC, whereas it does not account for rectal bleeding – a good indicator of disease severity in UC. More importantly, Raza and Shata make the assumption that anti-IL-17 (or anti-IL-17R) therapy may have failed in CD due to, according to their data, a lack of production of IL-17 in these patients, whereas they hypothesise that it may work in UC. It is important to emphasise that increased production of IL-17 in active UC and CD patients has been documented by several groups (apart from us) and it is well-known that clinical and endoscopic activity in both UC (measured using the Mayo score) and CD patients is accompanied by increased production of IL-17. Moreover, anti-IL-17 therapy appears to worsen disease in some patients suggesting that, as it has been seen in different animal models, lack of IL-17 may have deleterious effects to intestinal homeostasis. Given the evidence, we believe that the assumption that anti-IL-17 may be beneficial in UC, based on the data the authors provide in the letter, is misleading.
Seno,H.,等:“潘氏细胞破坏后肿瘤坏死因子α参与肠上皮细胞增殖”Scand J Gastroenterol.. 37. 154-160 (2002)
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