Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), University Hospital Marqués de Valdecilla and Universidad de Cantabria, Santander, Spain.
Service of Neurology, University Hospital Marqués de Valdecilla, Universidad de Cantabria and IDIVAL, Av. Valdecilla s/n, Santander, 39008, Spain.
BMC Gastroenterol. 2024 Aug 13;24(1):262. doi: 10.1186/s12876-024-03366-w.
The role of beta calcitonin gene-related peptide (beta-CGRP) in gastrointestinal tract is obscure, but experimental models suggest an effect on the homeostasis of the intestinal mucosa. We measured beta-CGRP circulating levels in a large series of subjects with a recent diagnosis of inflammatory bowel disease (IBD), in order to assess the potential role of this neuropeptide in IBD pathogenesis.
Morning serum beta-CGRP levels were measured by ELISA (CUSABIO, China) in 96 patients recently diagnosed of IBD and compared with those belonging from 50 matched healthy controls (HC) and 50 chronic migraine (CM) patients.
Beta-CGRP levels were lower in patients with IBD (3.1 ± 1.9 pg/mL; 2.9 [2.4-3.4] pg/mL) as compared to HC (4.7 ± 2.6; 4.9 [4.0-5.8] pg/mL; p < 0.001) and to CM patients (4.6 ± 2.6; 4.7 [3.3-6.2] pg/mL; p < 0.001). Beta-CGRP levels in CM were not significantly different to those of HC (p = 0.92). Regarding IBD diagnostic subtypes, beta-CGRP levels for ulcerative colitis (3.0 ± 1.9pg/mL; 2.5 [2.1-3.4] pg/mL) and Crohn's disease (3.3 ± 2.0 pg/mL; 3.2 [2.4-3.9] pg/mL) were significantly lower to those of HC (p < 0.01 and p < 0.05, respectively) and CM (p < 0.01 and p < 0.05, respectively).
We have found a significant reduction in serum beta-CGRP levels in patients with a recent diagnosis of all kinds of IBD as compared to two control groups without active intestinal disease, HC and CM, which may suggest a role for this neuropeptide in the pathophysiology of IBD. Our data indicate a protective role of beta-CGRP in the homeostasis of the alimentary tract.
β-降钙素基因相关肽(β-CGRP)在胃肠道中的作用尚不清楚,但实验模型表明其对肠道黏膜的稳态有影响。我们测量了最近诊断为炎症性肠病(IBD)的大量患者的血清β-CGRP 水平,以评估这种神经肽在 IBD 发病机制中的潜在作用。
采用酶联免疫吸附法(CUSABIO,中国)测定 96 例新近诊断为 IBD 的患者清晨血清β-CGRP 水平,并与 50 例匹配的健康对照(HC)和 50 例慢性偏头痛(CM)患者进行比较。
与 HC(4.7±2.6;4.9[4.0-5.8]pg/mL;p<0.001)和 CM 患者(4.6±2.6;4.7[3.3-6.2]pg/mL;p<0.001)相比,IBD 患者的β-CGRP 水平较低(3.1±1.9pg/mL;2.9[2.4-3.4]pg/mL)。CM 患者的β-CGRP 水平与 HC 患者无显著差异(p=0.92)。关于 IBD 的诊断亚型,溃疡性结肠炎(3.0±1.9pg/mL;2.5[2.1-3.4]pg/mL)和克罗恩病(3.3±2.0pg/mL;3.2[2.4-3.9]pg/mL)患者的β-CGRP 水平明显低于 HC(p<0.01 和 p<0.05)和 CM(p<0.01 和 p<0.05)。
与无活动性肠道疾病的两个对照组(HC 和 CM)相比,我们发现所有类型的 IBD 患者在最近诊断时血清β-CGRP 水平显著降低,这可能表明该神经肽在 IBD 的病理生理学中发挥作用。我们的数据表明,β-CGRP 在消化道的稳态中发挥保护作用。