Frokjaer Jens Brondum, Andersen Soren-Due, Ejskjaer Niels, Funch-Jensen Peter, Drewes Asbjorn-Mohr, Gregersen Hans
Center for Visceral Biomechanics and Pain, Department of Radiology, Aalborg Hospital, DK-9100 Aalborg, Denmark.
World J Gastroenterol. 2007 Sep 28;13(36):4881-90. doi: 10.3748/wjg.v13.i36.4881.
To investigate that both the neuronal function of the contractile system and structural apparatus of the gastrointestinal tract are affected in patients with longstanding diabetes and auto mic neuropathy.
The evoked esophageal and duodenal contractile activity to standardized bag distension was assessed using a specialized ultrasound-based probe. Twelve type-1 diabetic patients with autonomic neuropathy and severe gastrointestinal symptoms and 12 healthy controls were studied. The geometry and biomechanical parameters (strain, tension/stress, and stiffness) were assessed.
The diabetic patients had increased frequency of distension-induced contractions (6.0 +/- 0.6 vs 3.3 +/- 0.5, P < 0.001). This increased reactivity was correlated with the duration of the disease (P = 0.009). Impaired coordination of the contractile activity in diabetic patients was demonstrated as imbalance between the time required to evoke the first contraction at the distension site and proximal to it (1.5 +/- 0.6 vs 0.5 +/- 0.1, P = 0.03). The esophageal wall and especially the mucosa-submucosa layer had increased thickness in the patients (P < 0.001), and the longitudinal and radial compressive stretch was less in diabetics (P < 0.001). The esophageal and duodenal wall stiffness and circumferential deformation induced by the distensions were not affected in the patients (all P > 0.14).
The impaired contractile activity with an imbalance in the distension-induced contractions likely reflects neuronal abnormalities due to autonomic neuropathy. However, structural changes and remodeling of the gastrointestinal tract are also evident and may add to the neuronal changes. This may contribute to the pathophysiology of diabetic gut dysfunction and impact on future management of diabetic patients with gastrointestinal symptoms.
研究长期糖尿病合并自主神经病变患者胃肠道收缩系统的神经功能和结构装置是否均受影响。
使用基于超声的专用探头评估标准化气囊扩张诱发的食管和十二指肠收缩活动。研究了12例患有自主神经病变和严重胃肠道症状的1型糖尿病患者以及12名健康对照者。评估了几何和生物力学参数(应变、张力/应力和硬度)。
糖尿病患者扩张诱发收缩的频率增加(6.0±0.6对3.3±0.5,P<0.001)。这种反应性增加与病程相关(P = 0.009)。糖尿病患者收缩活动协调性受损表现为在扩张部位及其近端诱发首次收缩所需时间的不平衡(1.5±0.6对0.5±0.1,P = 0.03)。患者的食管壁尤其是黏膜下层厚度增加(P<0.001),糖尿病患者的纵向和径向压缩性伸展较小(P<0.001)。患者的食管和十二指肠壁硬度以及扩张引起的周向变形未受影响(所有P>0.14)。
收缩活动受损以及扩张诱发收缩不平衡可能反映了自主神经病变导致的神经异常。然而,胃肠道的结构改变和重塑也很明显,可能会加重神经变化。这可能有助于糖尿病肠道功能障碍的病理生理学,并影响未来对有胃肠道症状的糖尿病患者的管理。