Service de diabétologie, maladies métaboliques et nutrition, université de Nancy I, CIC Inserm, CHU de Nancy, 54511 Vandoeuvre-Les-Nancy, France.
Diabetes Metab. 2012 Nov;38(5):393-402. doi: 10.1016/j.diabet.2012.05.001. Epub 2012 Jun 27.
Diabetic gastroparesis is a component of autonomic neuropathy, and is the most common manifestation of gastrointestinal neuropathy. Diabetes is responsible for about one quarter of gastroparesis. The upper gastrointestinal symptoms are often non-specific and dominated by nausea, vomiting, early satiety, fullness, bloating. We also have to look for diabetic gastroparesis in case of metabolic instability, such as postprandial hypoglycaemia. The pathophysiology of diabetic gastroparesis is complex, partly due to a vagus nerve damage, but also to changes in secretion of hormones such as motilin and ghrelin. A decrease in the stem cell factor (SCF), growth factor for cells of Cajal (gastric pacemaker), was found in subjects with diabetic gastroparesis. These abnormalities lead to an excessive relaxation in the corpus, a hypomotility of antrum, a desynchronization antrum-duodenum-pylorus, and finally an abnormal duodenal motility. The treatment of diabetic gastroparesis is based on diabetes control, and split meals by reducing the fiber content and fat from the diet. The antiemetic and prokinetic agents should be tested primarily in people with nausea and vomiting. Finally, after failure of conventional measures, the use of gastric neuromodulation is an effective alternative, with well-defined indications. Introduced in the 1970s, this technology works by applying electrical stimulation continues at the gastric antrum, particularly in patients whose gastric symptoms are refractory to other therapies. Its efficacy has been recently reported in different causes of gastroparesis, especially in diabetes. Gastric emptying based on gastric scintigraphy, gastrointestinal symptoms, biological markers of glycaemic control and quality of life are partly improved, but not normalized. Finally, a heavy nutritional care is sometimes necessary in the most severe forms. The enteral route should be preferred (nasojejunal and jejunostomy if possible efficiency). However, in case of failure especially in patients with small bowel neuropathy, the long-term parenteral nutrition is sometimes required.
糖尿病性胃轻瘫是自主神经病变的一个组成部分，也是胃肠道神经病变最常见的表现。糖尿病约占胃轻瘫的四分之一。上消化道症状往往是非特异性的，主要表现为恶心、呕吐、早饱、饱胀、腹胀。我们还必须寻找代谢不稳定的糖尿病性胃轻瘫，如餐后低血糖。糖尿病性胃轻瘫的病理生理学很复杂，部分原因是迷走神经损伤，但也与胃动素和 ghrelin 等激素分泌的变化有关。在糖尿病性胃轻瘫患者中发现干细胞因子（SCF）减少，这是 Cajal 细胞（胃起搏）的生长因子。这些异常导致胃体过度松弛、胃窦蠕动减少、胃窦-十二指肠-幽门失同步，最终导致十二指肠运动异常。糖尿病性胃轻瘫的治疗基于糖尿病的控制，并通过减少纤维含量和饮食中的脂肪来分餐。止吐药和促动力药应主要在有恶心和呕吐的患者中进行测试。最后，在常规措施失败后，胃神经调节的使用是一种有效的替代方法，具有明确的适应证。该技术于 20 世纪 70 年代引入，通过对胃窦进行持续的电刺激来发挥作用，特别是在对其他治疗方法有抗性的患者中。最近在不同原因引起的胃轻瘫中，特别是在糖尿病中，报告了其疗效。基于胃闪烁扫描的胃排空、胃肠道症状、血糖控制的生物标志物和生活质量得到了部分改善，但没有正常化。最后，在最严重的情况下，有时需要进行严重的营养护理。应优先选择肠内途径（如果可能，经鼻空肠和空肠造口术）。然而，在失败的情况下，特别是在患有小肠神经病变的患者中，有时需要长期的肠外营养。
