Bharucha Adil E., Locke G. Richard, Murray Joseph A.
Dr. Adil E. Bharucha is Professor of Medicine, and a consultant in the Division of Gastroenterology and Hepatology and the Clinical Enteric Neuroscience Translational and Epidemiological Research Program, Mayo Clinic, Rochester, MN
Dr. G. Richard Locke is Professor of Medicine, and a consultant in the Division of Gastroenterology and Hepatology and the Clinical Enteric Neuroscience Translational and Epidemiological Research Program, Mayo Clinic, Rochester, MN
Although most attention has traditionally focused on the stomach, diabetes can affect the entire gastrointestinal (GI) tract, as implied by the term diabetic . This chapter details the epidemiology and summarizes the salient features of the pathophysiology, clinical features, and management of diabetic enteropathy. Diabetic enteropathy may be asymptomatic or manifest with upper (i.e., heartburn, dysphagia, dyspepsia, gastroparesis) or lower GI symptoms (i.e., diarrhea, constipation, and fecal incontinence). GI symptoms are not uncommon (abdominal pain experienced in 7.6%, vomiting in 1.7%) in patients with diabetes presenting for care. However, in community studies, the prevalence of GI symptoms is, for the most part, either not different or only slightly higher in type 1 and type 2 diabetes than in people without diabetes. For example, 17% of persons with type 1 diabetes and 14% of those without diabetes had constipation in one study. Limited data are available on the epidemiology, particularly risk factors, and natural history of these specific GI manifestations among patients with diabetes in the community. For example, the risk of developing gastroparesis over 10 years was 5% in type 1 diabetes and 1% in type 2 diabetes versus <1% in persons without diabetes. GI dysmotility in diabetes is multifactorial: extrinsic and intrinsic (i.e., enteric) neural dysfunction, hyperglycemia, and hormonal disturbances have been implicated. Delayed gastric emptying in diabetes is often asymptomatic and is associated with impaired glycemic control. Approaches to manage diabetic enteropathy primarily focus on correcting the motor disturbance, symptom relief, managing complications, and improving glycemic control. However, there is no evidence that improving glycemic control is beneficial in diabetic enteropathy. From a public health perspective, further studies to better understand the risk factors for diabetic enteropathy and the relationship between diabetic enteropathy and impaired glycemic control and to develop novel approaches to managing diabetic enteropathy are critical. Type 1 diabetes is associated with gluten-sensitive enteropathy (also known as celiac disease [CD]). CD is very common (approximately 5%) in patients with type 1 diabetes, is often overlooked clinically, and may be asymptomatic while patients accrue health consequences, including growth retardation, bone demineralization, and eventually, symptoms. CD is readily detectable, and at the very least, those looking after patients with type 1 diabetes should have a very low threshold for testing. Screening at initial diabetes diagnosis and yearly for at least 5 years later should be considered in children and at least once in adults. Conversely, there is also a twofold increase in type 1 diabetes in patients with a prior diagnosis of CD (hazard ratio 2.4, 95% confidence interval 1.9–3.0). Gastric autoantibodies are common in type 1 diabetes and can lead to progressive loss of parietal cell mass and hypochlorhydria (low stomach acid) in a significant percentage of patients. It behooves the physician to be aware of this association and vigilant of its consequences as the patient ages. In summary, studies suggest the prevalence of selected GI symptoms (e.g., constipation) are greater in individuals with diabetes than in controls. For other symptoms, the prevalence is generally not different in persons with diabetes compared to those without. Further studies are necessary to accurately estimate the prevalence of GI symptoms in people with diabetes and to identify the risk factors for these symptoms.
尽管传统上大多数注意力都集中在胃部,但正如“糖尿病性”这个术语所暗示的,糖尿病可影响整个胃肠道(GI)。本章详细介绍了糖尿病性肠病的流行病学,并总结了其病理生理学、临床特征和管理的显著特点。糖尿病性肠病可能无症状,或表现为上消化道症状(即烧心、吞咽困难、消化不良、胃轻瘫)或下消化道症状(即腹泻、便秘和大便失禁)。在就诊的糖尿病患者中,胃肠道症状并不罕见(腹痛发生率为7.6%,呕吐发生率为1.7%)。然而,在社区研究中,1型和2型糖尿病患者胃肠道症状的患病率在很大程度上与非糖尿病患者没有差异或仅略高。例如,在一项研究中,17%的1型糖尿病患者和14%的非糖尿病患者有便秘。关于这些糖尿病患者中特定胃肠道表现的流行病学,尤其是危险因素和自然史的数据有限。例如,1型糖尿病患者10年内发生胃轻瘫的风险为5%,2型糖尿病患者为1%,而非糖尿病患者<1%。糖尿病中的胃肠动力障碍是多因素的:外在和内在(即肠内)神经功能障碍、高血糖和激素紊乱都与之有关。糖尿病患者胃排空延迟通常无症状,且与血糖控制受损有关。糖尿病性肠病的管理方法主要集中在纠正运动障碍、缓解症状、处理并发症和改善血糖控制。然而,没有证据表明改善血糖控制对糖尿病性肠病有益。从公共卫生的角度来看,进一步研究以更好地了解糖尿病性肠病的危险因素以及糖尿病性肠病与血糖控制受损之间的关系,并开发管理糖尿病性肠病的新方法至关重要。1型糖尿病与麸质敏感性肠病(也称为乳糜泻[CD])有关。CD在1型糖尿病患者中非常常见(约5%),在临床上常被忽视,可能无症状,但患者会累积健康后果,包括生长发育迟缓、骨质脱矿质,最终出现症状。CD很容易检测到,至少,照顾1型糖尿病患者的人员应该有很低的检测阈值。儿童应在初次诊断糖尿病时进行筛查,并在至少5年后每年筛查一次,成人至少筛查一次。相反,先前诊断为CD的患者患1型糖尿病的风险也会增加两倍(风险比2.4,95%置信区间1.9 - 3.0)。胃自身抗体在1型糖尿病中很常见,在相当比例的患者中可导致壁细胞数量逐渐减少和胃酸过少(胃酸低)。随着患者年龄增长,医生有必要了解这种关联并警惕其后果。总之,研究表明糖尿病患者中某些胃肠道症状(如便秘)的患病率高于对照组。对于其他症状,糖尿病患者的患病率与非糖尿病患者通常没有差异。需要进一步研究以准确估计糖尿病患者胃肠道症状的患病率,并确定这些症状的危险因素。