Diagnosis and Classification of Diabetes Mellitus The information that follows is based largely on the reports of the Expert Committee on the Diagnosis and Classification of Diabetes (Diabetes Care 20:1183–1197, 1997, and Diabetes Care 26:3160–3167, 2003)
Diagnosis and Classification of Diabetes Mellitus The information that follows is based largely on the reports of the Expert Committee on the Diagnosis and Classification of Diabetes (Diabetes Care 20:1183–1197, 1997, and Diabetes Care 26:3160–3167, 2003)
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糖尿病的定义和描述糖尿病是一组代谢性疾病，其特征是由于胰岛素分泌、胰岛素作用或两者的缺陷而导致的高血糖症。糖尿病的慢性高血糖与不同器官的长期损害、功能障碍和衰竭有关，特别是眼睛、肾脏、神经、心脏和血管。糖尿病的发展涉及几种致病过程。其范围从自身免疫性破坏胰腺b细胞导致胰岛素缺乏到导致胰岛素抵抗的异常。糖尿病中碳水化合物、脂肪和蛋白质代谢异常的基础是胰岛素对靶组织的作用不足。胰岛素作用不足是由于胰岛素分泌不足和/或在激素作用的复杂途径中的一个或多个点对胰岛素的组织反应减弱所致。胰岛素分泌的损害和胰岛素作用的缺陷经常在同一患者中共存，并且通常不清楚哪种异常（如果单独存在）是高血糖症的主要原因。明显的高血糖症状包括多尿、烦渴、体重减轻，有时伴有多食和视力模糊。生长障碍和对某些感染的易感性也可伴随慢性高血糖症。糖尿病未控制的急性、危及生命的后果是高血糖伴酮症酸中毒或非酮症高渗综合征。糖尿病的长期并发症包括视网膜病变伴潜在视力丧失;肾病导致肾衰竭;周围神经病变伴足溃疡、截肢和夏科关节风险;自主神经病变引起胃肠道、泌尿生殖系统和心血管症状以及性功能障碍。糖尿病患者的动脉粥样硬化性心血管、外周动脉和脑血管疾病的发病率增加。高血压和脂蛋白代谢异常常见于糖尿病患者。绝大多数糖尿病病例分为两大类病因（下文将更详细地讨论）。1型糖尿病的病因是胰岛素分泌绝对不足。发展这种类型糖尿病的风险增加的个体通常可以通过胰岛中发生的自身免疫病理过程的血清学证据和遗传标记来鉴定。在另一种更普遍的类型2型糖尿病中，其原因是对胰岛素作用的抵抗和代偿性胰岛素分泌反应不足的组合。在后一类中，在检测到糖尿病之前，足以引起各种靶组织中的病理和功能变化但没有临床症状的高血糖程度可能存在很长一段时间。在此无症状期间，通过测量空腹状态下或口服葡萄糖负荷激发后的血糖或A1 C，可以证明碳水化合物代谢异常。高血糖的程度（如果有的话）可能会随着时间的推移而变化，这取决于潜在疾病过程的程度（图1）。疾病过程可能存在，但可能尚未进展到足以引起高血糖症。相同的疾病过程可导致空腹血糖受损（IFG）和/或葡萄糖耐量受损（IGT），而不满足糖尿病的诊断标准。在某些糖尿病患者中，通过减肥、运动和/或口服降糖药可实现充分的血糖控制。因此，这些人不需要胰岛素。其他有残余胰岛素分泌但需要外源性胰岛素来充分控制血糖的个体可以在没有胰岛素的情况下生存，而b细胞广泛破坏因而没有残余胰岛素分泌的个体则需要胰岛素来生存。代谢异常的严重程度可以进展、消退或保持不变。因此，高血糖的程度反映了潜在代谢过程的严重程度及其治疗，而不是过程本身的性质。
DEFINITION AND DESCRIPTION OF DIABETES MELLITUSdDiabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of different organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Several pathogenic processes are involved in the development of diabetes. These range from autoimmune destruction of the b-cells of the pancreas with consequent insulin deficiency to abnormalities that result in resistance to insulin action. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of hormone action. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycemia. Symptoms ofmarked hyperglycemia includepolyuria,polydipsia,weight loss,sometimes with polyphagia, and blurred vision. Impairment of growth and susceptibility to certain infections may also accompany chronic hyperglycemia. Acute, life-threatening consequences of uncontrolled diabetes are hyperglycemia with ketoacidosis or the nonketotic hyperosmolar syndrome. Long-term complications of diabetes include retinopathy with potential loss of vision; nephropathy leading to renal failure; peripheral neuropathy with risk of foot ulcers, amputations, and Charcot joints; and autonomic neuropathy causing gastrointestinal, genitourinary, and cardiovascular symptoms and sexual dysfunction. Patients with diabetes have an increased incidence of atherosclerotic cardiovascular, peripheral arterial, and cerebrovascular disease. Hypertension and abnormalities of lipoprotein metabolism are often found in people with diabetes. The vast majority of cases of diabetes fall into two broad etiopathogenetic categories (discussed in greater detail below). In one category, type 1 diabetes, the cause is an absolute deficiency of insulin secretion. Individuals at increased risk of developing this type of diabetes can often be identified by serological evidence of an autoimmune pathologic process occurring in the pancreatic islets and by genetic markers. In the other, much more prevalent category, type 2 diabetes, the cause is a combination of resistance to insulin action and an inadequate compensatory insulin secretory response. In the latter category, a degree of hyperglycemia sufficient to cause pathologic and functional changes in various target tissues, but without clinical symptoms, may be present for a long period of time before diabetes is detected. During this asymptomatic period, it is possible to demonstrate an abnormality in carbohydrate metabolism by measurement of plasma glucose in the fasting state or after a challenge with an oral glucose load or by A1C. The degree of hyperglycemia (if any) may change over time, depending on the extent of the underlying disease process (Fig. 1). A disease process may be present but may not have progressed far enough to cause hyperglycemia. The same disease process can cause impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) without fulfilling the criteria for the diagnosis of diabetes. In some individuals with diabetes, adequate glycemic control can be achieved with weight reduction, exercise, and/or oral glucose-lowering agents. These individuals therefore do not require insulin. Other individuals who have some residual insulin secretion but require exogenous insulin for adequate glycemic control can survive without it. Individuals with extensive b-cell destruction and therefore no residual insulin secretion require insulin for survival. The severity of the metabolic abnormality can progress, regress, or stay the same. Thus, the degree of hyperglycemia reflects the severity of the underlying metabolic process and its treatment more than the nature of the process itself.