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糖尿病的诊断、分类及发病机制。

Diagnosis, classification, and pathogenesis of diabetes mellitus.

作者信息

Lebovitz H E

机构信息

State University of New York Health Science Center at Brooklyn, USA.

出版信息

J Clin Psychiatry. 2001;62 Suppl 27:5-9; discussion 40-1.

PMID:11806489
Abstract

Diabetes mellitus is a metabolic disorder that is characterized by inappropriate hyperglycemia and is associated with both acute and chronic complications. Currently, diabetes mellitus is diagnosed by blood or plasma glucose levels. A random plasma glucose level > or = 200 mg/dL in an individual with classic symptoms is sufficient to make the diagnosis. Otherwise, a fasting plasma glucose level > or = 126 mg/dL or a 2-hour plasma glucose level > or = 200 mg/dL after an oral glucose challenge of 75 g on 2 occasions is sufficient evidence upon which to diagnose diabetes mellitus. The major types of diabetes mellitus are type 1 diabetes (insulin deficient) and type 2 diabetes (combination of insulin resistance and insulin deficiency). In both types, there is a genetic predisposition as well as environmental factors that contribute to the expression of the genetic predisposition. In type 1 diabetes, the primary abnormality is extensive deficiency of beta cell function. In type 2 diabetes, insulin resistance occurs, and the marked compensatory increases in insulin secretion necessary to maintain normal glucose tolerance cannot be achieved or maintained. As beta cell function continues to decrease, the individual progresses from normal glucose tolerance to impaired glucose tolerance to diabetes with primarily postprandial hyperglycemia to diabetes with fasting hyperglycemia. Drugs can cause diabetes by interfering with beta cell insulin secretion, by increasing insulin resistance, or by a combination of both. Atypical antipsychotic drugs have been reported to cause diabetic ketoacidosis, obesity and insulin resistance, type 2 diabetes, and hypertriglyceridemia. A monitoring system should be in place in patients started on treatment with these agents to detect metabolic abnormalities as they are evolving so that adequate and timely treatment can be initiated.

摘要

糖尿病是一种代谢紊乱疾病,其特征为血糖异常升高,并伴有急性和慢性并发症。目前,糖尿病通过血液或血浆葡萄糖水平进行诊断。对于有典型症状的个体,随机血浆葡萄糖水平≥200mg/dL足以确诊。否则,空腹血浆葡萄糖水平≥126mg/dL或口服75g葡萄糖后2小时血浆葡萄糖水平≥200mg/dL,两次检测结果均符合此标准,则足以作为诊断糖尿病的依据。糖尿病的主要类型为1型糖尿病(胰岛素缺乏型)和2型糖尿病(胰岛素抵抗与胰岛素缺乏并存型)。在这两种类型中,均存在遗传易感性以及促使遗传易感性表现出来的环境因素。在1型糖尿病中,主要异常是β细胞功能广泛缺乏。在2型糖尿病中,会出现胰岛素抵抗,且无法实现或维持为维持正常糖耐量所必需的胰岛素分泌显著代偿性增加。随着β细胞功能持续下降,个体从正常糖耐量发展为糖耐量受损,再发展为主要以餐后高血糖为主的糖尿病,最终发展为空腹高血糖的糖尿病。药物可通过干扰β细胞胰岛素分泌、增加胰岛素抵抗或两者兼而有之来引发糖尿病。据报道,非典型抗精神病药物可导致糖尿病酮症酸中毒、肥胖和胰岛素抵抗、2型糖尿病以及高甘油三酯血症。对于开始使用这些药物治疗的患者,应建立监测系统,以便在代谢异常发展过程中及时发现,从而能够启动充分且及时的治疗。

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