| The incidence rate of diabetes mellitus gets higher year by year within the scope of world, anticipating to rise to 5.4% till 2025. Type 2 diabetes mellitus(T2DM) is the most familiar type, occupying for 90% of diabetic. In the patients diagnosed as T2DM about 10% -25% of specific autoantibodies to pancreatic islet cells show positive. LADA has no united diagnosis standard till now, and the abroad literature generally consider T2DM who show ICA or GAD-Abs positive and get rise in adult as LADA. GAD-Ab and ICA are the two most important diagnosed indexes of LADA. LADA is namely latent autoimmune diabetes mellitus in adults. WHO puts forward the new suggestion on the diabetes mellitus division that is to make LADA belong to the subgroup of type 1 diabetes mellitus (slowly progressive autoimmune type)in 1997. But it is not completely similiar with classic type 1 diabetes mellitus in the aspects of immunopathology. Self-antigen can cause auto-immunoreaction after tolerating many years and go through at least six-month non-insulin dependent phase. Following progressive immune injury for 1-10 years, it enters the insulin dependent phase finally, appearing the ketosis tendency. Pathophysiology characteristics of T2DM are insulin resistance of liver, adipose tissue ,skeletal muscle and decreased secretion of islet βcell( namely β cell's function abnormality).Comprehensive action of these abnormal factors causes chronic hyperglycemia and serious chronic complications. In this study we considered GAD-Ab and ICA as signals of pancreas injuried to probe into whether there is difference between patients with T2DM or LADA in the aspect of general clinical data and biochemical characteristics. 415 clinical new-diagnosed patients with T2DM were examined and divided into LADA group and T2DM group according to positive/negative of antibodies. The age, gender, body mass index, blood glucose, blood pressure, blood lipid, HbA1c, C peptide, microdose albumin in urine, eye ground were examined. We also make clear whether they have complications such as hypertension, hyperlipemia, diabetic nephropathy and diabetic retinopathy. The mean of age, body mass indices, blood pressure, fasting and postprandial 2h blood glucose,blood lipid and HbA1c were showed as ±s. P value is above 0.05 by using Homogeneity assay and Two-sample t-test; incidence rate of each complications compared between groups was analysed using chi-square test and each P value is above 0.05 ; fasting and postprandial 2h C peptide was examined by t-test and P value are one between 0.01 and 0.025 and another less than 0.0005.Above all, we can draw a conclusion: 1 The clinical manifestation of LADA and T2DM at first diagnosed was resemble. There is no evidence difference of age, body mass index, blood pressure, fasting and postprandial 2h blood glucose,blood lipid and HbA1c between two groups.2 Fasting and Postprandial 2h C peptide both show the obvious difference ( P value all less than 0.05),but the difference of Postprandial 2h C peptide shows more obvious ( P<0.0005), expressing islet storage function is already obviously injured when LADA sufferers.3 The incidence of complications such as hypertension, hyperlipemia, diabetic nephropathy and diabetic retinopathy is similar between T2DM and LADA. There is no significant difference between them.Clinical manifestation of LADA in non-insulin dependent phase resembles to T2DM, and the symptom of three many one few is more obvious than T2DM , non-ketosis in 6 months after diagnosed,the lower serum C peptide level and the higher blood glucose level,controlled by using the food and/ or oral hyperglycemic agent .The function of islet β cell will be proceedly injuried during 1 -10 years and the insulin secrete will proceedly reduce. Then the sufferers will experience secondary invalidation of oral hyperglycemic agent and need insulin treatment. Finally Ketoacidosis tendency appears. So diagnosis emphasis of LADA should be in early non-insulin dependent phase ,in which we make theβcell at rest a...
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