Abstract：Objective To analyze the clinical features of 20 patients with acute onset type 1 diabetes (AT1DM), 11 patients with fulminant type 1 diabetes (FT1DM) and 23 patients with chronic onset type 1 diabetes (SPIDDM). Methods Data such as disease course, age, gender, body mass index, random blood glucose, HbA1c, C-peptide, creatinine, serum potassium, arterial blood pH, and white blood cell count were collected for statistical analysis, and the clinical characteristics of each subtype were further compared. Results The course of FT1DM was[(4.23±1.21)days] shorter than those of AT1DM[(146.25.±33)days] and SPIDDM[(518.2±64.6)days]. The blood glucose concentration at the onset of FT1DM[(38.23±15.41)(mmol/l)] was higher than those of AT1DM [(16.75±4.88)(mmol/l)] and SPIDDM[(13.44±4.12)(mmol/l)]. The FT1DM glycosylated hemoglobin concentration[(6.58±1.66)(mmol/l)] was lower than those of AT1DM[(12.83±3.81)(mmol/l)] and SPIDDM[(11.01±3.21)(mmol/l)]. The mean blood glucose concentration fluctuation range of FT1DM[(9.55±2.40) (mmol/l)] was higher than those of AT1DM[(5.54±1.84) (mmol/l] and SPIDDM[(5.13±1.31)(mmol/l). The difference between the maximum and minimum blood glucose concentration of FT1DM[(13.54±3.227)(mmol/l)] was higher than those of AT1DM[(7.46±3.44)(mmol/l)] and SPIDDM[(6.92±2.37)(mmol/l)]. Arterial blood pH of FT1DM (7.003±0.083) was lower than those of AT1DM (7.393±0.095) and SPIDDM (7.395±0.038). The fasting C-peptide concentration[(0.03-0.02)(ng/ml)] of FT1DM was lower than those of AT1DM[(0.91±0.43) (ng/ml)] and SPIDDM[(1.05±0. 47) (Ng/ml)]. The differences between the above indicators were statistically significant (P<0.01). Conclusion Compared with AT1DM and SPIDDM, FT1DM has a shorter duration of disease, greater fluctuations in mean blood glucose, more severe ketoacidosis, poorer islet function, and the more dangerous condition.
[1] MATSUMOTO H, MURASE-MISHIBA Y, YAMAMOTO N, et. al. Glycated albumin to glycated hemoglobin ratio is a sensitive indicator of blood glucose variability in patients with fulminant type 1 diabetes[J]. Intern Med, 2012,51(11):1315-1321. [2] AMERICAN DIABETES ASSOCIATION. Standards of medical care in diabetes-2007[J]. Diabetes Care, 2007,30(Suppl 1):S4-S41. [3] IMAGAWA, HANAFUSA T. Fuliminant type 1 diabetes mellitus immunoen-docrinology, Scientific and cllinical aspects[M]. New York: humanapress, 2011:331-342. [4] KAWASAKI E, MARUYAMA T, IMAGAWA A, et al. Diagnostic criteria for acute-onset type 1 diabetes mellitus(2012): Report of the Committee o f Japan Diabetes Society on the research of fulminant and Acute-onset Type 1 Diabetes Mellitus[J]. Journal of Diabetes Investigation, 2013,5(1):115-118. [5] KAWABATA Y, IKEGAMI H, AWATA T, et al. Differential association of HLA with three subtypes of type 1 diabetes: fulminant,slowlyprogressive and acute-onset[J]. Diabetologia, 2009,52 (12):2513-2521. [6] WANG Z, ZHENG Y, TU Y,et al. Immunological aspects of fulminant type 1 diabetes in Chinese[J]. J Immunol Res,2016(7):1-6. [7] 周智广,郑超.暴发性1型糖尿病:一种不容忽视的糖尿病急危重症[J].内科急危重症杂志,2008,14(4):169-170. [8] YASUDA H, JIN Z, NAKAYAMA M, et al. NO-mediated cyto-toxicity contributes to multiple low dose streptozotocin induceddiabetes but not to NOD diabetes[J]. Diabetes Research & ClinicalPractice,2009,83(2):200-207. [9] PAOLIP, ABRANNA F, TIRIBILL B, et al. Protein Homocysteinylation inducesthe Formation on of Toxic Amyloid Like Protofibrils[J]. Journalmal of Melocular Bilologoy, 2010,9(4):102-105. [10]SASTRY BK,INDIRA N.A case-control study Of plasma homocysteinelevels in South Indians and without coronary artery disease[J]. Indian Heart J, 2001,53(6):749-753.
