Narrative review: Ketosis-prone type 2 diabetes mellitus

被引:173
作者
Umpierrez, GE
Smiley, D
Kitabchi, AE
机构
[1] Emory Univ, Sch Med, Atlanta, GA 30303 USA
[2] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA
关键词
D O I
10.7326/0003-4819-144-5-200603070-00011
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Several investigators have reported that more than half of African-American persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immunologic features of type 2 diabetes during follow-up. These patients are usually obese, have a strong family history of diabetes, have a low prevalence of autoimmune markers, and lack a genetic association with HLA. Their initial presentation is acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a precipitating cause of metabolic decompensation. At presentation, they have markedly impaired insulin secretion and insulin action, but intensified diabetic management results in significant improvement in beta-cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within a few months of follow-up. On discontinuation of insulin therapy, the period of near-normoglycemic remission may last for a few months to several years. The absence of autoimmune markers and the presence of measurable insulin secretion have proven useful in predicting near-normoglycemic remission and long-term insulin dependence in adult patients with a history of diabetic ketoacidosis. This clinical presentation is commonly reported in African and African-American persons but is also observed in Hispanic persons and those from other minority ethnic groups. The underlying mechanisms for beta-cell dysfunction in ketosis-prone type 2 diabetes are not known; however, preliminary evidence suggests an increased susceptibility to glucose desensitization.
引用
收藏
页码:350 / 357
页数:8
相关论文
共 76 条
[21]  
Gosmanov A, 2003, DIABETES, V52, pA287
[22]   Impaired expression and insulin-stimulated phosphorylation of Akt-2 in muscle of obese patients with atypical diabetes [J].
Gosmanov, AR ;
Umpierrez, GE ;
Karabell, AH ;
Cuervo, R ;
Thomason, DB .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2004, 287 (01) :E8-E15
[23]   ISLET CELL ANTIBODIES IDENTIFY LATENT TYPE-I DIABETES IN PATIENTS AGED 35-75 YEARS AT DIAGNOSIS [J].
GROOP, LC ;
BOTTAZZO, GF ;
DONIACH, D .
DIABETES, 1986, 35 (02) :237-241
[24]   QUANTITATIVE ASSAY USING RECOMBINANT HUMAN ISLET GLUTAMIC-ACID DECARBOXYLASE (GAD65) SHOWS THAT 64K AUTOANTIBODY POSITIVITY AT ONSET PREDICTS DIABETES TYPE [J].
HAGOPIAN, WA ;
KARLSEN, AE ;
GOTTSATER, A ;
LANDINOLSSON, M ;
GRUBIN, CE ;
SUNDKVIST, G ;
PETERSEN, JS ;
BOEL, E ;
DYRBERG, T ;
LERNMARK, A .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 91 (01) :368-374
[25]   In vivo prevention of hyperglycemia also prevents glucotoxic effects on PDX-1 and insulin gene expression [J].
Harmon, JS ;
Gleason, CE ;
Tanaka, Y ;
Oseid, EA ;
Hunter-Berger, KK ;
Robertson, RP .
DIABETES, 1999, 48 (10) :1995-2000
[26]  
HSIN YE, 2001, DIABETIC MED, V18, P895
[27]   Clinical review 135 -: The importance of β-cell failure in the development and progression of type 2 diabetes [J].
Kahn, SE .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (09) :4047-4058
[28]   Editorial: Ketosis-prone diabetes - A new subgroup of patients with atypical type 1 and type 2 diabetes? [J].
Kitabchi, AE .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2003, 88 (11) :5087-5089
[29]  
Kitabchi AE, 2003, DIABETES CARE, V26, P2484, DOI 10.2337/diacare.26.8.2484-a
[30]   Small doses of subcutaneous insulin as a strategy for preventing slowly progressive beta-cell failure in islet cell antibody-positive patients with clinical features of NIDDM [J].
Kobayashi, T ;
Nakanishi, K ;
Murase, T ;
Kosaka, K .
DIABETES, 1996, 45 (05) :622-626