酮症倾向糖尿病

酮症倾向糖尿病是一组临床综合征,主要包括1型糖尿病和酮症倾向的2型糖尿病。1型糖尿病发生酮症的原因主要为自身免疫所致胰岛素缺乏。酮症倾向的2型糖尿病可能有某些遗传缺陷,对葡萄糖毒性或糖脂毒性诱导的氧化应激敏感性增加,导致胰岛β细胞功能衰竭和胰岛素抵抗而发生酮症。1型糖尿病需胰岛素终身治疗,而酮症倾向的2型糖尿病在酮症纠正后且密切随访胰岛功能的情况下,可以使用口服降糖药治疗。     

酮症倾向糖尿病

酮症倾向糖尿病是一组临床综合征，主要包括1型糖尿病和酮症倾向的2型糖尿病。1型糖尿病发生酮症的原因主要为自身免疫所致胰岛素缺乏。酮症倾向的2型糖尿病可能有某些遗传缺陷，对葡萄糖毒性或糖脂毒性诱导的氧化应激敏感性增加，导致胰岛β细胞功能衰竭和胰岛素抵抗而发生酮症。1型糖尿病需胰岛素终身治疗，而酮症倾向的2型糖尿病在酮症纠正后且密切随访胰岛功能的情况下，可以使用口服降糖药治疗。     

酮症和非酮症起病的新诊断2型糖尿病胰岛功能比较

酮症倾向糖尿病（ketosis－pronediabetes,KPD）指以自发酮症或酮症酸中毒起病的一类糖尿病,曾一度被认为是自身免疫性1型糖尿病的重要临床特征,但是近年来一类以自发性酮症起病的肥胖糖尿病患者开始引起人们的注意,这类患者有典型的高血糖症状伴自发性酮症起病,具有肥胖、短期内不依赖胰岛素治疗等2型糖尿病的临床特征。过去被称为1B型糖尿病、特发性1型糖尿病、不典型糖尿病等”…,近来更多学者称其为酮症倾向的2型糖尿病。本研究分析了酮症和非酮症起病的2型糖尿病患者其临床特征及胰岛β细胞功能,为治疗方案的选择提供依据。     

102例酮症倾向2型糖尿病患者的临床特征分析

目的探讨酮症倾向2型糖尿病的临床特征及治疗方法。方法102例酮症倾向2型糖尿病在胰岛素降糖治疗1个月后,停用胰岛素给予口服降糖药单用或联合治疗,接受至少1年的随访。根据最终的治疗方案,分为口服降糖药（OHA）组和胰岛素治疗（INS）组。结果（1）经过1年的随访,77．5％的患者通过口服药物可将血糖得到较满意的控制,22．5％的患者因严重高血糖或酮症需要再次接受胰岛素治疗。（2）酮症倾向的2型糖尿病具有普通2型糖尿病许多类似的临床特点和病理生理特征。（3）与INS组相比,OHA组起病时的血糖、HbA1c、胰岛素强化治疗达标时间、男性构成比较低,而BMI、甘油三酯、糖尿病家族史构成比较高（P〈0．05）。（4）在高血糖得到控制后,OHA组胰岛素分泌指数（MBCI）和MBCI的变化值均大于INS组（P〈0．05）。（5）多元回归分析发现,高血糖控制后的MBCI、：BMI为选择不同治疗方案（口服药治疗或胰岛素治疗）的主要参考因素。结论酮症倾向2型糖尿病可能是2型糖尿病的一个亚型。在短期胰岛素治疗后,大多数可以改用口服降糖药,高血糖控制后的MBCI、：BMI将有助于不同降糖方案的选择。     

如何模拟生理状态的胰岛素分泌？

患上糖尿病后，医生往往会根据患者的临床表现、伴随症状及实验室检查结果，将患者分为1型或2型糖尿病患者。两型糖尿病的发病机制不同，治疗也有很大的差异。1型糖尿病的特点是胰岛素绝对缺乏；如果没有外源胰岛素的替代治疗，患者将会发生一些危及生命的代谢紊乱如糖尿病酮症酸中毒等，所以1型糖尿病患者需要依赖胰岛素治疗。     

内分泌代谢系统的糖尿病试题与题解

A型题:请从A、B、C、D中选出一个最佳答案1.关于 1型糖尿病,下列哪项是错误的?A.起病较急,症状明显;B.对胰岛素不敏感;C.大多消瘦;D.有发生酮症酸中毒的倾向。(答案为B。1型糖尿病发病上是因绝对缺乏胰岛素,无胰岛素抵抗,故对胰岛素敏感。)2.病人空腹血糖为 6 5mmol/L,下列哪项     

酮症起病的糖尿病患者胰岛素抵抗的特点

对35例酮症起病、自身抗体阴性的糖尿病患者及38例无酮症的初诊2型糖尿病患者,应用胰岛素治疗3个月.计算治疗前后胰岛素抵抗指数.结果 表明酮症起病的糖尿病患者胰岛素抵抗较普通2型糖尿病轻,血糖控制后胰岛素敏感性恢复程度较小.     

以糖尿病酮症发病42例患者临床分析

42例以糖尿病酮症为首发患者临床特点、治疗转归等综合分析,并进行随访6～12个月。结果酮症时病情重,合并酸中毒,酮体消失时间长的患者倾向于T,DM,依赖于胰岛素治疗。酮症时病情轻,无酸中毒,酮体消失时间短的患者倾向于T2DM（胰岛素抵抗为主）,胰岛素促泌剂和／或胰岛素增敏剂治疗就能很好控制病情。结论以糖尿病酮症为首发症状的糖尿病患者可以根据发病时临床表现及短期病情进展划分为两类（即T1DMT、T2DM）。     

自发酮症起病的糖尿病87例临床特征及分型探讨

目的探讨自发酮症起病的糖尿病的临床特征及分型。方法将2003-01～2004-05南京鼓楼医院收治的自发酮症起病的糖尿病患者(87例)根据自身抗体阳性与否,分为抗体阴性组(67例)及抗体阳性组(1A型糖尿病组)(20例)。抗体阴性的患者依据是否依赖胰岛素治疗,进一步分为胰岛素依赖组(27例)及非胰岛素依赖组(40例)。不同组别的临床特征、生化指标之间进行比较。结果抗体阴性组男性发生率显著高于女性;具明显的家族遗传倾向;起病时体重指数显著高于1型糖尿病组,甘油三酯水平高于其他两组;空腹及餐后2hC肽水平介于2型及1型糖尿病组之间。胰岛素依赖组较胰岛素非依赖组具更强的男性易患性;超重和肥胖患者所占比例较低;酮症程度较重;血糖及空腹C肽水平两组之间差异无显著性;3个月后空腹C肽水平,非胰岛素依赖组显著高于胰岛素依赖组。结论酮症起病的糖尿病依据抗体阳性与否,分为抗体阴性和抗体阳性酮症起病的糖尿病,后者即为1A型糖尿病。抗体阴性酮症起病的糖尿病可依据是否依赖胰岛素治疗,分为酮症起病的2型糖尿病和特发性1型糖尿病(1B型糖尿病)。     

74例酮症倾向的2型糖尿病患者临床特点分析

目的 探讨酮症倾向的2型糖尿病患者的临床特征.方法 选取我院74例酮症倾向的2型糖尿病患者,与172例无酮症倾向的2型糖尿病患者及58例1型糖尿病患者临床特点进行回顾性分析.结果 酮症倾向的2型糖尿病患者有如下特点:(1)血糖水平明显高于无酮症倾向的2型糖尿病患者(P＜0.01);(2)与1型糖尿病患者相比,仍存留部分胰岛功能,空腹C肽、餐后C肽水平明显高于1型糖尿病患者(P＜0.01);(3)体重指数(BMI)、腰臀比(WHR)、血脂水平明显高于1型糖尿病患者(P＜0.01);(4)代谢综合征的发生率明显高于1型糖尿病患者(P＜0.01),与无酮症倾向的2型糖尿病患者相比,差异无统计学意义(P＞0.05).结论 以酮症起病的初发2型糖尿病患者具有较高的血糖水平,胰岛β细胞功能受损,代谢综合征发生率较高.     

Comparison of type 1, type 2, and atypical ketosis-prone diabetes at 4 years of diabetes duration

CONTEXT: Atypical ketosis-prone diabetes (KPD) is frequently detected in obese individuals at diagnosis of diabetes, yet its precise pathophysiology is not understood. AIM: The hypothesis tested in this study states that while individuals with atypical KPD are phenotypically similar to those with type 2 diabetes, metabolically, they behave more like individuals with autoimmune type 1 diabetes. METHODS: Thirty-seven individuals of Black, Hispanic, or White background and a diagnosis of diabetes mellitus for an average duration of 4 years participated in this cross-sectional study. Ten, 12, and 15 subjects had type 1, atypical, and type 2 diabetes, respectively. Insulin secretion was evaluated by a mixed-meal test. Insulin sensitivity and fuel oxidation were assessed by simultaneous euglycemic hyperinsulinemic clamp and indirect calorimetry. Lastly, a 12-h insulin withdrawal test was performed. RESULTS: Insulin secretion, insulin sensitivity, and the insulin withdrawal tests yielded significant differences for type 1 vs. atypical diabetes and type 1 vs. type 2 diabetes, while there were no significant differences between atypical vs. type 2 diabetes. The indirect calorimetry showed higher-than-normal basal nonprotein respiratory quotients (RQs) and lower-than-normal insulin-stimulated nonprotein RQs across the three study groups. CONCLUSIONS: After 4 years from diabetes diagnosis and while far from optimal glycemic control, atypical KPD resembles type 2 diabetes phenotypically and metabolically as well. Therefore, this study supports the classification of atypical KPD as ketosis-prone type 2 diabetes, and the concept that metabolic inflexibility occurs in the presence of insulin resistance in type 1 and type 2 diabetes.     

Preclinical and manifest diabetes mellitus in young patients with friedreich's ataxia: no evidence of immune process behind the islet cell destruction

Summary Friedreich's ataxia is known to be associated with diabetes mellitus in up to 20% of the patients. However, type, development and course of diabetes mellitus are not well characterised. We report on 3 patients (2 female and 1 male, age 13–20 years) with the combination of Friedreich's ataxia and diabetes mellitus. Diabetes mellitus was characterised as follows: (1) it was strictly insulin-dependent and ketosis-prone, (2) the average insulin requirement was 1 U/kg body weight, (3) the HLA haplotype was not typical of Type 1 (insulin-dependent) diabetes mellitus, (4) there were no positive immune parameters typical of Type 1 diabetes at the clinical onset of diabetes mellitus and (5) there was no remission. To evaluate a preclinical phase as in common autoimmune Type 1 diabetes, i.v. glucose tolerance tests (0.5 g glucose/kg body weight) were performed in 8 patients with Friedreich's ataxia without diabetes mellitus. Seven patients had normal early phase insulin response. In contrast, the glucose disappearance rate was slow in 4 and normal in 3 patients. One of the 8 patients showed a prediabetic metabolic state: the early-phase insulin response was abolished and the glucose disappearance rate was abnormal. The results suggest that diabetes in Friedreich's ataxia is caused by a loss of islet cells similar to common Type 1 diabetes but without HLA-association and without serologic evidence for autoimmune destruction of the islet cells.     

Diabetes in Africans. Part 2: Ketosis-prone atypical diabetes mellitus

Diabetes is increasing with ageing and changes in lifestyle in populations of African ancestry as described in the first part of this review. Apart from classical type 1 and Type 2 diabetes, atypical presentations are observed in these populations, especially "tropical" and "ketosis-prone" atypical diabetes. Ketosis-prone atypical diabetes that has been classified by ADA as idiopathic Type 1 diabetes or Type 1b is the most common atypical form. It is characterised by an acute initial presentation with severe hyperglycaemia and ketosis, as classical Type 1 diabetes. In the subsequent clinical course after initiation of insulin therapy, prolonged remission is often possible with cessation of insulin therapy and maintenance of appropriate metabolic control. Metabolic studies showed a markedly blunted insulin secretory response to glucose, partially reversible with the improvement of blood glucose control. Variable levels of insulin resistance are observed, especially in obese patients. Pancreatic B-cell autoimmunity is an exceptional finding. Association with type 1 susceptibility HLA alleles is variable. The molecular mechanisms underlining the insulin secretory dysfunction are still to be understood and may involve gluco-lipotoxicity processes, glucagon dysregulation, effect of stress, or may be genetically determined. The present review summarises the available clinical and metabolic features and suggests some pathogenetic hypotheses and principles of management for the ketosis-prone atypical diabetes of the Africans.     

Systematic review and meta-analysis of short-acting insulin analogues in patients with diabetes mellitus

BACKGROUND: This article compares the effect of treatment with short-acting insulin (SAI) analogues vs regular insulin on glycemic control, hypoglycemic episodes, quality of life, and diabetes-specific complications. METHODS: Electronic searches (Cochrane Library, MEDLINE, and EMBASE) and additional searching (pharmaceutical companies, experts, approval agencies, abstracts of diabetology meetings) were performed. Two reviewers independently screened randomized controlled trials to determine inclusion. RESULTS: Forty-two randomized controlled trials that assessed the effect of SAI analogues vs regular insulin in 7933 patients with type 1 diabetes mellitus, type 2 diabetes mellitus, and gestational diabetes mellitus were identified. The weighted mean difference between hemoglobin A(1c) values obtained using SAI analogues and regular insulin was -0.12% (95% confidence interval [CI], -0.17% to -0.07%) for adult patients with type 1 diabetes mellitus and -0.02% (95% CI, -0.10% to 0.07%) for patients with type 2 diabetes mellitus. The standardized mean difference for overall hypoglycemia (episodes per patient per month) was -0.05 (95% CI, -0.22 to 0.11) and -0.04 (95% CI, -0.12 to 0.04) comparing SAI analogues with regular insulin in adult patients with type 1 and type 2 diabetes mellitus, respectively. No differences between treatments were observed in children with type 1 diabetes, pregnant women with type 1 diabetes mellitus, and women with gestational diabetes. Concerning quality of life, improvement was observed only in open-label studies in patients with type 1 diabetes mellitus. No differences were seen in a double-blinded study of patients with type 1 or in the studies of patients with type 2 diabetes mellitus. CONCLUSION: Our analysis suggests only a minor benefit to hemoglobin A(1c) values in adult patients with type 1 diabetes mellitus but no benefit in the remaining population with type 2 or gestational diabetes from SAI analogue treatment.     

Looking to the future: focus on DPP-4 inhibitors for the treatment of type 2 diabetes and emerging therapies

Strong evidence exists demonstrating the benefits of tight glycemic control in type 1 and type 2 diabetes mellitus patients, but glycemic goals are not adequately achieved for many patients. Advancement in the knowledge surrounding the physiology of endogenous glucoregulatory peptide hormones, such as glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1, has led to new therapeutic targets for the treatment of type 2 diabetes mellitus. Dipeptidyl peptidase-4 (DPP-4) inhibitors provide practitioners with a novel mechanism of action to use for combination therapies for the treatment of type 2 diabetes mellitus. This article, part 3 of a 3-part series, reviews the new class of medications known as DPP-4 inhibitors as well as discusses a future buccal insulin formulation, Oral-Lyn, on the horizon for the treatment of diabetes mellitus.     

Insulin Dose Adjustment Following Bariatric Surgery,a Review of Available Literature

Bariatric surgery is a known and effective treatment for type 2 diabetes mellitus. Patients with type 1 diabetes mellitus and exogenous insulin-requiring type 2 diabetes mellitus require adjusted insulin dosing after surgery to avoid hypoglycemia. This review describes insulin dose adjustments following a variety of bariatric procedures. After searching the available literature and assessing for eligibility, 8 articles were included. The Johns Hopkins Research Evidence Appraisal Tool for literature appraisal was used. The results of this review reveal insulin dose adjustment varies based upon surgical procedure type and time of follow-up from the procedure.     

Double diabetes: possible but unpublished complication of insulin pump therapy

"Double diabetes," which refers to the coexistence of type 1 and type 2 diabetes mellitus, is a newly coined term in the diabetic literature. Excessive weight gain and a family history of type 2 diabetes in a patient with type 1 diabetes are the possible major causes. We report a case of double diabetes in a 45-year-old patient with type 1 diabetes mellitus that developed after insulin pump therapy. Insulin pump therapy is a valuable method used in the management of type 1 diabetes mellitus that may provide life comfort. However, this comfort may result in excessive weight gain, which, when combined with a family history of type 2 diabetes mellitus, may predispose to double diabetes. Clinicians must consider this pattern during the use of insulin pump therapy in patients with type 1 diabetes.