短期胰岛素强化治疗对肥胖2型糖尿病的影响

对初诊的2型糖尿病患者33例进行4周的强化胰岛素治疗.并对治疗成功组患者随访1年.结果4周的胰岛素强化治疗可以逆转初诊肥胖2型糖尿病患者β细胞的功能及改善他们的糖脂代谢指标.结论短期胰岛素强化治疗对初诊肥胖2型糖尿病患者血糖、血脂控制有良好的疗效,并能够改善这些患者的胰岛β细胞功能.     

胰岛素强化治疗及其疗程对初诊2型糖尿病长期缓解的影响

目的 探讨胰岛素强化治疗及疗程对初诊2型糖尿病患者胰岛β细胞功能与长期缓解的影响. 方法 将初诊2型糖尿病患者按胰岛素强化疗程分为15天、30天、60天3组,检测其治疗前后胰岛β细胞功能,并长期随访,分析影响糖尿病缓解的相关因素. 结果 3组患者治疗后胰岛功能明显改善.30天、60天组均较15天组胰岛素早时相分泌指标明显改善,长期缓解率明显提高.回归分析提示胰岛素强化疗程、△I30/△G30治疗后增高值与糖尿病缓解时间呈正相关. 结论 胰岛素强化治疗可显著改善初诊2型糖尿病患者胰岛β细胞功能.适当延长胰岛素强化疗程可更好地恢复胰岛素早时相分泌,更容易取得糖尿病的长期缓解.     

初诊2型糖尿病患者短期胰岛素强化治疗的临床观察

目的 探讨初诊2型糖尿病(T2DM)患者短期胰岛素强化治疗后获长期缓解的影响因素.方法 42例初诊T2DM患者,经2周胰岛素强化治疗后,先给予饮食及运动干预,若血糖不达标,则加用口服降糖药物.追踪观察至少1年. 结果 (1)与强化治疗前相比,强化治疗后以及1年后随访的FPG、曲线下葡萄糖面积、HOMA-IR明显降低,曲线下胰岛索面积、△I_(30)/△G_(30)明显增加(P<0.05或P<0.01).(2)与需口服降糖药物治疗患者相比,单纯饮食控制患者胰岛素强化治疗后FPG、强化治疗停止时胰岛素用量均明显降低,而△I_(30)/△G_(30).则明显增高(P<0.05). 结论 短期胰岛素强化治疗可改善糖尿病患者病理生理缺陷.以较低的胰岛素用量能良好控制血糖,β细胞功能得到较好恢复的初诊T2DM者将来获得病情缓解的可能性较大.     

初发2型糖尿病胰岛素强化治疗后不同治疗方案对胰岛β细胞功能的影响

目的 探讨初发2型糖尿病短期强化治疗后不同治疗方案对胰岛β细胞功能的影响.方法 对86例初发糖尿病患者经2周胰岛素泵强化治疗后,分别给予胰岛素及口服降糖药物治疗6个月,观察两组胰岛β细胞功能改变.结果 经强化血糖控制后继用胰岛素或口服降糖药治疗6个月后,患者空腹血糖、餐后2小时血糖和C肽、糖化血红蛋白（HbAlc）、胰岛β细胞功能指数（HOMA-β）、胰岛素抵抗指数（HOMA-IR）在治疗前后比较差异有统计学意义（P＜0.05）.结论 早期糖尿病严格血糖控制可明显改善胰岛β细胞功能,对于解除高血糖毒性后的患者不论继续采用胰岛素还是口服降糖药物治疗,均可良好控制血糖并进一步改善胰岛β细胞功能.     

胰岛素强化治疗对初诊2型糖尿病患者胰岛β细胞功能和胰岛素抵抗的影响

目的探讨阶梯式胰岛素强化治疗对初诊2型糖尿病（T2DM）患者胰岛β细胞功能和胰岛素抵抗（IR）的影响及机制。方法初诊T2DM患者61例,进行为期2周的胰岛素强化治疗和后续10周的预混胰岛素治疗,比较治疗前后FPG、2hPG、HbA1c、Fins、2hIns、FC-P、2hC-P、TC、TG、胰岛β细胞分泌指数（HOMA-β）和胰岛素抵抗指数（HOMA-IR）的变化。结果治疗后患者FPG、2hPG、HbA1 c和HOMA-IR显著下降,而Fins、2hIns、FC-P、2hC-P和HOMA-β显著上升。结论对血糖明显升高的初诊T2DM患者,短期胰岛素强化治疗及后续数周预混胰岛素皮下注射治疗可有效控制血糖,明显改善胰岛8细胞功能并减轻IR。     

短期胰岛素强化治疗对初诊2型糖尿病长期血糖控制观察

采用患者自身前后对照,观察30例新诊断2型糖尿病患者接受二周短期胰岛素强化治疗,结果治疗2周后显示快速稳定降糖效果,其中28例空腹血糖,餐后2h血糖均良好控制,未见明显低血糖,胰岛β细胞功能在治疗后获得明显改善,静脉注射葡萄糖后10分钟内出现明显的胰岛素、C肽分泌相.部分患者可见到胰岛素第一时相分泌高峰.结论短期胰岛素强化治疗可以显著恢复代表胰岛β细胞功能的血糖刺激的胰岛素第一时相分泌,使患者血糖良好控制.     

强化胰岛素治疗在重症急性胰腺炎中的作用

目的 探讨强化胰岛素治疗在重症急性胰腺炎中的作用.方法 将31例患者分成强化胰岛素治疗组(18例)和对照组(13例).强化胰岛素治疗组在常规综合治疗基础上给予强化胰岛素治疗,使血糖控制在4.4～6.1 mmol/L ;对照组当血糖超过11.9 mmol/L时用胰岛素将血糖控制在10.0～11.7 mmol/L.观察两组患者血和尿淀粉酶、血常规、血生化指标并进行APACHEⅡ评分,分析两组患者的并发症发生率和住院天数.结果 (1)强化胰岛素治疗组APACHEII评分显著下降的时间(1天)较对照组(3天)提前,且强化胰岛素治疗组3天起较对照组显著降低(P＜0.05);(2)强化胰岛素治疗组与对照组比较,患者的住院死亡率和并发症发生率有下降趋势,但无显著性差异;(3)强化胰岛素治疗组患者的住院时间较对照组明显缩短;(4)18例强化胰岛素治疗组患者中有4例发生低血糖血症,而对照组无低血糖血症发生.结论 强化胰岛素治疗可以促使重症急性胰腺炎的恢复,改善病情并减少患者的住院天数.     

新诊断2型糖尿病患者短期胰岛素强化治疗后一年临床观察

新诊断的2型糖尿病患者进行短期胰岛素强化治疗后随访1年，观察血糖控制和胰岛β细胞功能的改变，分析对于初发2型糖尿病患者经短期应用胰岛素强化治疗后是否需要进一步的干预治疗。     

短期胰岛素泵强化治疗对新诊断2型糖尿病患者胰岛素分泌和敏感性的影响

目的 探讨短期胰岛素泵强化治疗对新诊断2型糖尿病患者胰岛素敏感性和胰岛素分泌功能的影响.方法 选取2006年6月至2007年2月在本院就诊的新诊断2型糖尿病患者10例进行为期2周的胰岛素泵强化治疗,在治疗前和停泵24 h后分别进行两次静脉葡萄糖耐量试验(IVGTT)和高胰岛素-正葡萄糖钳夹试验.结果 (1)在治疗前所有糖尿病患者均缺乏急性胰岛素分泌(AIR),经2周强化治疗使血糖正常后,所有患者AIR均有了不同程度地恢复[(7.63±4.73 vs 0.83±1.96)mU/L,P＜0.01)].AIR恢复较好的患者略为年轻和肥胖.(2)糖耐量正常志愿者平均葡萄糖输注率(GIR)为(8.26±2.48)mg·kg-1·min-1,而初发2型糖尿病患者在胰岛素泵强化治疗前GIR为(2.30±0.81)mg·kg-1·min-1(与正常者比,P＜0.01),胰岛素泵强化治疗后GIR升高到(5.33±1.43)mg·kg-1·min-1(P＜0.01).GIR升高显著的患者腰围和体重指数低、治疗前的平均血糖高.结论 短期胰岛素泵强化治疗使血糖"正常化",同时可改善胰岛细胞功能,提高胰岛素敏感性.     

不同胰岛素抵抗状态的初诊2型糖尿病患者短期胰岛素强化疗效观察

对62例不同胰岛素抵抗状态的初诊2型糖尿病患者进行2周胰岛素强化治疗,结果显示胰岛素强化治疗降糖效果确切,能改善β细胞功能,但有明显胰岛素抵抗的患者治疗效果欠佳。     

两类达标血糖控制对急危重患者预后的影响

目的 观察两类达标血糖控制对急危重患者预后的影响. 方法 选取2011年1月至2013年9月我院急诊重症监护室（EICU）急性生理学与慢性健康评分（APACHEⅡ）＞15分且合并高血糖的危重患者200例,分为胰岛素强化治疗（IIT）组和常规控制（CIT）组,比较两组近期死亡率、3d及7d后APACHEⅡ、严重并发症、低血糖、院内感染发生率、住院时间和费用等指标. 结果 IIT组住院时间和费用、院内感染发生率、呼吸衰竭、心功能不全、3d及7d后APACHEⅡ较CIT组低（P＜0.05）.两组低血糖总发生率比较差异有统计学意义（29％ vs 13％,P＜0.01）,严重低血糖发生率、死亡率比较差异无统计学意义. 结论 IIT可能为临床带来较多益处,但增加急危重患者低血糖风险,对降低总死亡率可能无明显影响.     

应激性高血糖的临床研究进展

应激性高血糖在危重症患者中普遍存在并严重影响其预后。应激性高血糖正逐渐受到广泛重视和研究,其发生机制目前已经基本阐明。应激性高血糖的治疗主要是胰岛素治疗,研究表明胰岛素治疗可降低危重症患者的病死率并改善其预后。但由于胰岛素治疗在危重症患者中应用时间较短,胰岛素治疗的血糖控制目标仍然存在一定争议,目前临床上还没有统一的血糖控制目标。本文在简述应激性高血糖的流行病学特征的基础上,探讨了应激性高血糖的发生机制及其重要临床意义。回顾了胰岛素治疗的研究进展并分析了强化胰岛素治疗的优缺点,最后提出了胰岛素治疗的原则和对于不同患者的血糖控制目标。     

Cortisol response to critical illness: effect of intensive insulin therapy

CONTEXT: Both excessive and insufficient activation of the hypothalamic-pituitary-adrenal axis in response to critical illness is associated with increased mortality. OBJECTIVE: The objective of the study was to study the effect of intensive insulin therapy, recently shown to reduce mortality and morbidity of critically ill patients, on the cortisol response to critical illness. DESIGN: This was a preplanned subanalysis of a large randomized, controlled study measuring serum total cortisol, cortisol-binding globulin, and albumin and calculating free cortisol levels. SETTING: The study was conducted at a university hospital surgical intensive care unit. PATIENTS: Four hundred fifty-one critically ill patients dependent on intensive care for more than 5 d and 45 control subjects matched for gender, age, height, and weight participated in this study. INTERVENTION: The intervention was strict blood glucose control to normoglycemia with insulin. RESULTS: Total and calculated free cortisol levels were equally elevated upon admission in both patient groups and thereafter were lower in intensive insulin-treated patients. Lower cortisol levels statistically related to the outcome benefit of intensive insulin therapy. Cortisol-binding globulin levels and structure were affected by critical illness but not insulin therapy, and neither were albumin levels. Administration of hydrocortisone in so-called replacement dose resulted in severalfold higher total and free cortisol levels, indicating that reevaluation of the doses used is warranted. CONCLUSIONS: Lower serum cortisol levels in critically ill patients receiving intensive insulin therapy statistically related to improved outcome with this intervention. The lower cortisol levels were not related to altered cortisol-binding capacity.     

Regulation of the somatotropic axis by intensive insulin therapy during protracted critical illness

The catabolic state of critical illness has been linked to the suppressed somatotropic GH-IGF-binding protein (IGFBP) axis. In critically ill patients it has been demonstrated that, compared with the conventional approach, which only recommended insulin therapy when blood glucose levels exceeded 12 mmol/liter, strict maintenance of blood glucose levels below 6.1 mmol/liter with intensive insulin therapy almost halved intensive care mortality, acute renal failure, critical illness polyneuropathy, and bloodstream infections. Poor blood glucose control in diabetes mellitus has also been associated with low serum IGF-I levels, which can be increased by insulin therapy. We hypothesized that intensive insulin therapy would improve the IGF-I axis, possibly contributing to the clinical correlates of anabolism. Therefore, this study of 363 patients, requiring intensive care for more than 7 d and randomly assigned to either conventional or intensive insulin therapy, examines the effects of intensive insulin therapy on the somatotropic axis. Contrary to expectation, intensive insulin therapy suppressed serum IGF-I, IGFBP-3, and acid-labile subunit concentrations. This effect was independent of survival of the critically ill patient. Concomitantly, serum GH levels were increased by intensive insulin therapy. The suppression of IGF-I in association with the increased GH levels suggests GH resistance induced by intensive insulin therapy, which was reflected by the decreased serum GH-binding protein levels. Intensive insulin therapy did not affect IGFBP-3 proteolysis, which was markedly higher in protracted critically ill patients compared with healthy controls. Also, intensive insulin therapy did not suppress the urea/creatinine ratio, a clinical correlate of catabolism. In conclusion, our data suggest that intensive insulin therapy surprisingly suppressed the somatotropic axis despite its beneficial effects on patient outcome. GH resistance accompanied this suppression of the IGF-I axis. To what extent and through which mechanisms the changes in the GH-IGF-IGFBP axis contributed to the survival benefit under intensive insulin therapy remain elusive.     

Insulin therapy for critically ill hospitalized patients: a meta-analysis of randomized controlled trials

BACKGROUND: Hyperglycemia is common in critically ill hospitalized patients, and it is associated with adverse outcomes, including increased mortality. The objective of this meta-analysis was to determine the effect of insulin therapy initiated during hospitalization on mortality in adult patients with a critical illness. METHODS: An electronic search in the English-language articles of MEDLINE and the Cochrane Controlled Clinical Trials Register and a hand search of key journals and relevant review articles were performed. Randomized controlled trials that reported mortality data on critically ill hospitalized adult patients who were treated with insulin were selected. Data on patient demographics, hospital setting, intervention (formulation and dosage of insulin, delivery method, and duration of therapy), mortality outcomes, adverse events, and methodological quality were extracted. RESULTS: Thirty-five trials met the inclusion criteria. Combining data from all trials using a random-effects model showed that insulin therapy decreases short-term mortality by 15% (relative risk [RR], 0.85; 95% confidence interval [CI], 0.75-0.97). In subgroup analyses, insulin therapy decreased mortality in the surgical intensive care unit (RR, 0.58; 95% CI, 0.22-0.62), when the aim of therapy was glucose control (RR, 0.71; 95% CI, 0.54-0.93), and in patients with diabetes mellitus (RR, 0.73; 95% CI, 0.58-0.90). A near-significant trend toward decreasing mortality was seen in patients with acute myocardial infarction who did not receive reperfusion therapy (RR, 0.84; 95% CI, 0.71-1.00). No randomized trials of insulin in the medical intensive care unit were identified. CONCLUSION: Insulin therapy initiated in the hospital in critically ill patients has a beneficial effect on short-term mortality in different clinical settings.     

The Role of Insulin Therapy in Critically I11 Patients

Protracted critically ill patients have a seriously deranged metabolism, characterized by severe hyperglycemia, a disturbed serum lipid profile, and protein hypercatabolism. The severity of stress-induced hyperglycemia and insulin resistance in critically ill patients reflect the risk of death. A large, prospective, randomized, controlled study showed that maintaining normoglycemia with intensive insulin therapy reduces morbidity and mortality of surgical intensive care patients. These results were recently confirmed by two studies: one randomized controlled study of surgical intensive care patients and a prospective observational study of a heterogeneous patient population admitted to a mixed medical/surgical intensive care unit. The clinical benefits of intensive insulin therapy appear to be related both to prevention of glucose toxicity and to other direct insulin actions that are independent of glycemic control. Prevention of the toxic effects of high circulating glucose levels protected the ultrastructure and function of hepatocyte mitochondria. Benefits of the non-glycemic effects of insulin included partial correction of the deranged serum lipid profile and possibly counteraction of the catabolic state. In addition to its metabolic effects, intensive insulin therapy also prevented excessive inflammation and improved immune function.     

Challenges in Glycemic Control in Perioperative and Critically Ill Patients: Reducing Glycemic Variability in Intensive Care Unit Patients: A New Therapeutic Target?

Acute hyperglycemia is common in critically ill patients. Strict control of blood glucose (BG) concentration has been considered important because hyperglycemia is associated independently with increased intensive care unit mortality. After intensive insulin therapy was reported to reduce mortality in selected surgical critically ill patients, lowering of BG levels was recommended as a means of improving patient outcomes. However, a large multicenter multination study has found that intensive insulin therapy increased mortality significantly. A difference in variability of BG control may be one possible explanation why the effect of intensive insulin therapy varied from beneficial to harmful. Several studies have confirmed significant associations between variability of BG levels and patient outcomes. Decreasing the variability of the BG concentration may be an important dimension of glucose management. If reducing swings in the BG concentration is a major biologic mechanism behind the putative benefits of glucose control, it may not be necessary to pursue lower glucose levels with their attendant risk of hypoglycemia.     

Perioperative insulin therapy using a closed-loop artificial endocrine pancreas after hepatic resection

Postoperative hyperglycemia is common in critically ill patients, even in those without a prior history of diabetes mellitus. It is well known that hyperglycemia induced by surgical stress often results in dysregulation of liver metabolism and immune function, impairing postoperative recovery. Current evidence suggests that maintaining normoglycemia postoperatively improves surgical outcome and reduces the mortality and morbidity of critically ill patients. On the basis of these observations, several large randomized controlled studies were designed to evaluate the benefit of postoperative tight glycemic control with intensive insulin therapy. However, intensive insulin therapy carries the risk of hypoglycemia, which is linked to serious neurological events. Recently, we demonstrated that perioperative tight glycemic control in surgical patients could be achieved safely using a closed-loop glycemic control system and that this decreased both the incidence of infection at the site of the surgical incision, without the appearance of hypoglycemia, and actual hospital costs. Here, we review the benefits and requirements of perioperative intensive insulin therapy using a dosed-loop artificial endocrine pancreas system in hepatectomized patients. This novel intensive insulin therapy is safe and effectively improves surgical outcome after hepatic resection.     

内科危重病患者胰岛素抵抗相关因素研究

目的目的通过观察危重病患者早期血糖、胰岛素浓度及胰岛素抵抗(IR)的变化,这些指标与疾病。方法选取本院ICU内科危重病患者52例,于入院24h内进行急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分,次日清晨抽取空腹静脉血测血糖(FBG)和胰岛素(FINS)浓度,使用稳态模式法(HOMA)计算胰岛素抵抗指数(HOMA-IR)。52例中入ICU28d后仍存活者划入存活组,余为死亡组。另选择健康体检者30人为对照组,检测FBG、FINS及计算HO-MA-IR。结果内科危重病组FBG、FINS浓度及HOMA-IR均高于对照组(P均0.01)。死亡组FBG浓度、HOMA-IR及A-PACHEⅡ评分均高于存活组(P0.05);而FINS浓度两组比较差异无统计学意义。按APACHEⅡ评分分值≤10分、11～20分、≥21分3组,表现为随评分增加,各组FBG、FINS均显著增加(P0.05)。结论危重病应激状态下存在胰岛素抵抗。FBG及HOMA-IR可反映危重病严重程度及预后,部分患者表现为高胰岛素血症,但FINS不能准确反映危重病的病情及预后。