甘精胰岛素联合瑞格列奈对磺脲类继发失效老年糖尿病人的疗效和胰岛功能的影响

目的 探讨磺脲类药物继发性失效的老年糖尿病患者加用甘精胰岛素(GL)或中性鱼精蛋白锌胰岛素(NPH)的疗效和治疗前后胰岛功能的变化.方法 对磺脲类药物继发性失效的54例老年糖尿病患者,改用瑞格列奈,并分别于睡前注射GL(26例)或NPH(28例),观察16 w前后空腹血糖、餐后2 h血糖、糖化血红蛋白、空腹C肽、餐后C肽的变化.结果 两组均有显著的降血糖作用,且所用的胰岛素剂量相近,但GL组的低血糖事件明显少于NPH组,且GL组治疗后C肽水平明显升高.结论 睡前注射NPH或GL均对磺脲类药物继发性失效的老年糖尿病患者有很好的疗效,但应用GL低血糖发生率低,且可能改善胰岛功能.     

磺脲类继发失效糖尿病患者加用胰岛素疗效及胰岛B细胞功能变化

目的探讨磺脲类药物继发性治疗失效的2型糖尿病患者加用甘精胰岛素(IG)或中效精蛋白人胰岛素(NPH)后的疗效及胰岛B细胞功能的变化。方法2004-05—2004-11对上海市第一人民医院52例磺脲类药物继发性失效的糖尿病患者,改用格列吡嗪控释片,并分别睡前注射IG(20例)或NPH(32例),观察16周内多点空腹血糖变化及16周前后HbA1c、餐后血糖、空腹和餐后C肽。结果两组均有显著的降血糖效果,且疗效、所用剂量相近,但IG组低血糖事件明显少于NPH组,且治疗后血清C肽水平明显升高,而NPH组C肽无变化。结论睡前注射甘精胰岛素或中效人胰岛素对磺脲类继发性失效者均有较高的达标率,联用甘精胰岛素可改善胰岛B细胞功能。     

甘精胰岛素对老年危重疾病合并高血糖患者预后的影响

目的 为探讨磺脲类药物继发性失效的老年糖尿病患者加用甘精胰岛素(GI)或中性鱼精蛋白锌胰岛素(NPH)的疗效和治疗前后胰岛功能的变化.方法 对磺脲类药物继发性失效的54例老年糖尿病患者,改用瑞格列奈,并分别于睡前注射GI(26例)或NPH(28例),观察16 w前后空腹血糖、餐后2 h血糖、糖化血红蛋白、空腹C肽、餐后C肽的变化.结果 两组均有显著的降血糖作用,且所用的胰岛素剂量相近,但GI组的低血糖事件明显少于NPH组,且GI组治疗后C肽水平明显升高.结论 睡前注射中性鱼精锌蛋白胰岛素或GI均对磺脲类药物继发性失效的老年糖尿病患者有很好的疗效,但应用GI低血糖发生率低,且可能改善胰岛功能.     

甘精胰岛素联合口服降糖药与预混胰岛素对2型糖尿病患者血糖控制稳定性的影响

目的 对比短期内甘精胰岛素联合口服降糖药与预混胰岛素对2型糖尿病患者血糖控制、血糖稳定性及安全性的影响.方法 连续入选60例因血糖控制不佳初次使用胰岛素的2型糖尿病住院患者,随机分为甘精胰岛素联合口服降糖药物组(甘精组)和预混胰岛素组(预混组),分别给予甘精胰岛素每日一次皮下注射联合餐前口服降糖药以及给予门冬胰岛素30注射液每日两次皮下注射治疗.开始治疗2 w后,采用动态血监测测系统(CGMS)观察血糖波动情况,同时记录患者全天指血血糖并与人院时比较,记录患者胰岛素使用量以及低血糖情况.结果 两组患者入组时一般临床特征及生化指标无显著差异;治疗2 w后CGMS监测两组平均血糖(MBG),高血糖曲线下面积(AUC)无明显差别,甘精组血糖标准差(SD)、日内平均血糖波动幅度(MAGE)、低血糖曲线下面积(AUC)均显著低于预混组;甘精组胰岛素使用量及低血糖发生率显著低于预混组(均P＜0.05).结论 与预混胰岛素比较,甘精胰岛素联合口服降糖药物治疗2型糖尿病,降糖效果相当,血糖波动更小,低血糖发生率低.     

甘精胰岛素联合格列美脲用于老年2型糖尿病患者效果观察

目的探讨甘精胰岛素联合格列美脲用于老年2型糖尿病的效果及安全性。方法将100例口服降糖药物控制不佳的老年2型糖尿病患者随机分为观察组和对照组各50例。观察组每日1次早餐前口服格列美脲,每晚22时注射甘精胰岛素1次;对照组每日早、晚餐前分别注射优泌林70/30。均以空腹血糖5.0～7.0 mmol/L、餐后血糖6.0～10.0 mmol/L为治疗目标,共治疗16周;治疗期间根据血糖情况调整剂量。观察血糖水平及血清C肽水平和低血糖发生情况。结果治疗16周两组全天血糖谱均明显下降,C肽水平均明显升高（P均〈0.05）;观察组低血糖事件、胰岛素用量、体质量增加均明显少于对照组,P均〈0.05。结论甘精胰岛素联合格列美脲用于老年2型糖尿病不仅降糖效果好,且较为安全。     

降糖药致老年低血糖昏迷14例临床分析

低血糖昏迷是降糖药的严重副反应之一,随着糖尿病发病率的增高,临床上低血糖昏迷并不少见,其中又以老年人多见。现就我院近 10年来因降糖药所致的老年低血糖昏迷 14例分析如下。1　临床资料1 1　一般资料　我院 1994年 1月 ~2004年 1月共收治年龄≥60岁的降糖药物导致的老年低血糖昏迷 14例,年龄 61~82岁,平均 ( 73 6±5 1 )岁,男 11例,女 3例 (门诊 9例,住院 5例 )。诊断标准为病人呈现昏迷状态后即测血糖<2 8mmol/L。所用药物中,普通胰岛素 4例,分别为每日 30、20U皮下注射, 2例每日8、10U用于葡萄糖 胰岛素 钾极化液(GIK)中静滴而…     

急诊糖尿病低血糖昏迷病因及防范措施分析

目的探讨急诊糖尿病低血糖昏迷病因,总结相应的防范措施。方法选取该院2013年5月—2014年5月收治的60例糖尿病低血糖昏迷患者作为研究对象,对其临床资料进行回顾性分析,总结低血糖昏迷发病诱因。结果导致低血糖昏迷的可控因素包括进食减少(66.67%),磺脲类降糖药使用不合理(31.67%),自行购买使用降糖中药或应用新的降糖方案(26.67%),过量应用胰岛素(21.67%),调整降糖方案(3.33%)等。不可控因素包括该病程6年(38.33%),年龄≥65岁(60.00%),急性应激性事件(41.67%),慢性合并症(38.33%)等。结论临床上要积极预防糖尿病低血糖发生,以降低糖尿病低血糖昏迷发生风险,对于已发生低血糖昏迷的患者,要积极采取相应的治疗措施,以挽救患者生命。     

糖尿病合并低血糖诊断及规范治疗探讨

目的 探讨糖尿病合并低血糖诊断及规范治疗方案.方法 选取该院2013年2月-2014年3月收治的50例糖尿病合并低血糖的患者,采用胰岛素皮下注射联合口服降糖药治疗,比较治疗前后的生化检测,对治疗过程中血糖波动进行记录.结果 通过胰岛素皮下注射联合口服降糖药治疗,患者治疗后生化治疗较治疗前显著下降,与治疗前的检测结果相比较,有统计学差异（P＜0.05）;随访10周可见患者在降糖的过程中,血糖波动较小,达到了预期的治疗效果.结论 对于2型糖尿病合并低血糖患者,临床采用胰岛素皮下注射联合口服降糖药治疗,患者血糖控制效果好,披动小,减少了低血糖的发生率,适合于临床应用.     

合理使用α-糖苷酶抑制剂

糖尿病患者长期血糖增高可以引起各器官损害,造成多种急慢性并发症。因此,降低血糖,使血糖保持在合理范围之内是治疗糖尿病的中心环节。口服降糖药的作用机制主要包括促进胰岛素分泌（磺脲类和格列奈类）和提高胰岛素敏感性。减轻胰岛素抵抗（双胍类和胰岛素增敏剂）。此外还有α-糖苷酶抑制剂,该类药物可以延缓肠道糖类物质吸收,在降糖药物中独树一帜。     

药源性低血糖

低血糖最常见的原因为糖尿病患者注射过量的胰岛素或服大量的磺脲类降糖药物(如甲磺丁脲、优降糖、氯磺丙脲等),这种低血糖可导致昏迷、甚至死亡。因此,应认清各种药物发生低血糖的机理,以便早期诊断和治疗。1.胰岛素:多因剂量过大,又未接时进食,或     

C-peptide profiles in patients with non-insulin-dependent diabetes mellitus before and during insulin treatment.

The objective of the study was to evaluate the effect of insulin treatment on insulin secretion in patients with non-insulin-dependent diabetes mellitus (NIDDM). Ten patients with NIDDM were first investigated while still taking oral hypoglycemic agents, and then randomized to a crossover study with two eight-week periods of insulin treatment (oral treatment having been stopped) given either as mainly intermediate-acting insulin twice daily (2-dose) or as preprandial regular insulin and intermediate-acting insulin at bedtime (4-dose). In the patients treated with oral agents the 24-h C-peptide area under the curve was similar to that in the controls, but the profile was different with a rise at breakfast but with almost absent meal peaks during the rest of the day. Insulin treatment improved glycemic control markedly, lowered urinary C-peptide excretion and the serum C-peptide concentrations being reduced by more than 50%. The shape of the C-peptide profiles was unaltered and there were no significant differences between the two insulin regimens. The decrease in serum C-peptide concentration during insulin treatment correlated with the change in blood glucose. Fasting serum C-peptide concentrations correlated closely with the 24-h C-peptide area under the curve. In conclusion, insulin treatment of NIDDM patients with secondary failure to oral agents greatly reduces the insulin secretion, probably owing to the reduction in blood glucose.     

Clinical significance of circulating C-peptide in diabetes mellitus and hypoglycemic disorders.

Proinsulin is converted to insulin and C-peptide in the pancreatic in the pancreatic beta cells: the latter two peptides are secreted in equimolar concentrations. Thus, measurements of serum C-peptide provide a means of assessing pancreatic beta cell function in addition to that of insulin. This technique has proved particularly useful in insulin treated diabetic patients in whom the development of circulating insulin antibodies interferes with the radioimmunoassay of the hormone. The C-peptide assay has also been used to facilitate the diagnosis of various hypoglycemic conditions, including islet cell tumors and factitious injection of insulin. The extraction of C-peptide in the urine reflects average serum values over a period of time and urine C-peptide measurements are especially useful in children or individuals in whom repeated blood sampling is difficult.     

Frequency of diabetic ketoacidosis and hypoglycemic coma during treatment with continuous subcutaneous insulin infusion. Audit of medical care

The frequency of diabetic ketoacidosis and hypoglycemic coma in a large series of patients with insulin-dependent diabetes treated by long-term continuous subcutaneous insulin infusion was compared with the frequency of these events in a matched group of patients treated by conventional insulin injections at the same hospital over the same period of time. Ketoacidosis and hypoglycemic coma occurred no more frequently in continuous subcutaneous insulin infusion-treated patients. Therefore, intensified insulin therapy achieved by continuous subcutaneous insulin infusion does not appear to be associated with a greater risk of ketoacidosis or hypoglycemic coma than does conventional insulin therapy.     

Serum free C-peptide response to oral glucose loading as a parameter for the monitoring of pancreatic B-cell function in diabetic patients

As a parameter for evaluating pancreatic B-cell function, the accuracy of measuring serum free C-peptide immunoreactivity (CPR) was compared with that of measuring plasma immunoreactive insulin (IRI) and urine CPR in diabetic patients during a 100 g oral glucose tolerance test. In 25 non-obese patients receiving oral hypoglycemic agent or diet treatment alone, a positive correlation between the sum of serum free CPR (sigma serum free CPR) and the sum of plasma IRI (sigma plasma IRI) was noted (r = 0.68, P less than 0.001). However, the sum of blood glucose values was found to be negatively correlated to sigma free CPR (r = -0.56, P less than 0.0025), but not to sigma plasma IRI (r = -0.25, NS). In 23 patients receiving diet, oral hypoglycemic agent or insulin treatment, a positive correlation between sigma serum free CPR and urine CPR was noted (r = 0.75, P less than 0.001). However, no significant correlation was found when only insulin-treated patients were investigated (r = 0.37, NS, n = 17). In addition, patients with insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus were better differentiated by measuring sigma serum free CPR than urine CPR. Thus, we concluded that the measurement of serum free CPR during OGTT provides an extremely valuable method for monitoring pancreatic B-cell function in diabetic patients, whether they are receiving insulin treatment or not.     

Comparison of the inhibitory effect of insulin and hypoglycemia on insulin secretion in humans

Although both insulin and hypoglycemia are known to inhibit endogenous insulin secretion, their potency to suppress insulin secretion has not been directly compared thus far. The serum C-peptide concentration was measured during 28 euglycemic and 28 stepwise hypoglycemic (4.1,3.6, 3.1, and 2.6 mmol/L) clamp experiments using either a low-rate (1.5 mU x min(-1) x kg(-1)) or high-rate (15.0 mU x mU(-1) x kg(-1)) insulin infusion. The experiments lasted 6 hours and were performed in 28 lean healthy men. During both the euglycemic and hypoglycemic clamps, serum insulin was approximately 40-fold higher during the high-rates versus low-rate insulin infusion (euglycemia, 24,029 +/- 1,595 v 543 +/- 34 pmol/L; hypoglycemia, 23,624 +/- 1,587 v 622 +/- 32 pmol/L). Under euglycemic conditions, serum C-peptide decreased from 0.54 +/- 0.04 to 0.41 +/- 0.05 nmol/L during the low-rate insulin infusion (P < .05) and from 0.55 +/- 0.07 to 0.27 +/- 0.09 nmol/L during the high-rate insulin infusion (P < .001). Under hypoglycemic conditions, serum C-peptide decreased from 0.50 +/- 0.03 to 0.02 +/- 0.01 nmol/L during the low-rate insulin infusion (P< .001) and from 0.46 +/- 0.07 to 0.02 +/- 0.01 nmol/L during the high-rate insulin infusion (P< .001). In the euglycemic clamp condition, the high-rate insulin infusion reduced the C-peptide concentration more than the low-rate insulin infusion (P < .05). Independent of the rate of insulin infusion, the decrease in C-peptide was distinctly more pronounced during hypoglycemia versus euglycemia (P < .001). These data indicate that insulin inhibits insulin/C-peptide secretion in a dose-dependent manner. Hypoglycemia is a much stronger inhibitor of insulin secretion than insulin itself.     

口服红霉素治疗2型糖尿病的初步观察

目的 探讨红霉素对2型糖尿病患者血糖控制和胰岛素分泌的影响。方法 我们将98例初发2型糖尿病患者随机分为两组，治疗组48例，单独口服红霉素治疗，0．25g，每日3次；对照组50例，单独口服二甲双胍治疗，0．5g，每日3次。观察空腹及餐后2h血糖、糖化血红蛋白及血清胰岛素和C肽变化情况。结果 经治疗3个月后，两组患者的空腹血糖及餐后2h血糖和糖化血红蛋白都有明显降低(P＜0．01)，治疗组血清胰岛素及C肽明显升高(P＜0．01)，无低血糖反应。停药4周后重复治疗仍然有效。结论口服红霉素可以降低血糖及糖化血红蛋白，使血清胰岛素分泌增加，说明红霉素能改善糖尿病患者的糖代谢，可以用于糖尿病的治疗。     

芪连汤加降糖药治疗2型糖尿病胰岛素抵抗疗效观察

目的 观察芪连汤合用格列奇特治疗2型糖尿病（T2DM）患者胰岛素敏感性的作用。方法选择T2DM患者123例，随机分两组：口服格列奇特组（对照组），口服芪连汤加格列奇特组（治疗组）。治疗前后测定两组空腹血糖、胰岛素、C肽、计算胰岛素敏感指数（ISI）。结果治疗组较对照组：空腹胰岛素、C肽下降（P〈0．05），差异有统计学意义；结论芪连汤对改善胰岛素抵抗（IR）有效。     

Determinants of glucose and ketoacid concentrations in acutely hyperglycemic diabetic patients

Diabetic hyperosmolar coma is a syndrome of marked hyperglycemia and minimal ketoacidosis. In general, the serum glucose concentrations are not predictive of the serum ketoacid concentrations in acutely decompensated diabetes. The endocrine factors that modulate glucose concentrations may be different from those that modulate ketoacid concentrations in patients with acutely decompensated diabetes. To test this hypothesis, regression analysis was used to determine the endocrine and metabolic characteristics that correlated with serum concentrations of glucose and ketoacids in 26 diabetic patients with spontaneous, acute hyperglycemia. All patients had a serum glucose level greater than 390 mg/dl, and ketoacid levels were from 0.17 to 25.5 mM. Multiple regression analysis showed that increased serum glucose concentrations correlated with increased plasma glucagon levels (p = 0.0007, r2 = 0.45), but with no other factors. Increased total ketoacid levels (acetoacetate plus 3-hydroxybutyrate) correlated with increased free fatty acid levels (p = 0.0001), decreased C-peptide levels (p = 0.002), and increased body mass index (p = 0.002) (r2 = 0.72). Body mass index only correlated with ketoacid levels, when it was analyzed with C-peptide and free fatty acid levels. A model is proposed that predicts the serum glucose and ketoacid concentrations in patients with acutely decompensated diabetes. Glucagon modulates the serum glucose concentration in these patients with an absolute or relative insulin deficiency. Total serum ketoacid levels are determined by the serum free fatty acid concentration, residual pancreatic insulin secretion (as reflected by C-peptide), and the patient's body habitus. This model allows for the marked hyperglycemia and minimal ketosis of diabetic nonketotic hyperosmolar coma, as well as the glucose and ketoacid concentrations in other presentations of acutely decompensated diabetes.     

Secondary failure of oral antidiabetics. Value of intravenous insulin infusions

A temporary strict blood glucose control was achieved by means of intravenous insulin infusion in 37 non insulin-dependent diabetic patients with secondary drug failure to reinduce the efficacy of oral hypoglycemic agents. This procedure was successful in 18 patients (48.6%) resulting in better glycemic response to oral hypoglycemic agents. Results remained identical 6 and 12 months later. This improvement does not seem related to an increase in insulin secretion as urinary C-peptide and basal and glucagon-stimulated plasma C-peptide were identical before and after insulin infusion. We suggest that a decrease in insulin resistance, not tested in this study, may explain the beneficial effect or normoglycemia in our patients.     

Variation of endogenous insulin secretion in association with treatment status: assessment by serum C-peptide and modified urinary C-peptide.

The variation of endogenous insulin secretion in association with fasting plasma glucose (FPG) level and the modality of treatment was assessed using serum C-peptide levels before and after breakfast and the corrected value of 24-h urinary C-peptide (24 h-UCP) in inpatients with non-insulin-dependent diabetes mellitus. The corrected value calculated as 24 h-UCP/(urinary C-peptide to creatinine clearance (CCP/CCR) ratio in the fasting state x 10) was correlated with the sum of day-long serum C-peptide levels (r = 0.93) more closely than the measured value of 24 h-UCP (r = 0.79) in 9 patients. In 52 patients treated with diet alone, 38 with sulfonylurea and 28 with insulin, fasting serum C-peptide level did not vary with FPG level, and the increment of serum C-peptide level after breakfast and the corrected value of 24 h-UCP decreased with the rise in FPG level in each treatment. These indexes were the lowest in insulin treatment among the patients with similar FPG levels. In conclusion, 24 h-UCP was demonstrated to be able to reflect day-long endogenous insulin secretion more faithfully after the correction with the CCP/CCR ratio. It was estimated that the insulin response to breakfast and day-long insulin secretion decreased with the rise in FPG level, but basal insulin secretion was maintained over a wide range of FPG levels in each treatment. Endogenous insulin secretion seemed to be somewhat suppressed or rested by exogenous insulin in insulin-treated patients.