糖尿病患者伴抑郁症临床分析

正糖尿病(diabetes mellitus,DM)属于慢性非传染性疾病,由于目前临床尚无有效治愈措施,患者需终身用药控制血糖水平~([1])。本文选取我院2014-01—12收治的糖尿病伴抑郁症患者60例,探讨糖尿病患者伴抑郁症临床正确治疗措施及应用效果,现总结如下。1资料与方法1.1一般资料60例糖尿病伴抑郁症患者中男24例,女36例,年龄49~84(62.31±1.27)岁,糖尿病病程2~18(6.71±0.24)a。按照就诊序号分为研究组(单)、对照组(双),每组30例。2组一般资料对比差异无统计学意义(P0.05),具有可比性。     

基于老年综合评估的护理干预对老年糖尿病合并抑郁症患者的影响

目的探讨基于老年综合评估的护理干预对老年糖尿病合并抑郁症患者的影响。方法选取我院2014年12月~2016年3月收治的老年糖尿病合并抑郁症患者84例为本研究对象,将其随机分为研究组和对照组,各42例。两组均采用基础治疗,对照组采用常规护理,研究组采用基于老年综合评估的护理干预。比较两组护理前后相关血糖指标及抑郁症改善情况。结果两组护理前空腹血糖(FBG)、餐后2h血糖(2h PBG)、糖化血红蛋白(Hb Alc)水平差异无统计学意义(P0.05),护理后各项血糖水平均降低,且研究组低于对照组(P0.05);护理前两组抑郁和焦虑评分无统计学差异(P0.05),护理后评分均降低,且研究组低于对照组,差异有统计学意义(P0.05)。结论基于老年综合评估的护理干预,可有效改善老年糖尿病合并抑郁症患者的血糖水平及抑郁症程度。     

糖尿病伴发抑郁症临床初步研究

目的调查糖尿病伴发抑郁症的临床特征、药物疗效.方法(1)实验对象34例符合CCMD-Ⅲ中抑郁症的诊断标准及美国糖尿病协会Ⅱ型糖尿病诊断标准的患者.(2)治疗方法口服盐酸氟西汀,每日一次,20 mg/日,观察十二周.(3)临床评价治疗前及治疗第2、4、6、8、12周末分别进行空腹血糖、HAMD17、HAMA、CGI评定;于治疗前及治疗后进行糖化血红蛋白、SDS评定;于治疗第2、4、6、8、12周末进行TESS评定.结果(1)糖尿病伴发抑郁症患者具有年龄大、文化水平低、糖尿病病程长、合并并发症者多的临床特征.(2)盐酸氟西汀治疗前后患者的抑郁及焦虑症状的改善具有显著性意义.(3)治疗前后空腹血糖及糖化血红蛋白的变化具有显著性差异.结论糖尿病伴发抑郁症患者趋于老龄、低文化程度、有并发症、慢性病程等,盐酸氟西汀对缓解患者伴发的抑郁症状以及协同降低血糖有一定疗效.     

SSRI类药物对抑郁症患者esRAGE水平及血糖的影响

目的 探讨SSRI类药物对抑郁症患者血清内源性分泌型糖基化终产物受体(esRAGE)水平及血糖的影响.方法 采用SSRI类药物对28例抑郁症患者进行为期6周的治疗,分别在治疗前和治疗6周后,用酶联免疫法测定抑郁症患者血清中esRAGE浓度和血糖水平,并与34例正常对照者比较.结果 (1)抑郁症组治疗后esRAGE浓度[(0.56±0.17)ng/ml]高于治疗前[(0.49±0.21)ng/ml],但均低于正常对照组[(0.66±0.10)ng/ml],组间比较差异有显著统计学意义(P＜0.001).(2)抑郁症组治疗后空腹血糖[(4.91±0.50)mmol/L]低于治疗前[(5.38±0.39)mmol/L],差异有显著统计学意义(P=0.000),但与正常对照组空腹血糖[(5.08±0.41)mmol/L]比较差异无统计学意义(P=0.172).(3)Pearson相关分析显示,esRAGE与空腹血糖成中等程度负相关(P＜0.05).结论 SSRI类药物能升高抑郁症患者的esRAGE水平,同时降低血糖水平.     

住院抑郁症患者糖尿病患病率调查

目的:调查抑郁症患者糖尿病的患病率,分析与2型糖尿病患病率有关的危险因素。方法:以2003年内的抑郁症出院病例为研究对象,以世界卫生组织关于糖尿病的诊断标准(1997年)观察血糖和血脂的动态变化,了解抑郁症患者中糖尿病的患病率;用Logistic回归分析影响糖尿病发生的相关因素。结果:248例抑郁症患者中糖尿病患者为27例,抑郁症患者中糖尿病的患病率为10.9%;进入单因素非条件Logistic回归方程的有性别、年龄、文化程度、高脂血症、伴发躯体疾病数目和抑郁症发病诱因;选入多因素非条件Logistic回归方程的有高脂血症、伴发躯体疾病数目和抑郁症发病诱因。结论:抑郁症患者中糖尿病的患病率为10.9%,高脂血症、伴发躯体疾病数目和发病诱因是抑郁症合并糖尿病的独立危险因素。     

米氮平对2型糖尿病患者合并抑郁症的疗效观察

目的 探讨果氮平对2型糖尿病患者合并抑郁症的疗效.方法 将120例合并抑郁症的2型糖尿病患者,随机分为研究组和对照组,每组60例.对照组仅用降糖药治疗,研究组在常规降糖药治疗基础上联用米氮平( 15～45mg/d)治疗,治疗8周.在治疗前和治疗8周末均进行汉密尔顿抑郁量表(HAMD)评定和空腹血糖、餐后2h血糖、糖化血...     

沉默信息调控因子1和血糖与抑郁障碍的关系

目的:探索沉默信息调控因子1(SIRT1)和血糖与抑郁障碍的关系。方法:采用17项汉密尔顿抑郁量表(HAMD-17)评定93例首发抑郁障碍患者(病例组)病情;并检测其空腹血糖(GLU)和血清SIRT1水平,结果与106名健康志愿者(对照组)比较;分析抑郁障碍患者的病情与GLU、血清SIRT1水平的关系。结果:病例组GLU水平显著高于对照组,血清SIRT1水平显著低于对照组(P均<0.01);病例组中,高血糖亚组HAMD总分显著高于正常血糖亚组,血清SIRT1水平显著低于正常血糖组(P<0.05或P<0.01);HAMD总分与GLU呈正相关(t=3.10,P=0.003),与血清SIRT1水平呈负相关(t=-3.65,P<0.01);Pearson相关分析显示,抑郁障碍患者的GLU与血清SIRT1水平呈负相关(r=-0.33,P=0.002)。结论:高GLU和低SIRT1水平增加抑郁障碍的发生风险,并与抑郁症状严重程度有关。     

抑郁症昼夜节律变化与免疫功能的关系

目的:探讨抑郁症昼夜节律的特征与细胞因子浓度的关系. 方法:对符合美国精神障碍诊断和统计手册第4版重性抑郁发作诊断标准的49例患者(抑郁症组)和38名健康人(对照组),采用酶联免疫吸附法测定其早7:00和晚7:00血浆白细胞介素-1β(IL-1β)、白细胞介素-2(IL-2)、白细胞介素-6(IL-6)及肿瘤坏死因子(TNF)的浓度,比较各指标早、晚浓度及早晚差值在抑郁症组中有晨重夕轻、无晨重夕轻和对照组之间的差异. 结果:抑郁症组中不论有、无晨重夕轻,其早晨IL-1β浓度及TNF浓度均明显低于对照组(P均<0.05或P<0.01));晚间IL-6浓度均较对照组显著增高(P均<0.05),IL-2浓度较对照组显著降低(P均<0.01);IL-6浓度早晚差值均较对照组显著增大(P均<0.05).结论:抑郁症患者在晚间存在广泛的免疫激活,血浆IL-6的昼夜节律较对照组有异常改变.     

缺血性脑血管病发病临界点的研究

目的 探讨同时患高血压病和糖尿病患者发生缺血性脑血管病(ICVD)的好发时段及变化规律，寻求对其预防和治疗的策略。方法 选择82例同时患高血压病、糖尿病在凌晨时段发病的ICVD患者(观察组)，测定凌晨时段1：00～7：00时的血压及血糖的变化。并与70例(对照组)无高血压病和糖尿病的ICVD患者进行对照。结果 观察组中，凌晨1：00-6：00时血压逐渐下降64例(78．05％)；从3：00时开始血糖逐渐升高67例(81．71％)。两者变化曲线形成交点，有68例(82．93％)在该交点后发病。对照组两者变化曲线不形成交点。结论 该点是高血压和糖尿病患者发生ICVD的临界点，在临界点后的凌晨时段发病率增高，寻找临界点是预防ICVD的重要措施。     

抑郁症和糖尿病共病患者的瘦素水平

目的:探讨抑郁症和糖尿病共病患者血清瘦素水平的特点。方法:采用放射免疫方法测定抑郁症和糖尿病共病患者(共病组:n=30)和单纯抑郁症患者(单纯抑郁症组:n=30)给予抗抑郁药治疗前后的血清瘦素水平,并与正常人(正常对照组:n=30)的血清瘦素水平进行比较。结果:治疗前共病组血清瘦素水平与单纯抑郁症组差异有统计学意义(t=3.42,P<0.01);与正常对照组差异无统计学意义(t=0.35,P>0.05);治疗后共病组与单纯抑郁症组血清瘦素水平均较治疗前显著下降(t分别=2.455,7.002;P<0.05或P<0.001);共病组与正常对照组差异有统计学意义(t=-4.18,P<0.001)。结论:抑郁症和糖尿病共病可能存在瘦素分泌不足,抗抑郁药可降低血清瘦素水平。     

The plasma dexamethasone window: evidence supporting its usefulness to validate dexamethasone suppression test results

Two doses of dexamethasone (DEX) (0.5 and 1.0 mg) were administered in a randomized crossover design to 31 patients with major depression, 9 healthy controls, and 14 nondepressed psychiatric patients. Using this modified Dexamethasone Suppression Test (DST), minimum DEX levels of 6 nmol/liter at 8:00 AM and 2.0 nmol/liter at 4:00 PM were required to achieve reliable suppression of cortisol in healthy controls and nondepressed psychiatric patients. Failure to achieve these minimum plasma DEX levels was associated with similar rates of nonsuppression in both depressed and nondepressed patients, thereby reducing the specificity of the DST. Conversely, high DEX levels greater than 13 nmol/liter at 8:00 AM or 4.0 nmol/liter at 4:00 PM were associated with abnormal "suppressibility" in depressed patients, thereby reducing the sensitivity of the test. Controlling for plasma DEX concentrations by selecting a test result that fell within a plasma DEX window at 8:00 AM and 4:00 PM increased the sensitivity and specificity of the DST. Significant differences in plasma DEX between suppressors and nonsuppressors were no longer evident when comparing patients with adequate DEX levels, thus ensuring that cortisol escape reflected HPA axis changes associated with depression and not peripheral mechanisms responsible for the availability of DEX. These results suggest that the clinical utility of the DST would be significantly enhanced by extending the standard 1.0-mg DST and retesting those patients with levels outside the DEX window with a higher or lower dose. The data also indicate that the measurement of plasma DEX is essential to validly interpret DST status and highlight the need to standardize DEX assays to compare DST results between research centers.     

Monoamine oxidase and cortisol response in depression and schizophrenia.

The relationship between hypothalamic-pituitary-adrenal (HPA) axis function and platelet monoamine oxidase (MAO) activity was examined in drug-free depressed (n = 32) and schizophrenic (n = 36) inpatients. HPA function was measured by determining plasma cortisol levels at 8:30 a.m. and 11 p.m. before, and 8:30 a.m., 4 p.m., and 11 p.m. after administration of 1 mg of dexamethasone (DEX). There was a significant correlation between platelet MAO activity and all post-DEX cortisol levels (8:30 a.m., 4 a.m., and 11 p.m.) in depressed patients, and MAO activity and pre-DEX cortisol levels (11 p.m.) in schizophrenic patients. MAO activity was significantly higher in depressed DST nonsuppressors than in suppressors, and there were more DST nonsuppressors in high-MAO groups as compared with low-MAO groups. Our results thus suggest a strong relationship between platelet MAO activity and HPA function in depressed patients. These biochemical markers are potentially useful in the identification of biochemically and clinically homogeneous subgroups of depressed patients.     

The prevalence of impaired glucose regulation in psychiatric patients with sleep disorders and its relationship with altered hypothalamopituitary–adrenal and hypothalamopituitary–thyroid axis activity

BackgroundSleep restriction, an important symptom of psychiatric diseases, is associated with adverse effects on glucose regulation, but few studies have examined its association with impaired glucose regulation and altered hypothalamic activity. Our study was designed to evaluate the sleep duration, fasting glucose, tolerance glucose, and concentration of plasma insulin; to assess the function of both the hypothalamopituitary–thyroid (HPT) and hypothalamopituitary–adrenal (HPA) axis; and to investigate the relationship of altered hypothalamic function with glucose metabolism in psychiatric patients with a sleep disorders.MethodsFrom January 2010 to December 2011, 324 women (64.7%) and 177 men (35.32%) with a diagnosis of a sleep disorder participated in our cross-sectional study in the psychiatric outpatient department of the West China Hospital of Sichuan University. Results from 75-g glucose tolerance tests, insulin-releasing tests, morning (8:00 am) serum cortisol, and thyroid-stimulating hormone (TSH) (TT_3, TT_4, FT_3, FT₄) were collected, as well as body mass index and waist–hip ratio to assess the prevalence of impaired glucose regulation and function of the HPA and HPT axis. Sleep quality was assessed through self-reported questionnaires.ResultsThere were 301 patients previously diagnosed with an anxiety disorder (78%), and 200 patients previously diagnosed with depression and other psychiatric diseases (22%). Crude prevalence rates were 15.0% for diabetes mellitus (DM), 11.6% for impaired glucose tolerance, 15.8% for impaired fasting glucose, and 11.6% for impaired glucose regulation (impaired glucose tolerance [IGT] + impaired fasting glucose [IFG]). Total prevalence of impaired glucose regulation in patients with a sleep disorder was 48.8%. Mean cortisol level was 463.5 ± 178.8 nmol/L, and the cortisol concentration at 8:00 am was significantly associated with a higher prevalence of impaired glucose regulation and insulin resistance. TSH values above 2.5 mU/L accounted for over 58% and were significantly associated with insulin resistance.ConclusionsThese results partially confirm that a high level of cortisol and an increased activity of the HPT axis are associated with impaired glucose regulation. Therefore, as a pathophysiologic event abnormal activity of the hypothalamic function of psychiatric patients with sleep disorders could be viewed as a potential risk factor for increasing incidence of DM.     

HPA hyperactivity with increased plasma cortisol affects dexamethasone metabolism and DST outcome

Data suggests that dexamethasone bioavailability or pharmacokinetic factors contribute importantly to the outcome of the dexamethasone suppression test, and a relationship between plasma cortisol and plasma dexamethasone levels has been shown. To evaluate these data further, we studied plasma dexamethasone pharmacokinetics in 24 patients with major depression (15 suppressors and nine nonsuppressors) who received a 1 mg IV dexamethasone bolus at 09:00 h with blood samples collected at intervals over the next 14 h. We found that nonsuppressors had significantly shorter plasma dexamethasone half-life (P=0.003) as well as significantly lower dexamethasone levels 10 h (P=0.02) following IV dexamethasone administration. Moreover, upon clinical improvement of patients, the shortened dexamethasone half-life and lower dexamethasone levels disappeared in the five patients who switched from nonsuppression to suppression and were restudied by IV bolus. These 10-h post IV plasma dexamethasone level findings paralleled the results of the 1 mg overnight oral DST performed in these depressed patients (N=22) where we found significantly lower 10 h plasma dexamethasone levels in nonsuppressors on admission compared to suppressors (P=0.002) and again at discharge (P=0.007). Interestingly, in the few patients who switched from suppression to nonsuppression over the course of hospitalization, 10-h post dose plasma dexamethasone levels simultaneously dropped. No difference in dexamethasone half-life was observed in the patients studied by oral and IV dexamethasone administration. These findings support the concept that metabolism of dexamethasone is significantly related to the activity of the HPA axis (particularly by plasma cortisol levels), and that dexamethasone pharmacokinetics can be modified by state-dependent phenomena.     

Plasma ACTH and cortisol concentrations before and after dexamethasone

Alteration in the hypothalamic-pituitary-adrenal (HPA) axis occurs in up to 50% of depressed patients and is demonstrated by the failure to suppress cortisol concentrations after dexamethasone administration. Evidence suggesting that these cortisol abnormalities reflect hypothalamic-pituitary dysfunction has been inconsistent. We administered the dexamethasone suppression test to 28 psychiatric inpatients, including 17 cortisol suppressors and 11 nonsuppressors. Adrenocorticotropic hormone (ACTH) concentrations at 8 a.m. pre- and postdexamethasone were significantly greater in cortisol nonsuppressors than in suppressors. Our data support the hypothesis that pituitary ACTH secretion is altered in depressed patients who have HPA axis abnormalities demonstrated by plasma cortisol measurements.     

The dexamethasone suppression test: importance of dexamethasone concentrations

Plasma dexamethasone concentrations and cortisol response to dexamethasone were measured in 29 normal healthy volunteers, 23 depressed patients, and 10 patients with anorexia nervosa at 4:00 PM postdexamethasone. In each of the 3 groups, nonsuppressors had lower dexamethasone concentrations than suppressors. Of the subjects with plasma dexamethasone at or below 0.7 ng/ml, a significantly higher proportion (48%) were nonsuppressors compared to the proportion above 0.7 ng/ml (14%), all of whom were patients. Plasma dexamethasone concentrations in a subgroup of depressed nonsuppressors were high (mean 1.35 ng/ml), whereas the remainder were low (0.42 ng/ml) and were similar to the normal nonsuppressors (0.35 ng/ml), suggesting different mechanisms for nonsuppression in the subgroups. Plasma dexamethasone concentrations were similar in nonendogenous and endogenous depressives, in men and women, and in medicated and drug-free patients. None of the variables of age, weight, history of weight loss, Hamilton depression rating score, predexamethasone cortisol, or postdexamethasone cortisol were significantly correlated with plasma dexamethasone, except for body weight and a history of weight loss in the depressed group only. Mean plasma dexamethasone concentrations increased significantly from week 1 to week 2 in 7 depressed patients, whereas plasma cortisol decreased; however, the relationship between dexamethasone and cortisol varied considerably for individual patients.     

Evidence of basal pituitary-adrenal overactivity in first episode, drug naïve patients with schizophrenia

BACKGROUND: Evidence for basal hypothalamic-pituitary-adrenal (HPA) axis dysfunction in schizophrenia is less consistent than that seen in major depression. Potential reasons include sampling procedures and the use of patients on antipsychotic medications which may suppress the HPA axis. Therefore, the objective of this study was to determine whether first episode, drug na?ve patients with schizophrenia have evidence of basal HPA axis dysfunction by measuring plasma levels of AVP, ACTH and cortisol from 13:00 to 16:00 h, a time frame which is believed to reflect 24 h concentrations of HPA axis activity. METHOD: In this cross-sectional study, plasma levels of AVP, ACTH and cortisol were measured in 12 (7 males and 5 females) (mean age +/-SD=33.6+/-12.6 years) patients with DSM-IV schizophrenia and compared with those found in age- and sex-matched healthy controls. RESULTS: Patients and controls did not differ in terms of their 13:00 h cortisol and AVP. However, patients with schizophrenia had higher levels of ACTH as compared to control subjects at 13:00 h (41.3+/-14.6 vs. 12.4+/-1.1 pg/ml respectively; t=1.99, df=11, p <0.05). In comparison to controls subjects, patients with schizophrenia, had higher mean (+/-SE) AUC of ACTH (26.3+/-6.2 vs. 13.9 nmol/l, respectively; t=2.86, df=11, p <0.02) and cortisol (279.4+/-26.0 vs. 213.1+/-18.4 nmol/l, respectively; t=3.72, df=11, p <0.01). Though, patients with schizophrenia, in comparison to control subjects, had lower mean (+/-SE) AUC of AVP (0.87+/-0.24 vs. 1.42+/-0.34 pmol/l, respectively; t=2.29, df=11, p <0.02). CONCLUSIONS: First episode, drug na?ve patients with schizophrenia show evidence of basal overactivity of the pituitary-adrenal axis.     

Impaired fasting glucose tolerance in first-episode,drug-naive patients with schizophrenia

OBJECTIVE: This study examined the prevalence of impaired fasting glucose tolerance in first-episode, drug-naive patients with schizophrenia. METHOD: In this cross-sectional study, fasting plasma levels of glucose, insulin, lipids, and cortisol were measured in 15 male and 11 female hospitalized Caucasian patients with DSM-IV schizophrenia (mean age=33.6 years) and age- and sex-matched healthy comparison subjects. The patients and comparison subjects were also matched in terms of various life-style and anthropometric measures. RESULTS: More than 15% of the drug-naive, first-episode patients with schizophrenia had impaired fasting glucose tolerance, compared to none of the healthy volunteers. Compared with the healthy subjects, the patients with schizophrenia had significantly higher fasting plasma levels of glucose (mean=88.2 mg/dl, SD=5.4, for the healthy subjects versus mean=95.8 mg/dl, SD=16.9, for the patients), insulin (mean=7.7 micro u/ml, SD=3.7, versus mean=9.8 micro u/ml, SD=3.9), and cortisol (mean=303.2 nmol/liter, SD=10.5, versus mean=499.4 nmol/liter, SD=161.4) and were more insulin resistant, as measured with homeostasis model assessment (mean=1.7, SD=0.7, for the healthy subjects versus mean=2.3, SD=1.0, for the patients). CONCLUSIONS: First-episode, drug-naive patients with schizophrenia have impaired fasting glucose tolerance and are more insulin resistant and have higher levels of plasma glucose, insulin, and cortisol than healthy comparison subjects.     

The dexamethasone and cortisol suppression test in depression: beta-endorphin as a useful marker

To investigate the mechanism underlying disturbances in hypothalamopituitary-adrenal (HPA) function in depressed patients, the dexamethasone suppression test (DST) was compared with a cortisol suppression test (CST) and placebo treatment in depressed patients and control subjects. Plasma levels of cortisol, ACTH and beta-endorphin were assessed at 3 times during the day after treatment with a single dose of exogenous steroid. Both dexamethasone and cortisol treatment resulted in suppression of cortisol, ACTH and beta-endorphin in control subjects, while neither treatment had any effect on the hormone levels in those depressed patients who showed cortisol nonsuppression after dexamethasone. In the depressed patients who were cortisol suppressors after dexamethasone, cortisol treatment only slightly changed plasma levels of beta-endorphin, although they were suppressed after dexamethasone treatment. In addition, high levels of both cortisol and beta-endorphin were observed after placebo treatment in all depressed patients compared to control subjects, probably due to the absence of the normally occurring decrease of these hormones during the day in these patients. Cortisol treatment, but not dexamethasone treatment, discriminated depressed patients from controls with respect to their beta-endorphin plasma levels. However, it is not yet clear whether these different effects of the two steroids are related to a different mode of action of these steroids in depressed patients. beta-Endorphin seems to be a useful marker in detecting disturbances in HPA function among depressed patients.     

Function of the adrenal cortex in patients with major depression

Failure to suppress cortisol secretion after administration of dexamethasone occurs in up to 50% of depressed patients. To test whether this hypothalamic-pituitary-adrenal (HPA) overactivity is associated with adrenocortical hyperresponsiveness, we performed dexamethasone suppression tests (DSTs) and adrenocorticotropic hormone (ACTH) stimulation tests in depressed subjects and subjects with other psychiatric disorders. Three groups were defined: depressed nonsuppressors, depressed suppressors, and other suppressors. While predexamethasone and postdexamethasone cortisol concentrations were greater in the depressed nonsuppressor group, ACTH concentrations did not differ among groups. After receiving alpha-ACTH[1-24] (4.2 micrograms/kg), depressed nonsuppressors had greater increases in stimulated cortisol secretion than the other groups. These results demonstrate that in a subgroup of depressed patients, HPA overactivity is associated with adrenocortical hyperresponsiveness.