Investigation of serum BDNF levels in drug-naive patients with schizophrenia

The role of brain-derived neurotrophic factor (BDNF) is to promote and modulate the neuronal responses across neurotransmitter systems in the brain. Therefore, abnormal BDNF signaling may be associated with the pathophysiology of schizophrenia. Decreased BDNF levels in the brain and the serum of patients with psychotic disorders have been reported. In the present study, we assessed serum BDNF levels in a group of 14 drug-naive first-episode patients with schizophrenia (FEP), compared to 15 healthy controls. The serum BDNF levels in the sample of FEP patients was significantly reduced compared to normal controls (23.92+/-5.99 ng/ml vs. 30.0+/-8.43 ng/ml, F=5.01, df=1, p=.034). Negative correlations were shown between serum BDNF levels of the patients and the PANSS Positive and Negative subscale scores. Our findings indicate that BDNF levels at the onset of schizophrenia may reflect associated pathophysiological processes as well as the severity of positive and negative psychotic symptoms.     

The evaluation of vitamin D levels in patients with carpal tunnel syndrome

The aim of this study was to evaluate the relationship between 25-hydroxyvitamin D (25(OH)D) levels and carpal tunnel syndrome (CTS). 25(OH)D levels were checked in 108 consecutive patients with CTS symptoms and 52 healthy controls. All patients underwent nerve conduction studies and completed Boston Carpal Tunnel Questionnaire (BQ) symptom severity and functional status scales to quantify symptom severity, pain status and functional status. There were 57 patients with electrophysiological confirmed CTS (EP+ group) and 51 electrophysiological negative symptomatic patients (EP? group). 25(OH) D deficiency (25(OH)D < 20 ng/ml) was found in 96.1 % of EP? group, in 94.7 % of EP+ group and in 73.8 % of control group. 25(0H) D level was found significantly lower both in EP+ and EP? groups compared to control group (p = 0.006, p < 0.001, respectively). Although mean vitamin D level in EP? group was lower than EP+ group, statistically difference was not significant between EP+ and EP? groups (p = 0.182). BQ symptom severity and functional status scores and BQ pain sum score were not significantly different between EP+ and EP? groups. We found no correlation with 25(OH) D level for BQ symptom severity, functional status and pain sum scores. 25(OH) D deficiency is a common problem in patients with CTS symptoms. As evidenced by the present study, assessment of serum 25(OH)D is recommended in CTS patients even with electrophysiological negative results.     

重复经颅磁刺激对首发精神分裂症患者血清脑源性神经营养因子的影响

目的分析高频重复经颅磁刺激(rTMS)对首发精神分裂症患者血清脑源性神经营养因子(BDNF)的影响。方法选取82例以阴性症状为主的首发精神分裂症患者,使用随机数表将82例患者分为对照组41例和观察组41例,2组均使用常规药物治疗,观察组同时予以真刺激治疗,对照组予以假刺激治疗,对比2组治疗结果。结果治疗4周后观察组PANSS(阳性和阴性症状量表)总分、阴性症状评分、一般病理评分及血清BDNF浓度均优于治疗前,且优于对照组(P0.05);对照组PANSS总分、阴性症状评分、阳性症状评分、一般病理评分及血清BDNF浓度与之前相比无明显变化(P0.05)。观察组BDNF浓度变化与PANSS总分及各因子的变化无明显相关性(P0.05)。结论rTMS可显著增加首发精神分裂症患者的血清BDNF水平,但血清BDNF水平变化与其临床症状的改善无明显相关性。     

GC and VDR SNPs and Vitamin D Levels in Parkinson’s Disease: The Relevance to Clinical Features

Vitamin D deficiency is suggested to be associated with Parkinson’s disease (PD). Our aim was to investigate the serum 25-hydroxyvitamin D₃ (25OHD) levels of PD patients in Turkish cohort, to investigate any association of vitamin D binding protein (GC) genotypes with PD due to the significant role of GC in vitamin D transport, to determine whether vitamin D receptor (VDR) haplotype that we previously demonstrated to be a risk haplotype for AD is also a common haplotype for PD and to investigate any relevant consequence of serum 25OHD levels, GC or VDR genotypes on clinical features of PD. Three hundred eighty-two PD patients and 242 healthy subjects were included in this study. The serum 25OHD levels were investigated by CLIA, and GC and VDR SNPs were evaluated with LightSnip. Our results indicated a strong relationship between low serum 25OHD levels and PD (p < 0.001). rs7041 of GC and ApaI of VDR were associated with the PD risk (p < 0.05). Minor allele carriers for BsmI of VDR gene in both PD patients and healthy subjects had significantly higher levels of serum 25OHD (p < 0.05). The homozygous major allele carriers for rs2282679, rs3755967 and rs2298850 of GC gene in PD patients with slower progression had significantly higher levels of serum 25OHD (p  < 0.05). Minor allele carriers for FokI of VDR gene were more frequent in patients with advanced-stage PD (p < 0.05). Consequently, this is the first study demonstrating GC gene as a risk factor for PD. The relationship between PD’s clinical features and low 25OHD or risk genotypes might have effects on PD independently.     

Decreased serum BDNF levels in chronic institutionalized schizophrenia on long-term treatment with typical and atypical antipsychotics

Accumulating evidence showed that brain-derived neurotrophic factor (BDNF) may be involved in the pathophysiology of schizophrenia. Decreased BDNF levels have been found in the serum of schizophrenic patients with mixed results. In the present study, we assessed serum BDNF levels in a large group of 364 schizophrenic patients (157 on clozapine, 89 on risperidone and 118 on typical antipsychotics), compared to 323 healthy control subjects matched for age and gender. The schizophrenia symptomatology was assessed by the Positive and Negative Syndrome Scale (PANSS), and serum BDNF levels were measured by sandwich ELISA. The results showed that BDNF levels were significantly lower in chronic patients with schizophrenia than in healthy control subjects (9.9 ± 2.0 ng/ml vs.11.9 ± 2.3 ng/ml, p < 0.0001). Lower BDNF levels were observed in patients treated with risperidone (9.3 ± 2.3 ng/ml) compared to those with clozapine (10.2 ± 2.0 ng/ml, p < 0.001) and typical antipsychotics (10.0 ± 2.1 ng/ml, p < 0.01). Furthermore, a stepwise multiple regression analysis identified types of antipsychotic drugs (beta = − 0.37, t = − 3.15, p = 0.001) and BDNF levels (beta = − 0.26, t = − 2.51, p = 0.014) as the influencing factor for the positive symptom subscore of PANSS. In addition, there was a sex difference in BDNF levels in patients with schizophrenia (9.7 ± 1.9 ng/ml for males vs.10.4 ± 2.1 ng/ml for female, p < 0.005), but not in normal controls. Our findings indicated decreased BDNF serum levels in chronic patients with schizophrenia, which may be related to clinical phenotypes, including gender, antipsychotic treatment and the severity of psychotic symptoms.     

Vitamin D deficiency might pose a greater risk for ApoEɛ4 non-carrier Alzheimer’s disease patients

Vitamin D is a secosteroid hormone that shares a synthetic pathway with cholesterol. ApoE, which is involved in the transport of cholesterol, is the most significant genetic risk factor for sporadic Alzheimer’s disease (AD). Surprisingly, recent studies have indicated the presence of an evolutionary juncture between these two molecules. To demonstrate this possible relationship, we investigated serum levels of 25-hydroxyvitamin-D₃ (25OHD) in patients with early onset-AD (EOAD; n:22), late onset-AD (LOAD; n:72), mild cognitive impairment (MCI; n:32) and in healthy subjects (n:70). We then analyzed the correlation between 25OHD and cytokines, BDNF and Hsp90 with respect to ApoE alleles, as these molecules were investigated in our previous studies. The LOAD patients had low levels of 25OHD, but these low levels originated only from ApoE?4 non-carrier patients. Negative correlations were observed between serum 25OHD and TNFα, IL-1β or IL-6 levels in healthy subjects or MCI patients, but these same correlations were positive in LOAD patients. ApoE alleles indicated that these positive correlations exist only in ?4 carrier LOAD patients. Consequently, our results indicate that vitamin D deficiency presents a greater risk for ApoE?4 non-carrier AD patients than for ?4 carriers. Therefore, it might be beneficial to monitor the vitamin D status of ApoE?4 allele non-carrier AD patients.     

Brain derived neurotropic factor in first-episode psychosis

There is much interest, derived from current neurochemical, genetic, and therapeutic research, in the role of brain neurotrophins in schizophrenia. Neurotrophins play key roles in neuronal development and differentiation (i.e., promoting dendritogenesis and synaptogenesis), and in orchestrating the neuronal response to stress/noxious stimuli. Additionally, neurotrophins are modulators across monominergic (dopamine and serotonin), gabaergic and cholinergic systems. These roles focus on important areas of the etiopathophysiology of schizophrenia. Clinical studies show reductions in brain-derived neurotrophic factor (BDNF) and nerve growth factor (NFG) in schizophrenic patients as compared to normal control subjects, as well as differences in patients receiving first-generation antipsychotics (FGAs) or second-generation antipsychotics (SGAs). We now report on BDNF levels in subjects with first-episode psychosis in comparison with normal healthy controls. Compared to normal controls (N=14; 290.5+/-38.81 pg/ml), first-episode psychotic patients showed significant reduction (N=15; 135+/-21.77 pg/ml; P=0.001; f=12.873) in plasma BDNF. Additionally, plasma BDNF levels showed a significant negative correlation (N=13' r=0.584, P=0.0362) only with positive symptom scores at base line and no significant correlations were found with any of the cognitive performance test battery or motor function test scores. Low BDNF levels at the onset of psychosis suggest that it may contribute to the pathogenesis of schizophrenia and/or perhaps could be a helpful neurobiological marker for possible early treatment intervention.     

Low serum levels of brain-derived neurotrophic factor in patients with schizophrenia do not elevate after antipsychotic treatment

Brain-derived neurotrophic factor (BDNF) has been suggested to be involved in the etiology of schizophrenia. There is a line of evidence that disruption of neurotrophins could play a role in the etiology of schizophrenia, and antipsychotics show their effect by altering levels of neurotrophins. The aim of this study was to evaluate the effect of antipsychotics on serum BDNF levels and their relationship with the symptoms in patients with schizophrenia. Twenty-two schizophrenia patients were enrolled in the study. The control group consisted of 22 age- and sex-matched physically and mentally healthy volunteers (7 male, 15 female). Serum BDNF levels and the positive and negative syndrome scale (PANSS) scores were recorded at baseline and after 6 weeks of treatment. Serum BDNF levels were also recorded in the control group. Schizophrenia patients who failed to meet 30% improvement in PANSS score were excluded from the study. The baseline serum BDNF levels of schizophrenia patients were lower than those of controls (t = 4.56; df = 21; p < 0.001). There was no correlation between serum BDNF levels and PANSS scores in patients with schizophrenia (p > 0.05). Although PANSS (for positive symptoms p < 0.001, for negative symptoms p < 0.001) and general psychopathology (t = 20.9; df = 22; p < 0.001) scores improved significantly after 6 weeks of antipsychotic treatment; there was no change in BDNF levels in patients' serum (p > 0.05). Our results support the view that BDNF would be associated with schizophrenia. However, we could not conclude that treatment with antipsychotics alters serum BDNF levels in patients with schizophrenia.     

Serum levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in depressed patients with schizophrenia

Aim: Brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are neurotrophins—proteins that induce the survival, development, and function of neurons. Their role in the development of schizophrenia and mood disorders is widely studied. This study was aimed to determine whether depression affects levels of BDNF and NT-3 in patients with schizophrenia. Methods: Data for 53 Caucasian adult hospitalized patients with chronic paranoid schizophrenia was compared with 27 healthy subjects. Clinical symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS) and positive, negative and general sub-scores, the Calgary Depression Scale for Schizophrenia (CDSS), the Hamilton Depression Rating Scale (HDRS), and the Clinical Global Impressions scale (CGI). Patients were defined as depressed (SHZ-DEP) with scores CDSS?>?6 and HDRS?>?7, otherwise they were included into the non-depressed group (SHZ-nonDEP). Results: In total, 17 patients (32.1%) with schizophrenia met criteria for depression. SHZ-DEP patients had higher scores in HDRS, CDSS, PANSS total, PANSS negative, PANSS general and CGI (p?p?=?0.045. NT-3 levels were higher in SHZ-DEP compared to SHZ-nonDEP: 133.31?±?222.19 versus 56.04?±?201.28 pg/mL, p?=?0.033. Conclusion: There were no differences in neurotrophin levels between patients with schizophrenia and controls. We found lower BDNF and higher NT-3 serum levels in depressed patients with schizophrenia.     

Thiol/Disulfide Homeostasis in Schizophrenic Patients

To determine serum thiol/disulfide homeostasis in schizophrenic patients. Serum native thiol, total thiol, and disulfide levels measuremented in the patients with 42 schizophrenia and 42 the healthy subjects. Serum native thiol, total thiol, and disulfide levels measuremented with a novel automated method. The thiol/disulfide ratio was also calculated. The Positive and Negative Syndrome Scale (PANSS) was used to assess the patients. The native thiol (p < 0.001) and total thiol (p < 0.001) levels, and the native thiol/total thiol (p = 0.018) ratio were significantly lower, whereas disulfide/native thiol (p = 0.002) and disulfide/total thiol (p = 0.002) ratio significantly increased in the schizophrenia patient group compared to the control group. A statistically significantly positive relationship was found between PANSS positive subscale with disulfide (r = 0.43, p = 0.01). Significantly positive relationships were found between PANSS total subscale with disulfide/total thiol (r = 0.308, p = 0.047). Our results suggest that the disulfide/thiol ratio is significantly greater in schizophrenia patients and disulfide/thiol ratio is closely related with the patients’ clinical symptoms.     

A positive correlation between serum levels of mature brain-derived neurotrophic factor and negative symptoms in schizophrenia

A meta-analysis study reported serum brain-derived neurotrophic factor (BDNF) levels as a potential biomarker for schizophrenia. However, at the time, commercially available human ELISA kits were unable to distinguish between pro-BDNF (precursor BDNF) and mature BDNF, because of limited antibody specificity. Here, we used new ELISA kits, to examine serum levels of mature BDNF and matrix metalloproteinase-9 (MMP-9), which converts pro-BDNF to mature BDNF in schizophrenia. Sixty-three patients with chronic schizophrenia and 52 age- and sex-matched healthy controls were enrolled. Patients were evaluated using the Brief Psychiatry Rating Scale, the Scale for the Assessment of Negative Symptoms (SANS) and neuropsychological tests. Neither serum mature BDNF nor MMP-9 levels differed between patients and controls. In male subgroups, serum MMP-9 levels of smoking patients were higher than those of non-smoking patients, but this was not observed in male controls or the female subgroup. In patients, serum mature BDNF levels were associated with SANS total scores and the Information subtest scores of the Wechsler Adult Intelligence Scale Revised (WAIS-R), while serum MMP-9 levels were associated with smoking and category fluency scores. These findings suggest that neither mature BDNF nor MMP-9 is a suitable biomarker for schizophrenia, although further studies using large samples are needed.     

Expression Analysis of Vitamin D Signaling Pathway Genes in Epileptic Patients

Vitamin D deficiency has been detected in epileptic patients. Vitamin D participates in neuroprotection, brain cell proliferation, and differentiation. Consequently, vitamin D supplementation has been suggested as an alternative treatment in epileptic patients. We aimed at assessment of vitamin D signaling pathway in epileptic patients. In the present study, we evaluated vitamin D serum concentration as well as expression of vitamin D receptor (VDR) gene and genes encoding for vitamin D activating enzyme 1-alpha-hydroxylase (CYP27B1) and deactivating enzyme 24-hyroxylase (CYP24A1) in epileptic patients compared with healthy individuals. We found significant lower levels of vitamin D in epileptic patients compared with healthy subjects. Expression analyses showed significant downregulation of VDR expression in peripheral blood of epileptic patients compared with healthy subjects (relative expression (REx)?=?0.16, P?<?0.001). However, there was no significant difference in CYP24A1 expression between epileptic patients and normal subjects. CYP27B1 expression analysis showed significant upregulation in male patients aged between 30 and 40 (REx?=?5.43, P?=?0.013). After using two-way ANCOVA for adjusting the effects of sex and age, there was a statistically significant difference in the VDR expression values between patient and control groups (P?<?0.001). Spearman’s correlation analysis showed no significant correlation between genes expression levels and patients’ age or vitamin D serum concentrations. However, we found significant correlations between VDR expression levels and CYP24A1/ CYP27B1 expression levels in epileptic patients (r?=?0.435 and P?<?0.001; r?=?0.26 and P?=?0.02 respectively). There was also a significant correlation between the expression levels of CYP24A1 and CYP27B1 (r?=?0.349 and P?=?0.001). Our study shows a possible role for VDR in the pathogenesis of epilepsy.     

Associations of serum brain-derived neurotrophic factor with cognitive impairments and negative symptoms in schizophrenia

Brain-derived neurotrophic factor (BDNF) may be involved in the pathophysiology of schizophrenia. The aim of this study was to examine the associations of serum BDNF levels with the cognition and clinical characteristics in patients with schizophrenia. Sixty-three patients with schizophrenia and 52 age- and sex-matched healthy controls were examined with neuropsychological tests. Serum BDNF levels were determined by enzyme-linked immunosorbent assay (ELISA). There were no significant differences in serum BDNF levels between normal controls and patients with schizophrenia. Serum BDNF levels of normal controls showed negative correlations with verbal working memory, but this was not the case with schizophrenic patients. Meanwhile, serum BDNF levels of schizophrenic patients showed positive correlations with the scores of the Scale for the Assessment of Negative Symptoms (SANS) and the Information subtest scores of Wechsler Adult Intelligence Scale Revised (WAIS-R). Serum BDNF levels are related with the impairment of verbal working memory and negative symptoms in patients with schizophrenia.     

The initial glycemic variability is associated with early neurological deterioration in diabetic patients with acute ischemic stroke

The association between glycemic variability and early neurological deterioration (END) in acute ischemic stroke remains unclear. This study attempted to explore whether initial glycemic variability increases END in diabetic patients with acute ischemic stroke. We enrolled type 2 diabetic patients undergoing acute ischemic stroke from November 2015 to November 2016. A total of 336 patients within 72 h from stroke onset were included. The serum glucose levels were checked four times per day during the initial 3 hospital days. The standard deviation of blood glucose (SDBG) values and the mean amplitude of glycemic excursions (MAGE) were calculated for glycemic variability. END was defined as an increase in the National Institutes of Health Stroke Scale (NIHSS) ≥?2 points between hospital days 0 and 5. The frequencies of END and HbA1c were significantly different in subjects grouped according to tertiles of MAGE (9.09, 12.07 and 50.00%, p?<?0.001 for END; 7.36?±?1.91, 7.83?±?1.93 and 8.56?±?1.79, p?<?0.001 for HbA1c). Compared to patients without END, patients with END had significantly higher HbA1c levels (8.30?±?1.92 vs 7.80?±?1.93, p?=?0.043), increased SDBG (3.42?±?1.14 vs 2.60?±?0.96, p?<?0.001), and increased MAGE (6.46?±?2.09 vs 4.59?±?1.91, p?<?0.001). In a multivariable logistic regression, stroke etiology (OR 0.675; 95% CI 0.485–0.940, p?=?0.020), baseline NIHSS (OR 1.086; 95% CI 1.004–1.175, p?=?0.040), and MAGE (OR 1.479; 95% CI 1.162–1.882, p?=?0.001) were significantly associated with END. Initial glycemic variability is associated with END in diabetic patients with acute ischemic stroke.     

The relationship between brain-derived neurotrophic factor and metabolic syndrome in patients with chronic schizophrenia: A systematic review

Background & aimsSchizophrenia is a serious long-term disorder in which the metabolic complications and abnormalities of the brain-derived neurotrophic factor (BDNF) can be found. In this study, we conducted a systematic review of the relationship between BDNF, metabolic syndrome (MetS) and its components in schizophrenic patients.MethodsData were collected mainly from PubMed, Google Scholar, Scopus, and ProQuest databases. The keywords related to the BDNF, MetS, schizophrenia were searched. Two reviewers independently screened 1061 abstracts. And eventually, a total of 7 studies (6 observational and 1 interventional) was included in the systematic reviews.ResultsFour of the 7 study ascertained statistically significant inverse relationship between serum BDNF levels and MetS in schizophrenic patients. While in the other two studies, there was no inverse relationship. In the last selected study, the researchers found a weak association between the Val66Met polymorphism in BDNF Gene and clozapine-induced MetS.ConclusionAlthough this relationship could not be determined but BDNF levels appear to be reduced in schizophrenic patients with MetS and factors such as sex and antipsychotic class differentiation, sampling and methodology and episodes of illness could play a role in the results and outcomes.     

Serum brain-derived neurotrophic factor level in relation to illness severity and episode duration in patients with major depression

BackgroundSince there are few data on the possible association between BDNF levels and characteristics of major depression, the present study assesses brain-derived neurotrophic factor (BDNF) levels in three drug-free patient samples, and explores whether episode duration, and severity correlate with serum BDNF levels.MethodSerum BDNF levels were measured in 42 drug-free patients with major depression. The duration of the index episode and the presence of psychotic features were assessed with the Schedule for Affective Disorders and Schizophrenia, and the severity of depression was measured with the 17-item Hamilton Rating Scale for Depression. The sample was divided into three groups: severely depressed inpatients without psychotic features, severely depressed inpatients with psychotic features, and moderately depressed outpatients.ResultsMean serum BDNF level in the total sample was 18.0 ± 2.8 ng/ml, with no significant difference between the three patient samples (F = 1.80, df = 2, p = 0.18). Mean serum BDNF level was significantly lower in patients with an index episode over one year, compared with patients who had a shorter index episode (F = 4.90, df = 1, p = 0.033).ConclusionThese data show that patients with a long index episode have significantly lower serum BDNF levels. We found no influence of the presence of psychotic features and severity of depression on serum BDNF levels.     

Serum brain-derived neurotrophic factors in Taiwanese patients with drug-naïve first-episode schizophrenia: Effects of antipsychotics

Objectives: Brain-derived neurotrophic factors (BDNF) are known to be related to the psychopathology of schizophrenia. However, studies focussing on drug-naïve first-episode schizophrenia are still rare.

Methods: Over a 5-year period, we investigated the serum BDNF levels in patients with first-episode drug-naïve schizophrenia and compared them to age- and sex-matched healthy controls. We also explored the association between antipsychotic doses, positive and negative syndrome scale (PANSS) scores, and serum BDNF levels before and after a 4-week antipsychotic treatment.

Results: The baseline serum BDNF levels of 34 patients were significantly lower than those of the controls (df?=?66, P?=?.001). Although the PANSS scores of 20 followed-up patients improved significantly after antipsychotic treatment, the elevation of the serum BDNF levels was not statistically significant (P?=?.386). In addition, Pearson’s correlation test showed significant correlations between pre-treatment negative scale scores and percentage changes in BDNF (P?=?.002).

Conclusions: The peripheral BDNF levels in Taiwanese patients with drug-naïve first-episode schizophrenia, compared with healthy controls, did not elevate after antipsychotic treatment, and pre-treatment negative symptoms played a pivotal role in trajectories of serum BDNF levels. Large samples will be needed in future studies to verify these results.     

男性慢性精神分裂症患者血清脑源性神经营养因子和胶质源性神经营养因子水平及认知功能的对照研究

目的:探讨慢性精神分裂症患者血清脑源性神经营养因子(BDNF)、胶质源性神经营养因子水平(GDNF)和神经认知功能的变化及它们之间关系。方法:入组慢性精神分裂症患者57例和正常对照39名。采用阳性与阴性症状量表(PANSS)评估患者的精神症状。使用酶联免疫吸附法检测血清BDNF、GDNF蛋白水平,采用数字划消测验、连线测验(TMT)、WMS-III空间广度测验(WMS-III SST)、定步调连续加法任务测验(PASAT)、Stroop测验、木块图评估神经认知功能。结果:患者组血清BDNF水平低于对照组,差异有统计学意义(t=9.112,P0.01),患者组血清GDNF与对照组相比差异无统计学意义(t=1.513,P0.05)。患者组数字划消测验、TMT-A、TMT-B、Stroop测验、木块图、WMS-III SST逆行分、PASAT成绩均差于对照组(P0.05)。患者组血清BDNF水平与PANSS阳性症状分、数字划消测验中的错误个数呈负相关(分别为r=-0.295,P=0.026;r=-0.262,P=0.049),血清GDNF水平与Stroop色词干扰测验分呈正相关(r=0.263,P=0.048)。结论:慢性稳定期的精神分裂症患者仍存在广泛的神经认知损害。BDNF可能是精神分裂症的一种素质性标记,可能参与了患者的注意障碍。     

Quality of Life and Hormonal,Biochemical, and Anthropometric Profile Between Olanzapine and Risperidone Users

This cross-sectional study compared quality of life and side effects in 108 users of olanzapine or risperidone suffering schizophrenia and being attended at psychiatric ambulatory services in Rio Grande do Norte, Brazil. Economic, socio-demographic, anthropometric, biochemical, and hormonal variables were compared. The EuroQoL Five-Dimension Scale (EQ-5D) was used to evaluate quality of life, and side effects were assessed using the Udvalg for Kliniske Undersøgelser (UKU) Side Effect Rating Scale and the Simpson–Angus Scale. Data were analysed using the χ² test and Student’s t test, with a significance level of 5 %.The household incomes of approximately 80 % of patients were <2.0 minimum wages ($678). Anthropometric variables (waist circumference, hip circumference, weight, waist-to-hip ratio) and systolic and diastolic blood pressure were noted among male olanzapine users (all p < 0.05). EQ-5D scores showed that olanzapine use significantly impacted self-help ability (p < 0.001). Risperidone users had a mean quality-adjusted life year value of 1. Mean total Simpson–Angus Scale scores was 0.38 for olanzapine users and 0.11 for risperidone users (p < 0.02). Significant differences in UKU were observed for the following items: asthenia/lassitude/fatigue (higher among olanzapine users, p = 0.02), dystonia (higher among olanzapine users, p = 0.01), tremors (higher among olanzapine users, p = 0.03), gynecomastia (higher among risperidone users, p < 0.02), and ejaculatory dysfunction (higher among risperidone users, p < 0.02). Olanzapine users had impaired quality of life, which can be explained in part by adverse motor, biochemical, and hormonal effects characteristic of metabolic syndrome.