精神分裂症与抑郁症患者视觉P300电位的随访比较

目的　探讨精神分裂症和抑郁症患者事件相关电位 (ERPs)P3 0 0 的P3 波异常的意义。方法　对 2 1例精神分裂症、15例抑郁症患者在未服药和停药半年后的发病期及 2年缓解期后采用视觉图像辨认作业引出中央点P3 0 0 ,并与 2 4名正常对照者进行比较。结果　两病例组在发病期P3 潜伏期 [精神分裂症组 (431± 42 )ms,抑郁症组 (40 5± 32 )ms]延长、波幅 [精神分裂症组 (4 7± 2 0 ) μV ,抑郁症组 (5 3± 2 7) μV]下降 ,与对照组 [(36 7± 13)ms、(9 3± 3 1) μV]间的差异有显著性 ;缓解期复查仅精神分裂症组P3 潜伏期 [(410± 30 )ms]及波幅 [(7 1± 3 3) μV]异常较明显 ,抑郁症组潜伏期[(374± 9)ms,波幅为 (8 1± 4 1) μV]与对照组间的差异无显著性。结论　精神分裂症P3 波异常具一定跨状态稳定性 ,其中潜伏期的延长更为稳定 ;而在抑郁症则与临床状态有关。     

利培酮和氟哌啶醇对精神分裂症患者超氧化物歧化酶及催乳素影响的临床对照研究

目的 探讨经第一、二代抗精神病药治疗的精神分裂症患者体内超氧化物歧化酶(SOD)、催乳素(PRL)与精神症状间的关系.方法 符合美国精神障碍诊断与统计手册第4版诊断标准的78例精神分裂症患者,随机分为利培酮组(41例),剂量为6 mg/d;氟哌啶醇组(37例),剂量为20mg/d;观察疗程均为12周.使用阳性和阴性症状量表(PANSS)评定临床疗效.采用放射免疫法在治疗前后分别测定患者血浆SOD及PRL浓度.以30名正常人为正常对照组.结果 利培酮组(40例)、氟哌啶醇组(33例)患者的基线SOD浓度[(794±126)ng/mg Hb,(750±101)ng/mg Hb]均明显高于正常对照组[(483±110)ng/mg Hb],而PRL浓度[(6±7)μg/L,(6±8)μg/L]均明显低于正常对照组[(18±12)μg/L],差异均有统计学意义(P均＜0.05).利培酮组和氟哌啶醇组患者的治疗前SOD与PRL间存在显著负相关(n=70,P＜0.05).治疗第12周末,利培酮组和氟哌啶醇组的SOD浓度[(499±98)ng/mg Hb,(482±76)ng/mg Hb]明显降低,而PRL浓度[(33±19)μg/L,(25±16)μg/L]则明显升高.利培酮组与氟哌啶醇组间治疗前后的SOD、PRL的差异均无统计学意义(P均＞0.05).治疗前后,阴性症状改善与SOD浓度差值(P＜0.05)、阳性症状改善与PRL浓度差值(n=70,P＜0.01)有相关性.结论 精神分裂症患者SOD及PRL浓度异常,两者间存在着相互作用,且对抗精神病药的临床疗效有影响.     

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.     

强迫症患者血小板5-羟色胺、血浆催乳素及地塞米松抑制试验的研究

目的　从神经递质与神经内分泌角度探讨强迫症的生化病理机制。方法　采用高效液相色谱法及放射免疫测定法 ,分别测定 2 9例强迫症患者和 2 8名正常对照者血小板 5 羟色胺 (5 HT)含量及血浆催乳素 (PRL)含量 ,并进行地塞米松抑制试验 (DST)。结果　强迫症组血小板 5 HT水平[(0 8± 1 0 )nmol/10 9个血小板 ]低于正常对照组 [(1 4± 1 2 )nmol/10 9个血小板 ],差异有显著性 (P <0 0 5 ) ;而血浆PRL水平 [(337± 192 )nmol/L]与对照组 [(2 87± 116 )nmol/L]相比 ,差异无显著性 (P >0 0 5 ) ;强迫症组于晨 8时的血浆基础皮质醇含量 [(375± 15 2 )nmol/L]高于正常对照组 [(2 6 2± 138)nmol/L],差异有非常显著性 (P <0 0 1) ,其DST阳性率为 2 4 %～ 17% ,与正常对照组 (14 %～ 11% )相比 ,差异无显著性 (P >0 0 5 )。结论　强迫症患者存在 5 HT能低下和神经内分泌功能的紊乱 ,强迫症的 5 HT能假说能解释其某些内分泌功能紊乱。     

老年精神分裂症患者血浆脂蛋白磷脂酶A2浓度与BPRS评分的相关性

目的分析老年精神分裂症患者血浆脂蛋白磷脂酶A2(Lp-PLA2)浓度及与简明精神病评定量表(BPRS)评分的相关性,探讨血浆Lp-PLA2浓度在老年精神分裂症发病中的作用。方法采用简单随机抽样方法选取2015年1月-12月在南京医科大学附属脑科医院住院的老年精神分裂症患者为病例组(n=72),以同时段在本院体检的所有健康退休员工为对照组(n=72)。采用免疫增强比浊法检测两组血浆Lp-PLA2浓度,使用简明精神病评定量表(BPRS)评定老年精神分裂症患者的精神症状,分析BPRS评分与血浆Lp-PLA2浓度的相关性。结果病例组血浆Lp-PLA2浓度高于对照组[(232.5±125.7)ng/m L vs.(185.4±74.6)ng/m L,t=2.734,P0.05]。61例慢性病例组血浆Lp-PLA2浓度与11例首发病例组比较,差异无统计学意义[(119.8±15.3)ng/m L vs.(160.4±48.4)ng/m L,t=0.479,P0.05]。老年精神分裂症病例组BPRS评分为(50.9±10.5)分,与血浆Lp-PLA2浓度无相关性。结论老年精神分裂症患者可能存在膜磷脂代谢异常,血浆Lp-PLA2浓度可能不能作为判断老年精神分裂症临床症状严重程度的标准。     

广泛性焦虑症与抑郁症患者免疫、内分泌及单胺递质的对照研究

目的探讨广泛性焦虑症(GAD)与抑郁症(MD)患者在免疫、内分泌和单胺递质方面的差异。方法 对30例GAD患者(焦虑症组)、38例MD患者(抑郁症组)在治疗(5-羟色胺再摄取抑制剂治疗6~8周)前后分别检测血清白细胞介素2(IL-2)、白细胞介素6(IL-6)、白细胞介素1β(IL-1β)、白细胞介素8(IL-8)、可溶性白细胞介素6受体(SIL-6R)、肿瘤坏死因子α(TNF-α)、皮质醇(CS)、促肾上腺皮质激素(ACTH)、肾上腺素(EPH)和去甲肾上腺素(NE)水平。选择30名年龄和性别与患者组相匹配的健康人为对照组。结果 (1)焦虑症组治疗前IL-8[(122±76)ng／L]、SIL-6R[(2 065±790)ng／L]水平均高于对照组(99±68)ng／L]、[(294±48)ng／L,IL-6水平为(1.6±0.7)ng／L,低于对照组[(5.3±2.7)ng／L],差异均有显著性意义(P<0.05);抑郁症组治疗前IL-2[(7.7±6.7)ng／L]、IL-8[(119±67)ng／L]、SIL-6R[(1308±371)ng／L]水平均高于对照组,差异均有显著性意义(均P<0.05)。经治疗后,焦虑症组IL-6[(4.3±1.2)ng／L]水平较治疗前升高,IL-8[(39±9)ng／L]水平较治疗前降低(P<0.05);抑郁症组IL-2[(2.4±1.2)ng／L]、IL-8[(47±15)ng／L]水平较治疗前降低(P<0.05);均接近于对照组水平(均P>0.05)。(2)焦虑症组治疗前ACIH[(49±28)ng／L]、EPH[(67±45)ng／     

抑郁症患者血清维生素D水平的研究

目的:探讨抑郁症患者血清维生素D水平及其与抑郁症病情的相关性。方法:随机抽取门诊抑郁症患者80例(抑郁症组),以电发光化学法测定血清25(OH)D3;并与50名性别、年龄相匹配的体检者(对照组)比较;采用汉密尔顿抑郁量表(HAMD)24项对抑郁症患者进行评估,分析血清25(OH)D3水平与HAMD评分的关系。结果:抑郁症组血清25(OH)D3[(25.54±7.09)ng/ml]明显低于对照组[(42.03±10.21)ng/ml](P0.01);抑郁症组血清维生素D不足率(60%)或缺乏率(25%)明显高于对照组(8%,0)(P均0.01);抑郁症患者血清25(OH)D3水平与HAMD评分呈负相关(r=-0.73,P0.01)结论:抑郁症患者血清维生素D水平降低,并与其病情相关。     

抑郁症患者睡眠行为及睡眠生理障碍的研究

目的　探讨抑郁症患者睡眠行为及睡眠生理的变化。方法　采用调查表对 32例抑郁症患者的睡眠行为障碍和睡眠生理进行调查 ,检测其全夜多导睡眠图 ,并与 2 1名正常人进行对照。结果　 (1)抑郁症组的入睡困难、早醒、睡眠维持障碍及睡眠过多的发生率高于对照组 (P <0 0 5～0 0 1) ;(2 )与对照组比较 ,抑郁症组存在睡眠潜伏期长 [(36 1± 17 2 )min],醒觉时间、觉醒次数、醒觉睡眠比高 ,睡眠效率和睡眠维持率低 (P <0 0 5～ 0 0 1) ,快速眼动睡眠潜伏期短 [(6 1 8± 31 2 )min]等。结论　抑郁症患者存在睡眠行为与睡眠生理相一致的异常改变 ,其睡眠障碍的病理机制可能同源于抑郁症的发病机制。     

精神分裂症、情感性精神障碍患者血超氧化物歧化酶的研究

目的探讨精神分裂症、情感性精神障碍患者血超氧化物歧化酶(SOD)含量与精神疾病的相关意义.方法采用放射免疫法测定130例精神分裂症患者、58例情感性精神障碍患者及50名健康人(对照组)的血SOD含量(ng/mg血红蛋白),并对其中64例精神分裂症患者经12周治疗后再次测定SOD;同时用简明精神病评定量表(BPRS)、汉密尔顿抑郁量表(HAMD)和Bech-Rafaelson躁狂量表(BRMS)分别对患者进行评定.结果精神分裂症、躁狂症患者的血SOD含量分别为1077±420、1044±292,均明显高于对照组(579±237),P＜0.01.抑郁症组SOD含量为701±267,与对照组的差异无显著性,P＞0.05;精神分裂症病程＜5年患者的SOD含量(1105±451)与≥5年组SOD含量(1035±346)的差异无显著性(P＞0.05);64例精神分裂症患者经12周治疗后的血SOD含量(627±217)低于治疗前(1009±364),P＜0.01.结论血SOD含量的增高也许能够反映精神疾病的存在,但不能有效区别是何种精神疾病.     

阿立哌唑治疗利培酮所致精神分裂症女性患者高催乳素血症的研究

目的 探讨阿立哌唑治疗利培酮所致女性患者高催乳素血症的疗效及安全性.方法 117例利培酮所致高催乳素血症的女性患者,随机分为治疗组(60例)和对照组(57例).维持原有利培酮治疗不变,治疗组加用阿立哌唑5 mg,对照组加用安慰剂治疗,疗程均为6周.于治疗第0,6周末检测催乳素,评定简明精神病量表(BPRS)、治疗中需处理的不良反应症状量表(TESS).结果 (1)治疗第6周末,治疗组催乳素[(26±6)μg/L]较基线[(112±40)μg/L]下降,差异有统计学意义(P=0.000);对照组催乳素[(99±44)μg/L]与基线[(104±34)μg/L]比较,差异无统计学意义(P=0.180).(2)治疗第6周末,治疗组催乳素下降率[(75±8)%]、正常率(82%),均高于对照组[分别为(5+30)%,4%];P均=0.000.(3)治疗第6周末,治疗组[(20.4±2.1)分]、对照组[(20.8±1.9)分]BPRS评分均较基线[分别为(21.1±1.8)分,(21.4±1.9)分]下降,P均=0.045;两组不良反应发生率相近(P=0.553).结论 阿立哌唑治疗利培酮所致精神分裂症女性患者的血高催乳症有效、安全.     

Biological measures and cellular immunological function in depressed psychiatric inpatients

Thirty depressed psychiatric inpatients, including 18 with a diagnosis of major depression, and 25 hospital staff controls were compared with respect to cellular immune function--that is, mitogen responsiveness to concanavalin A (con A), phytohemagglutinin (PHA), and pokeweed mitogen (PWM); natural killer cell (NK) activity; and T cell subsets, including helper/inducer T cells (CD4) and suppressor/cytotoxic cells (CD8). Only physically healthy subjects, who had not used psychoactive medications (except for low dose benzodiazepines) or other medications known to affect the immune system for at least 14 days, were included. Paired comparisons of the immune measures of patients with a DSM-III diagnosis of major depression (n = 18) with their controls demonstrated a statistically significant reduction of the patients' con A response. In addition, the patients with major depression had significantly lower con A and PHA responses than the combined patients with other forms of depression (atypical, dysthymic, or atypical bipolar). There was no indication that severity of depression, dexamethasone suppression test status, benzodiazepine use, or age accounted for the differences in immune function. A possibly important, unexpected finding was that antihistamine use was associated with lower immune function.     

Altered levels of the synaptosomal associated protein SNAP-25 in hippocampus of subjects with mood disorders and schizophrenia.

SNAP-25 levels were measured in ventral hippocampus in subjects with unipolar depression (n = 12), bipolar disorder (n = 13), schizophrenia (n = 15) and controls (n = 15) using quantitative immunocytochemistry. SNAP-25 levels were reduced significantly in stratum oriens of bipolar patients compared with controls (p < 0.05); they were also reduced significantly in st. oriens (p < 0.01 vs schizophrenia), in alveous (p < 0.01 vs schizophrenia) and in presubiculum (p < 0.05 vs depressed). SNAP-25 levels were also reduced in several layers of schizophrenics, only significantly so in st. granulosum (p < 0.05 vs controls). In contrast, depressed SNAP-25 levels increased in st. moleculare (p < 0.01 vs schizophrenics) and presubiculum (p < 0.05 vs controls and bipolars; p < 0.01 vs schizophrenics). SNAP-25 values were not affected by age, sex, race, post-mortem interval, brain pH, side of brain, age of onset of disease, family history of psychiatric disease, drug or alcohol use, antipsychotic drug treatment, or mode of death. The reported changes in SNAP-25 levels appear to be disease specific, separating synaptic pathology in unipolar depression from that observed in schizophrenia and bipolar disorders.     

Altered levels of Reelin and its isoforms in schizophrenia and mood disorders.

Reelin is a secreted extracellular matrix protein approximately 410 kDa mol. wt that is reduced in brains of patients with schizophrenia, autism, bipolar disorder and major depression. Recent reports also indicate its near absence in sera of some patients with an autosomal recessive form of lissencephaly. Moreover, Reelin is involved not only in normal cortical lamination of the brain during mammalian embryogenesis but is also implicated in cell signaling systems subserving cognition in adult brain. Here, we show that blood levels of Reelin and its isoforms are altered in three psychiatric disorders, namely, schizophrenia, bipolar disorder and major depression. The changes include significant increases in 410 kDa Reelin moiety of 49% in schizophrenic patients (p < 0.022) of four ethnic compositions (Caucasian, Vietnamese, Hmong and Laotian) and non-significant increases in depressed patients by 34% vs control blood. In contrast, 410 kDa Reelin levels decreased by 33% in bipolar blood, albeit non-signficantly, vs. controls. There was a significant increase of 90% (p < 0.0061) in 330 kDa Reelin in Caucasian schizophrenics; the depressed value was elevated by 30% vs. control but non-significantly. Again, in contrast, bipolar 330 kDa value decreased by 31% vs control (p < 0.0480). Finally, all 180 kDa Reelin values varied minimally in schizophrenics vs controls. In contrast, the 180 kDa Reelin values dropped significantly by 49% (p < 0.0117) and 29% (p < 0.0424) in bipolar and depressed patients, respectively, compared with controls. The alterations in blood Reelin values appear to be specific since levels of two other blood proteins, ceruloplasmin and albumin did not vary significantly between all psychiatric subjects and controls. These findings suggest that blood Reelin levels and its isoforms may be used as potential peripheral markers to diagnose presence of several psychiatric disorders and may also serve as targets for future therapeutic interventions.     

Lytic effector cell function in schizophrenia and depression

Natural killer (NK) cell activity and antibody-dependent cellular cytotoxicity (ADCC) were tested in patients with schizophrenia or depression. It was found that NK activity as well as ADCC were significantly lower in both groups, as compared to healthy control individuals (P less than 0.001). Psychopharmacologic treatment with neuroleptics and antidepressives resulted in a significant increase in NK activity and ADCC (P less than 0.005) in patients with schizophrenia but not in treated patients with depression. In patients with schizophrenia, no correlation could be established between the dose of neuroleptic given and the increase in NK activity. Lithium also did not produce an increase in NK activity and ADCC. The addition of serum, derived from untreated patients with schizophrenia, to cell cultures in concentrations of 10 and 20% had an inhibitory effect upon the ADCC and, to a lesser degree, upon NK activity (20% serum concentration only); sera from treatment schizophrenics produced no inhibition of NK activity, but did affect ADCC. No serum-derived inhibitory effect upon either NK activity or ADCC was found to be present in sera from patients with depression. We conclude that lytic effector mechanisms are impaired in patients with schizophrenia or depression and that this defect is reversed in schizophrenic patients on treatment, but not in depressives on therapy. Patients with schizophrenia also tend to have a reversible serum-mediated inhibition of NK activity which is absent in patients with depression.     

A comparative study on quality of life of patients of schizophrenia with and without depression

Depression in schizophrenia has been recognized as one of the important factors influencing the Quality of Life (QOL). For this study 60 patients with a clinical diagnosis of schizophrenia as per ICD-10 (DCR version) were divided into two groups (with and without depression) on the basis of their score on Calgary Depression Rating Scale for Schizophrenia (CDSS). Thereafter, all patients were assessed on Positive and Negative Syndrome Scale for Schizophrenia (PANSS) for psychopathology, on Lehman Quality of Life Interview (QOLI)-brief version for QOL, on World Health Organization Disability Assessment Schedule-II (WHODAS-II) for disability, on UKU Side Effect Rating Scale for side effects of drugs and on Social Support Questionnaire (SSQ) for perceived social support. The two (depressed and non-depressed schizophrenia) groups differed significantly on symptoms of general psychopathology of PANSS and disability as per WHODAS-II, with the depressed group scoring higher. In the total sample, positive symptoms and the symptoms of general psychopathology of PANSS had a strong negative correlation with all three (subjective, objective and combined) domains of QOL, whereas, disability and medication side effects had a negative correlation with subjective and combined domains of QOL. CDSS total score did not significantly correlate with QOL. General psychopathology symptoms of PANSS emerged as the sole significant predictor of subjective and combined QOL, while positive symptoms of PANSS emerged as the sole predictor of objective QOL. Hence, it can be concluded that general psychopathology on PANSS had significant effect whereas depression as rated on CDSS had no significant effect on QOL in patients with schizophrenia. Treatments to improve QOL in schizophrenia should focus on symptoms of general psychopathology of PANSS.     

Cross-sectional similarities and differences between schizophrenia, schizoaffective disorder and mania or mixed mania with mood-incongruent psychotic features.

BACKGROUND: The cross-sectional clinical differentiation of schizophrenia or schizoaffective disorder from mood-incongruent psychotic mania or mixed mania is difficult, since pathognomonic symptoms are lacking in these conditions. AIMS OF THE STUDY: To compare a series of clinical variables related to mood and cognition in patient groups with DSM-III-R diagnosis of schizophrenia, schizoaffective disorder, mood-incongruent psychotic mania and mood-incongruent psychotic mixed mania. METHODS: One hundred and fifty-one consecutive patients were evaluated in the week prior to discharge by using the structured clinical interview for DSM-III-R-patient edition (SCID-P). Severity of psychopathology was assessed by the 18-item version of the brief psychiatric rating scale (BPRS) and negative symptoms by the scale for assessment of negative symptoms (SANS). Level of insight was assessed with the scale to assess unawareness of mental disorders (SUMD). RESULTS: There were no differences in rates of specific types of delusions and hallucinations between subjects with schizophrenia, schizoaffective disorder, psychotic mania and psychotic mixed mania. SANS factors scores were significantly higher in patients with schizophrenia than in the bipolar groups. Patients with mixed state scored significantly higher on depression and excitement compared to schizophrenia group and, to a lesser extent, to schizoaffective group. Subjects with schizophrenia showed highest scores on the SUMD indicating that they were much more compromised on the insight dimension than subjects with psychotic mania or mixed mania. CONCLUSION: Negative rather than affective symptomatology may be a useful construct to differentiate between schizophrenia or schizoaffective disorders from mood-incongruent psychotic mania or mixed mania.     

Anhedonia in the deficit syndrome of schizophrenia.

Previous studies have shown that anhedonia characterizes the deficit syndrome of schizophrenia. Anhedonia is also one of the main symptoms of the depressive state. The purpose of this study was to examine the relationships between anhedonia and depression in the deficit syndrome of schizophrenia. Self-evaluations of anhedonia and depression were performed by three groups of subjects (32 deficit schizophrenics, 32 major depressives, 35 healthy subjects) matched for sociodemographic variables. Deficit schizophrenics and major depressives are more anhedonic than controls, but there is no difference between the two study groups. Contrarily to what is evidenced for major depressives and for healthy subjects, the depressive symptomatology correlates with anhedonia in deficit schizophrenics. When deficit schizophrenics are dichotomized into depressed versus non-depressed patients, no difference is observed concerning anhedonia. These results suggest that anhedonia in the deficit syndrome of schizophrenia has no specificity but appears independent of coexisting depression and covaries with several characteristics of depression (retardation, cognitive distortions). Our results support the hypothesis that the deficit syndrome of schizophrenia could constitute a non-depressive mood disorder.     

血可溶性白细胞介素2受体与不同精神疾病的相关性研究

为了解精神疾病与可溶性白细胞介素２受体（ＳＩＬ－２Ｒ）的关系，采用双抗体夹心步骤的酶联免疫吸附测定（ＥＬＩＳＡ）来检测精神分裂症４０例、躁狂症１８例、抑郁症２０例及４９名健康者的血清ＳＩＬ－２Ｒ含量。结果显示，精神分裂症和抑郁症患者血清ＳＩＬ－２Ｒ基础值较健康对照组显著升高（Ｐ＜０．０１），躁狂症组较对照组显著降低（Ｐ＜０．０１），而精神分裂症和抑郁症患者经治疗后血清ＳＩＬ－２Ｒ显著降低（Ｐ＜０．０１），躁狂症则明显增高（Ｐ＜０．０１）。提示精神疾病患者存在有免疫缺陷，血清ＳＩＬ－２Ｒ是可供判断免疫缺陷和精神症状演变的一个参考指标。     

Plasma-soluble interleukin-2 and transferrin receptor in schizoprenia and major depression

This study was carried out to examine some components of in vivo immune function in major depression and schizophrenia. Toward this end, plasma concentrations of interleukin-1 (IL-1) and IL-6, soluble IL-2 receptor (sIL-2R), and transferrin receptor (TfR) were measured in 28 normal controls, 11 schizophrenics and 13 major-depressed patients. Schizophrenic and major-depressed patients showed significantly higher plasma sIL-2R and TfR than normal controls. There was a trend toward higher plasma IL-6 in the psychiatric patients, and particularly in schizophrenic patients, than in normal volunteers. In normal controls and in the total study group, there were highly significant and positive correlations between plasma TfR and sIL-2R concentrations. It is suggested that schizophrenia and major depression are characterized by immune disorders that may indicate activation of cell-mediated immunity such as T-cell activation.     

精神分裂症血清肌酸磷酸激酶活性研究

目的：探讨精神分裂症患者血清肌酸磷酸激酶（CPK）活性与病情的关系。方法：对195例精神分裂症患者于治疗前、治疗4和8周末分别进行CPK检测，同时以简明精神病量表（BPRS）、阴性症状量表（SANS）和阳性症状量表（SAPS）评定其情严重度。选取同期本地区健康体检者69名为对照组。结果：精神分裂症在发病期的CPK活性极显著高于对照组，治疗后显著下降，4周末已降至正常范围；在发病期的CPK值与BPRS总分、思维障碍因子分、激活性因子分和SAPS因子分呈显著正相关，好转后相关性降低，至8周末已无相关性；病例组CPK变化值与BPRS总分减分值、激活性因子的减分值和SAPS总分的减分值呈显著正相关。结论：精神分裂症患者在发病期的CPK活性显著升高，与病情关系密切，与阳性症状相平等，这可能是精神分裂症的神经－免疫、代谢相互作用的结果。