二甲双胍对奥氮平致体质量增加精神分裂症患者肝脏脂肪含量的影响

目的探讨二甲双胍对奥氮平致体质量增加精神分裂症患者肝脏脂肪含量的影响。方法选取我院2012-03—2015-03收治的奥氮平致体质量增加精神分裂症患者65例,随机分为观察组(n=34)和对照组(n=31),对照组保持原有奥氮平药物治疗,观察组在原有服用奥氮平的基础上给予二甲双胍治疗,对比2组治疗前后的肝脏脂肪含量,以及观察组治疗前后的低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、甘油三酯(TG)、胆固醇(TC)、胰岛素抵抗指数(HOMA-IR)。结果治疗后观察组肝脏脂肪含量低于对照组,差异具有统计学意义(P0.05);观察组治疗后的HDL-C指标高于治疗前,TG、TC、HOMA-IR指标低于治疗前,差异有统计学意义(P0.05)。结论二甲双胍可降低奥氮平致体质量增加精神分裂症患者TG、TC等指标含量以及肝脏脂肪含量,效果良好,具有较高的实用价值。     

帕利哌酮和奥氮平对精神分裂症患者阳性症状、血脂、体质量的影响

目的对比帕利哌酮与奥氮平对精神分裂症患者阳性症状、血脂、体质量的影响。方法将70例精神分裂症患者随机分为帕利哌酮组和奥氮平组各35例。分别使用帕利哌酮缓释剂和奥氮平治疗,疗程均为8周。2组均采用阳性与阴性症状量表(PANSS)评定疗效,同时对比血脂、体质量的影响,评定不良反应。结果 2组疗效均显著,组间比较差异无统计学意义(P>0.05);帕利哌酮缓释剂组在导致体质量增加的不良反应明显低于奥氮平组(P<0.05),在对血脂的影响方面2组比较无统计学意义(P>0.05)。结论帕利哌酮可作为精神分裂症的一线用药和维持治疗用药,疗效可靠,导致体质量增加的不良反应少于奥氮平。     

非典型抗精神病药急性期治疗致精神分裂症患者体质量增加的影响因素

目的:探讨非典型抗精神病药(APS)急性期治疗致精神分裂症患者体质量增加的影响因素。方法:158例急性期精神分裂症患者给予APS单药治疗8周;治疗前后测量体质量并计算体质量指数(BMI)及血脂、血糖,以治疗后体质量是否增加≥7%为界将患者分为两组,分析APS致患者体质量增加的相关因素。结果:治疗8周后,有39例(24. 7%)患者较治疗前体质量增加,各种药物发生率依次为氯氮平43. 6%、奥氮平30. 8%、利培酮23. 1%、喹硫平2. 6%;男性发生率(32. 4%)明显高于女性(8%)。单因素分析显示性别、年龄、药物、基线BMI是体质量增加的危险因素(P 0. 05或P 0. 001);多因素Logistic回归分析发现体质量增加与性别(OR=0. 033,95%CI:0. 006～2. 185; P 0. 001)、药物(OR=2. 013,95%CI:1. 405～2. 883; P 0. 001)有关。结论:性别、药物是APS急性期治疗致精神分裂症患者体质量增加的危险因素。     

奥氮平与利培酮治疗精神分裂症对照研究

目的:比较奥氮平与利培酮治疗精神分裂症的疗效和安全性。方法:将60例精神分裂症随机分两组,分别给予奥氮平与利培酮治疗8周。用阳性与阴性症状量表(PANSS)、治疗中出现的症状量表(TESS)评定疗效及不良反应。结果:奥氮平与利培酮的疗效差异无显著性。奥氮平主要不良反应是嗜睡、体质量增加,利培酮主要是锥外系反应、失眠。结论:奥氮平与利培酮均是治疗精神分裂症安全有效的非典型抗精神病药,可根据患者的情况分别选择。     

齐拉西酮与奥氮平对初治精神分裂症的疗效评价

目的探讨齐拉西酮与奥氮平治疗初治精神分裂症的临床疗效。方法将2012-09—2015-12我院接受治疗的114例初治精神分裂症患者纳入本研究。按照入院顺序抽签后随机分为齐拉西酮组和奥氮平组,分别采取齐拉西酮和奥氮平治疗,观察治疗效果。结果齐拉西酮组总有效率85.96%,奥氮平组为87.82%,差异无统计学意义(P0.05)。2组治疗后阳性症状、阴性症状、一般精神病理症状、PANSS总评分均低于治疗前,差异有统计学意义(P0.05)。齐拉西酮组失眠发生率高于奥氮平组,体质量增加、血糖升高发生率低于奥氮平组,差异有统计学意义(P0.05)。齐拉西酮组T淋巴细胞亚群CD3、CD4、CD8、CD4/CD8水平均低于奥氮平组,差异有统计学意义(P0.05)。结论齐拉西酮与奥氮平治疗初治精神分裂症的效果相当,齐拉西酮治疗失眠率较高,奥氮平治疗体质量增加、血糖升高发生率较高,奥氮平治疗患者CD3、CD4、CD8、CD4/CD8水平恢复较好。     

二甲双胍对奥氮平所致精神分裂症患者体质量增加的影响

目的 验证二甲双胍预防奥氮平引起精神分裂症患者的体质量增加和糖代谢紊乱的效果.方法 将37例未服过抗精神病药的精神分裂症患者,随机分为奥氮平(15 mg/d)联合二甲双胍组(750 ms/d;A组,18例)和奥氮平(15 mg/d)联合安慰剂组(B组,19例),治疗12周.于治疗前和治疗第4周末、8周末及12周末测定空腹血糖、胰岛素(INS)、身高、体质量、腰围、臀围,计算体质量指数(BMI)、腰臀比(WHR)、胰岛素抵抗指数(IRI)及治疗12周末体质量增加大于7%的比率.用阳性症状量表(SAPS)、阴性症状量表(SANS)于治疗前和治疗12周末评定疗效.结果 治疗12周末,A、B两组的体质量、BMI、WHR及B组患者的空腹INS和IRI较治疗前均升高(P＜0.05).治疗第8,12周末,B组的体质量、BMI、空腹INS和IRI的变化值高于A组(P＜0.05).B组体质量增加大于7%的比率(63%,12例)高于A组(17%,3例;P＜0.01).A、B两组的SAPS及SANS评分均显著低于治疗前(均P＜0.05),但组间差异均无统计学意义(P＞0.05).结论 二甲双胍能有效减轻奥氮平引起的体质量增加和糖代谢紊乱.     

金刚烷胺治疗奥氮平所致精神分裂症患者体质量增加的Meta分析

目的探讨金刚烷胺治疗奥氮平所致精神分裂症患者体质量增加的效果。方法计算机检索英文数据库(PubMed、PsycINFO、EMbase和Cochrane Library)和中文数据库(中国期刊全文数据库、万方数据库和中国生物医学文献数据库),纳入关于金刚烷胺治疗奥氮平所致精神分裂症患者体质量增加的随机对照研究(RCT),检索时限均从建库至2015年12月,手工检索相关的已发表文献。由两位研究者独立进行文献筛选、资料提取和方法学质量评价后,采用RevMan 5.3软件进行Meta分析。结果最终纳入3篇RCTs,共207例患者(干预组103例,对照组104例),观察时间8~16周。3篇RCTs均为双盲设计。Meta分析结果显示,干预结束时,干预组体质量减轻值优于对照组(WMD=-2.22,95%CI:-3.58~-0.86,P=0.001),干预组体质量下降7%的例数多于对照组(RR=2.74,95%CI:1.09~6.86,P=0.03);差异均有统计学意义。结论金刚烷胺在一定程度上能有效减轻奥氮平所致精神分裂症患者的体质量增加。受样本量及方法学质量的影响,可能会降低本研究结论的可靠性,需要更多高质量的RCTs来验证上述结论。     

奥氮平联用氟西汀治疗精神分裂症阴性症状的疗效及安全性meta分析

目的通过meta分析系统评价奥氮平联用氟西汀治疗精神分裂症患者阴性症状的疗效及其安全性。方法检索Pubmed、Medline、Web of science、EMBASE、Cochrane Library、CNKI、万方数据库在1990年1月至2017年5月公开发表的关于奥氮平联用氟西汀治疗精神分裂症的中英文文献,提取奥氮平联用氟西汀组与奥氮平组阴性症状、阳性症状及TESS量表副作用的数据,采用Review Manager 5.3软件进行文献质量评估,并按照Cochrane系统评价员学习手册进行meta分析。结果共纳入5项研究,其中中文3项,英文2项。Meta分析结果提示,奥氮平联用氟西汀治疗精神分裂症患者的阴性症状效果与单用奥氮平无统计学差异(标准化均数差(standradized mean difference,SMD)=-0.61,95%CI:-1.30~0.08,P=0.08)。因国内外研究患者纳入标准有差异,异质性较大(I2=83%),故对国内外研究进行亚组分析:仅国内研究显示奥氮平联用氟西汀治疗以阴性症状为主精神分裂症患者的阴性症状更具优势(SMD=-1.19,95%CI:-1.52~-0.86,P0.01),并且奥氮平联用氟西汀治疗所致体质量增加的风险低于单用奥氮平(SMD=0.28,95%CI:0.13~0.57,P0.01)。结论仅国内研究初步提示奥氮平联用氟西汀较单用奥氮平治疗以阴性症状为主精神分裂症患者的阴性症状疗效更佳,并且体质量增加的风险更低。     

氨磺必利替换奥氮平治疗对伴有代谢综合征精神分裂症患者的影响

目的:观察氨磺必利替换奥氮平治疗对伴有代谢综合征精神分裂症患者的影响。方法:92例奥氮平治疗伴代谢综合征的精神分裂症患者随机分为氨磺必利组(治疗组)及奥氮平组(对照组)各46例。治疗组在2周内将奥氮平换为氨磺必利,对照组维持奥氮平治疗,观察12周。入组时及第6、12周末测量腰围、血压、体质量指数(BMI)及空腹血糖(FBS)、高密度脂蛋白(HDL)、三酰甘油(TG)水平。应用阳性和阴性症状评定量表(PANSS)和治疗中出现的症状量表(TESS)进行疗效和安全性评定。结果:治疗12周末,治疗组腰围、收缩压、BMI、TG、FBS均显著低于对照组(P0.05或P0.01),两组PANSS评分差异无统计学意义(P0.05),而TESS评分治疗组低于对照组(P0.05)。结论:氨磺必利替换奥氮平治疗对精神分裂症患者体质量增加及代谢综合征有显著改善作用。     

奥氮平联合金刚烷胺治疗精神分裂症首次发病患者的随机双盲对照研究

目的:探讨金刚烷胺添加对奥氮平治疗精神分裂症首次发病患者疗效及脂代谢的影响。方法:采用随机双盲法,将61例精神分裂症首次发病的患者随机分为研究组(31例)和对照组(30例),在奥氮平治疗的基础上,研究组及对照组分别添加金刚烷胺200 mg/d及安慰剂;疗程8周。治疗前及治疗4、8周进行阳性和阴性症状量表(PANSS)及治疗过程中出现的症状量表(TESS)评定,测量体质量,检测血三酰甘油(TG)、低密度脂蛋白(LDL)、总胆固醇(TC)水平。结果:治疗后研究组PANSS阴性症状减分值显著大于对照组(P0.05);TESS评分两组间差异无统计学意义;两组体质量和TG增加值差异无统计学意义;对照组LDL、TC增加值显著大于研究组(P均0.05)。结论:添加小剂量金刚烷胺短期内可明显增加奥氮平对精神分裂症患者阴性症状的改善作用,减少血LDL和TC水平升高;但不能改善奥氮平所致的体质量增加。     

The association of weight gain with mood symptoms and functional outcomes following a first manic episode: prospective 12‐month data from the Systematic Treatment Optimization Program for Early Mania (STOP‐EM)

Bond DJ, Kunz M, Torres IJ, Lam RW, Yatham LN. The association of weight gain with mood symptoms and functional outcomes following a first manic episode: prospective 12‐month data from the Systematic Treatment Optimization Program for Early Mania (STOP‐EM). Bipolar Disord 2010: 12: 616–626. © 2010 The Authors. Journal compilation © 2010 John Wiley & Sons A/S. Objectives: Up to 75% of patients with bipolar I disorder (BD‐I) are overweight or obese. Obesity is associated with an increased liability for mood episodes in patients with established BD‐I, but data from early in the illness are lacking. Obesity in the general population is also consistently associated with functional impairment, but the relationship between weight gain and functional outcomes in BD‐I has received little attention. Methods: We measured rates of clinically significant weight gain (CSWG), defined as gaining ≥ 7% of baseline weight, over 12 months in 46 patients with BD‐I who recently recovered from their first manic episode. We compared patients with and without CSWG for (i) the amount of time spent with mood symptoms, assessed using standard clinical rating scales and National Institute of Mental Health Life Charts, and (ii) functioning at 12 months, measured using the Multidimensional Scale of Independent Functioning (MSIF). Results: A total of 41% of patients (n = 19) experienced CSWG by 12 months. We did not detect an association between CSWG and the number of days with mood symptoms. Patients with CSWG had significantly poorer 12‐month global functioning than those without CSWG [MSIF score = 2.26 (SD = 1.24) versus 1.74 (0.98); p = 0.011]. Functional impairment was independent of recent or current mood symptoms, which were entered as covariates in our analyses. Conclusions: Weight gain may be an overlooked, but potentially modifiable, cause of functional impairment in BD‐I. Clinicians should consider the possibility of weight gain when making the earliest treatment decisions in BD‐I.     

Attenuation of olanzapine-induced weight gain with reboxetine in patients with schizophrenia: a double-blind,placebo-controlled study

OBJECTIVE: Since increased norepinephrine availability may account for the weight-reducing effect of appetite suppressants, the authors hypothesized that the addition of the selective norepinephrine reuptake inhibitor reboxetine may prevent or attenuate olanzapine-induced weight gain. METHOD: Twenty-six patients hospitalized for first-episode DSM-IV schizophrenic disorder participated in the study. In addition to 6 weeks of treatment with olanzapine, 10 mg/day, patients were randomly allocated in a double-blind design to receive either reboxetine, 4 mg/day, (N=13) or placebo (N=13). RESULTS: Ten patients in each group completed the 6-week trial. Patients given olanzapine and reboxetine demonstrated a significantly lower increase in body weight (mean=2.5 kg, SD=2.7) than those given olanzapine and placebo (mean=5.5 kg, SD=3.1). Significantly fewer patients in the olanzapine/reboxetine group (N=2 of 10) than in the olanzapine/placebo group (N=7 of 10) gained at least 7% of their initial weight, the cutoff for clinically significant weight gain. The addition of reboxetine to olanzapine treatment was safe and well tolerated by the patients. A between-group difference in the reduction of Hamilton depression scale scores was seen that favored the olanzapine/reboxetine group (mean difference=-3.1, SD=1.25). CONCLUSIONS: The selective norepinephrine reuptake inhibitor reboxetine may reduce olanzapine-induced weight gain in schizophrenia patients, and activation of the adrenergic system may attenuate weight gain induced by atypical antipsychotic agents.     

Long-term olanzapine treatment: weight change and weight-related health factors in schizophrenia

BACKGROUND: Weight change and the weight-related health factors of nonfasting serum glucose, serum cholesterol, and diastolic blood pressure levels were analyzed in patients with DSM-III-R schizophrenia and related disorders who received treatment with olanzapine for up to 3 years, and comparisons were made to patients treated with haloperidol. Baseline body mass index (BBMI; kg/m2) and dose (mg/day) were investigated as predictors of long-term weight change experienced during olanzapine treatment. METHOD: This analysis retrospectively examined 573 patients receiving olanzapine and 103 patients receiving haloperidol for 39 weeks or more from a study of 1,996 patients randomly assigned 2:1 to either olanzapine, 5 to 20 mg/day, or haloperidol, 5 to 20 mg/day. After 6 weeks of acute therapy, patients continued for 1 year or more with either double-blind or open-label olanzapine therapy or double-blind haloperidol therapy. RESULTS: Mean weight gain for olanzapine-treated patients observed for a median of 2.54 years trended toward a plateau after the first 39 weeks of treatment with a last-observation-carried-forward mean weight change of 6.26 kg (13.8 lb) and a median of 5.90 kg (13.0 lb). This was significantly higher than that for haloperidol-treated patients, whose mean weight gain was 0.69 kg (1.5 lb) after 1.15 years (p < .001). Patients with higher BBMI (> 27.6) gained significantly less weight during treatment with olanzapine than their lighter counterparts (BBMI < 27.6) (p < .001). The effect of olanzapine dose on weight was not significant (p > or = . 183). Median serum glucose at endpoint was not significantly associated (p = .096) with weight change for olanzapine. Median serum cholesterol and diastolic blood pressure for olanzapine-treated patients at endpoint showed a relationship with weight change that was statistically (p < or = .001) but not clinically significant. The difference in incidence of elevated serum glucose, cholesterol, or diastolic blood pressure between olanzapine and haloperidol therapy groups was not different (p > .05). CONCLUSION: Mean weight gain during olanzapine treatment trended toward a plateau after the initial 39 weeks of treatment with no further significant gain out to 3 years. Higher BBMI was predictive of a lower long-term weight gain, while dose was not a significant predictor of greater longer term weight change. The relationship between weight change and glucose was not statistically significant. The association between weight change and changes in cholesterol as well as changes in diastolic blood pressure was statistically significant but not considered clinically relevant based on the ranges observed.     

Weight gain induced by haloperidol, risperidone and olanzapine after 1 year: findings of a randomized clinical trial in a drug-naïve population

BACKGROUND: There is little information about weight gain induced by antipsychotics at long-term. OBJECTIVE: To quantify the weight gain induced by first (haloperidol) and second generation antipsychotics (olanzapine and risperidone) in a cohort of drug-na?ve subjects after 1 year of treatment. METHODS: This is a prospective, randomized clinical trial, including a representative sample of first episode psychotic incident cases from a population area of 555.000 people. The main outcome measures were changes in body weight and body mass index at 3 months and at 12 months. Both a per protocol analysis and an intention to treat analysis were conducted. RESULTS: A total of 164 drug-na?ve patients were included. At 12 months 144 patients were evaluated. Of them, 66% completed the protocol and 34% needed treatment switch. We found statistically significant differences in weight gain at 3 months: 3.8 kg (+/-4.1) for haloperidol, 5.9 kg (+/-5.1) for risperidone and 8.4 kg (+/-5.0) for olanzapine (F=7.045; p=0.002). After 1 year the difference in weight gain had disappeared: 9.7 kg (+/-5.7) for haloperidol, 8.9 kg (+/-8.8) for risperidone and 10.9 kg (+/-7.2) for olanzapine (F=0.817; p=0.445). CONCLUSIONS: Drug-na?ve patients experience an extraordinary weight gain after 1 year of treatment with haloperidol, olanzapine or risperidone. The main difference among these treatments is the pattern of weight gain but not the final amount of weight gain.     

A Survey of Inhalant Use Disorders among Delinquent Youth: Prevalence, Clinical Features, and Latent Structure of DSM-IV Diagnostic Criteria

Background

This study focuses on exploring the relationship between changes in appetite or eating behaviors and subsequent weight change for adult patients with schizophrenia or bipolar disorder treated with olanzapine and adjunctive potential weight mitigating pharmacotherapy. The aim is not to compare different weight mitigating agents, but to evaluate patients' characteristics and changes in their eating behaviors during treatment. Identification of patient subgroups with different degrees of susceptibility to the effect of weight mitigating agents during olanzapine treatment may aid clinicians in treatment decisions.

Methods

Data were obtained from 3 randomized, double-blind, placebo-controlled, 16-week clinical trials. Included were 158 patients with schizophrenia or bipolar disorder and a body mass index (BMI) ≥ 25 kg/m² who had received olanzapine treatment in combination with nizatidine (n = 68), sibutramine (n = 42), or amantadine (n = 48). Individual patients were analyzed for categorical weight loss ≥ 2 kg and weight gain ≥ 1 kg. Variables that were evaluated as potential predictors of weight outcomes included baseline patient characteristics, factors of the Eating Inventory, individual items of the Eating Behavior Assessment, and the Visual Analog Scale.

Results

Predictors/correlates of weight loss ≥ 2 kg included: high baseline BMI, low baseline interest in food, and a decrease from baseline to endpoint in appetite, hunger, or cravings for carbohydrates. Reduced cognitive restraint, increase in hunger, and increased overeating were associated with a higher probability of weight gain ≥ 1 kg.

Conclusion

The association between weight gain and lack of cognitive restraint in the presence of increased appetite suggests potential benefit of psychoeducational counseling in conjunction with adjunctive pharmacotherapeutic agents in limiting weight gain during antipsychotic drug therapy.

Trial Registration

This analysis was not a clinical trial and did not involve any medical intervention.     

第二代抗精神分裂症药物对体重与代谢的影响

目的评价首发精神分裂症单一使用第二代抗精神病药物治疗对体重和代谢的影响。方法采用历史性队列研究方法评估62例首发精神分裂症单一使用抗精神病药物治疗2,4周末体重和代谢改变,并且对这些患者2年后的体重和代谢情况进行随访。结果62例患者随着治疗延长,体重迅速明显增加,平均体重从基线时的（55．5±15．6）kg,第2周末增加至（56．2±15．1）kg,第4周末进一步增加至（57．3±15．0）kg。第二代抗精神病药物对体重均有影响,其中奥氮平（增加5．24％）最为突出,利培酮（增加2．6％）、喹硫平（增加2．1％）次之。治疗第4周末,部分患者的糖脂代谢出现异常。在治疗2年后共随访到47例患者,其中27例继续治疗,20例因各种原因中断治疗,其中6例患者因为体重增加而停药。持续治疗的患者中,体重全部增加,半数体重增加10％～30％,1例患者体重增加50％。结论第二代抗精神病药物在首发精神分裂症急性期治疗会影响体重和糖脂代谢,进而影响患者的躯体健康和服药依从性。     

Weight gain associated with olanzapine and risperidone in adolescent patients: a comparative prospective study

OBJECTIVE: To evaluate weight gain associated with olanzapine, risperidone, and haloperidol treatment and its clinical risk factors in adolescent patients. METHOD: The study was conducted at three adolescent psychiatric departments in two mental health centers in the Tel Aviv area. All patients were Jewish Israelis. Weight and body mass index (BMI) of hospitalized adolescents treated with olanzapine (n = 21), risperidone (n = 21), or haloperidol (n = 8) were prospectively monitored on a weekly basis for the first 12 weeks of treatment. Various clinical risk factors were tested for association with weight gain. RESULTS: The olanzapine and risperidone groups experienced significant weight gain between baseline and endpoint (p < .01), whereas the average weight of the haloperidol group did not change. Average weight gain was significantly higher for the olanzapine group (7.2 +/- 6.3 kg, 11.1% +/- 7.8%) than for the risperidone (3.9 +/- 4.8 kg, 6.6% +/- 8.6%) and haloperidol (1.1 +/- 3.3 kg, 1.5% +/- 6.0%) groups. Extreme weight gain (>7%) was recorded in 19 patients (90.5%), 9 patients (42.9%), and 1 (12.5%) patient, respectively Gender (males), low concern about gaining weight (females), low baseline BMI, and paternal BMI were positively correlated with weight gain, whereas previous neuroleptic history, neuroleptic dosage, response to treatment, and illness duration were not. CONCLUSIONS: Olanzapine and risperidone are associated with extreme weight gain in adolescents, much higher than that reported in adults. This side effect should be taken into consideration before prescribing these medications, especially in patients at high risk.     

Long-term weight gain in patients treated with open-label olanzapine in combination with fluoxetine for major depressive disorder

OBJECTIVE: Patients with major depressive disorder (MDD) treated with olanzapine in combination with fluoxetine (OFC) demonstrate robust improvement in their depressive symptoms. Treatment with olanzapine may impact a patient's weight; thus, long-term weight gain and potential predictors (e.g., age and gender) and correlates (e.g., cholesterol and glucose levels) of weight gain were investigated in OFC-treated patients with MDD. METHOD: Outpatients who met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, diagnostic criteria for MDD were included (N = 549) in the current analyses of this 76-week, open-label study (February 2000 to July 2002). Maximum, endpoint, and potentially clinically significant (PCS; > or = 7% increase from baseline) weight gain; time to PCS weight gain; and predictors and correlates of weight change were assessed. Patients were treated once daily with oral olanzapine (6, 12, or 18 mg) plus fluoxetine (25, 50, or 75 mg) capsules. Statistical significance for all tests was based upon p < or = .05. RESULTS: Mean baseline-to-endpoint weight change was 5.6 +/- 6.6 kg (12.3 +/- 14.6 lb). Weight gain plateaued by 52 weeks. Fifty-six percent of patients met criteria for PCS weight gain by 76 weeks, and the median time to PCS weight gain was 16 weeks. Low baseline body mass index (BMI), female gender, younger age, and increased fluoxetine dose were predictors of weight gain; olanzapine dose was not. Patients with early (< or = 6 weeks) rapid PCS weight gain were 4.6 times more likely to gain substantial (> or = 15%) weight long-term (weeks 7-76). Changes to endpoint in total cholesterol and systolic blood pressure values were positively correlated with weight change. CONCLUSION: Long-term (76 weeks) OFC treatment may lead to a large percentage (56%) of patients meeting criteria for PCS weight gain (> or = 7%). The risk of weight gain may be significantly increased for OFC-treated patients who have a low BMI or who are female, younger, or taking high-dose fluoxetine. It is important that prescribers balance the risk of weight gain with the benefit of treatment for individual patients with depression.     

H(2) antagonist nizatidine may control olanzapine-associated weight gain in schizophrenic patients.

BACKGROUND: Olanzapine is temporally associated, in a number of patients with schizophrenia, with weight gain. H(2) antagonists, like nizatidine, have been shown to control appetite in overweight patients. METHODS: A patient with olanzapine temporally associated weight gain was treated with nizatidine as "add-on" therapy. RESULTS: Nizatidine treatment was associated with good control and subsequent reduction of weight after 4 to 5 weeks of therapy in a patient with repetitive episodes of weight gain during olanzapine treatment. Olanzapine was otherwise well tolerated and effective in controlling psychopathology. CONCLUSIONS: H(2) antagonist treatment with olanzapine may be a valid medical strategy in preventing and/or reducing weight gain in patients with schizophrenia. Controlled studies are recommended to confirm this observation.