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接受高剂量抗精神病药物治疗并进行精神康复的重症精神疾病患者的代谢综合征

Metabolic syndrome in patients with severe mental illness undergoing psychiatric rehabilitation receiving high dose antipsychotic medication.

作者信息

Ravindranath Bapu V

机构信息

Consultant Psychiatrist, Rathbone Low Secure Unit, Liverpool, UK.

出版信息

Indian J Psychol Med. 2012 Jul;34(3):247-54. doi: 10.4103/0253-7176.106021.

DOI:10.4103/0253-7176.106021
PMID:23439746
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3573576/
Abstract

BACKGROUND

To review evidence of chronic antipsychotic medication and the association with metabolic syndrome in mentally ill patients. This evidence was used to analyse a cohort of patients with severe mental illness and to deduce a correlation between the prevalence of metabolic syndrome and their dose regimens.

MATERIALS AND METHODS

Twenty-four male patients undergoing Psychiatric rehabilitation underwent a review of current medication and assessment of risk factors for metabolic syndrome. Assessment criteria was based upon National Cholesterol Education Programme expert panel on detection, evaluation and treatment of high blood cholesterol in adults (Adult Treatment Panel III) (NCEP ATP III) criteria, incorporating waist circumference, raised triglycerides, reduced high density lipoprotein, raised blood pressure and fasting blood glucose. PubMed, Nature and Science Direct databases have been used to compile the medical and scientific background on metabolic syndrome and antipsychotic medication and the effect on patients particularly on high dose.

RESULTS

Out of 24 patients, 10 patients (41.7%) were receiving high dose antipsychotics (HDA) and four were on maximum dosage limits of 100%. 8.3% (2/24) patients were receiving only one first generation antipsychotics (FGA), 37.5% (9/24) patients were receiving only one second generation antipsychotic (SGA), 45.8% patients (11/24) were receiving two or more SGA only, and only one patient was receiving two or more FGA. One patient was receiving a combination of FGA and SGA. PRN ("as needed") therapy was not included in this study as their usage was limited. Clozapine was mostly prescribed in these patients (10/24, 41.6%). Four out of the 24 patients refused blood tests therefore were excluded from the following results. In the patients evaluated, 55% (11/20) had confirmed metabolic syndrome. In these patients with metabolic syndrome, 45.4% (5/11) were on HDA and 27.3% (3/11) were on maximum British National Formulary (BNF) limits of 100% of dosage. Four out of the nine remaining patients not diagnosed with metabolic syndrome were on HDA.

CONCLUSIONS

Evidence supports the association between antipsychotic medication and metabolic syndrome. The data extrapolated from this cohort of mentally ill patients demonstrates that there is an increase in risk factors for metabolic syndrome and weight gain in the majority of patients on antipsychotic medication. The data however does not support any further predisposition to metabolic syndrome in these patients taking HDA. It also cannot be assumed antipsychotic medication is independently associated with the prevalence of these abnormalities.

摘要

背景

回顾慢性抗精神病药物治疗的证据以及与精神病患者代谢综合征的关联。该证据用于分析一组重症精神病患者,并推断代谢综合征患病率与其剂量方案之间的相关性。

材料与方法

24名接受精神康复治疗的男性患者接受了当前用药情况复查及代谢综合征危险因素评估。评估标准基于美国国家胆固醇教育计划成人高血胆固醇检测、评估和治疗专家小组(成人治疗小组III)(NCEP ATP III)标准,包括腰围、甘油三酯升高、高密度脂蛋白降低、血压升高和空腹血糖。已使用PubMed、《自然》和《科学直通车》数据库来汇编关于代谢综合征和抗精神病药物的医学和科学背景以及对患者的影响,尤其是高剂量时的影响。

结果

24名患者中,10名患者(41.7%)接受高剂量抗精神病药物(HDA)治疗,4名患者的剂量达到了100%的最大剂量限制。8.3%(2/24)的患者仅接受一种第一代抗精神病药物(FGA)治疗,37.5%(9/24)的患者仅接受一种第二代抗精神病药物(SGA)治疗,45.8%(11/24)的患者仅接受两种或更多种SGA治疗,只有1名患者接受两种或更多种FGA治疗。1名患者接受FGA和SGA联合治疗。本研究未纳入按需(PRN)治疗,因为其使用有限。氯氮平在这些患者中最常被处方(10/24,41.6%)。24名患者中有4名拒绝进行血液检测,因此被排除在以下结果之外。在接受评估的患者中,55%(11/20)确诊患有代谢综合征。在这些患有代谢综合征的患者中,45.分4%(5/11)接受HDA治疗,27.3%(3/11)的剂量达到英国国家处方集(BNF)100%的最大剂量限制。其余9名未被诊断为代谢综合征的患者中有4名接受HDA治疗。

结论

有证据支持抗精神病药物与代谢综合征之间的关联。从这组精神病患者中推断出的数据表明,大多数服用抗精神病药物的患者代谢综合征危险因素增加且体重增加然而,数据并不支持服用HDA的这些患者更容易患代谢综合征。也不能假定抗精神病药物与这些异常情况的患病率独立相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/e1ef41ccb32d/IJPsyM-34-247-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/79b7e80f8a3b/IJPsyM-34-247-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/5e2eb17fce64/IJPsyM-34-247-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/00ad6c9b58e2/IJPsyM-34-247-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/e1ef41ccb32d/IJPsyM-34-247-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/79b7e80f8a3b/IJPsyM-34-247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/4be65897e9b1/IJPsyM-34-247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/88cb7b49404e/IJPsyM-34-247-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/5e2eb17fce64/IJPsyM-34-247-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c2/3573576/e1ef41ccb32d/IJPsyM-34-247-g008.jpg

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