Perry Benjamin Ian, McIntosh Gemma, Weich Scott, Singh Swaran, Rees Karen
Coventry and Warwickshire Partnership NHS Trust, Coventry, UK; Department of Mental Health and Wellbeing, University of Warwick, Coventry, UK.
University Hospitals Birmingham, Birmingham, UK.
Lancet Psychiatry. 2016 Nov;3(11):1049-1058. doi: 10.1016/S2215-0366(16)30262-0. Epub 2016 Oct 5.
Schizophrenia might share intrinsic inflammatory disease pathways with type 2 diabetes. We aimed to assess whether first-episode psychosis, which could be described as developing schizophrenia, is associated with prediabetic markers, or developing diabetes, to determine whether intrinsic disease links could cause the disorders to develop in unison. We hypothesised that biochemical measures of prediabetic states would be more common in antipsychotic naive patients with first-episode psychosis than in healthy matched controls.
For this systematic review and meta-analysis, using PRISMA criteria, we searched Embase, MEDLINE, PsycINFO, Web of Science, and Google Scholar for clinical studies published between database inception and Jan 6, 2016. We assessed case-control studies with biochemical assessment of prediabetic states in patients with first-episode psychosis alongside matched controls. We sought data at the summary estimate level. Several measurements were used to test for prediabetes, including fasting plasma glucose, insulin resistance (measured by the Homeostatic Model Assessment), and impaired glucose tolerance. We calculated standardised mean differences for each outcome. We used the inverse variance method, for which the weight given to each study was the inverse of the variance of the effect estimate. For dichotomous outcomes, we entered the number of events and number in each group into RevMan 5.3 and used the Mantel-Haenszel method to pool studies.
We identified 1436 studies, of which 12 were included in final analysis, including 1137 participants. Pooled analyses found first-episode psychosis to be related to insulin resistance (mean difference 0·30 [95% CI 0·18 to 0·42]), impaired glucose tolerance (mean difference 1·31 [0·37 to 2·25]), and the number of patients with impaired glucose tolerance (odds ratio 5·44 [2·63 to 11·27]), but not fasting plasma glucose (mean difference 0·03 mmol/L [-0·04 to 0·09]).
Our findings suggest a potential link between prediabetic markers, in particular impaired glucose tolerance and insulin resistance, and first-episode psychosis. However, we cannot establish causality, and the studies contributing to this review were at some risk of bias. Nevertheless, the findings might help to explain the increased prevalence of type 2 diabetes in patients with schizophrenia and could have implications for the management of patients with schizophrenia.
None.
精神分裂症可能与2型糖尿病共享内在炎症性疾病途径。我们旨在评估首次发作精神病（可描述为精神分裂症的发病过程）是否与糖尿病前期标志物或糖尿病的发生有关，以确定内在疾病联系是否会导致这些疾病同时发生。我们假设在首次发作精神病的未使用抗精神病药物的患者中，糖尿病前期状态的生化指标比健康匹配对照组更为常见。
对于这项系统评价和荟萃分析，我们使用PRISMA标准，在Embase、MEDLINE、PsycINFO、Web of Science和谷歌学术中检索了从数据库建立至2016年1月6日发表的临床研究。我们评估了对首次发作精神病患者以及匹配对照组进行糖尿病前期状态生化评估的病例对照研究。我们在汇总估计水平上寻求数据。使用了几种测量方法来检测糖尿病前期，包括空腹血糖、胰岛素抵抗（通过稳态模型评估测量）和糖耐量受损。我们计算了每个结局的标准化均数差。我们使用逆方差法，赋予每项研究的权重是效应估计值方差的倒数。对于二分结局，我们将每组的事件数和总数输入RevMan 5.3，并使用Mantel-Haenszel方法汇总研究。
我们识别出1436项研究，其中12项纳入最终分析，包括1137名参与者。汇总分析发现首次发作精神病与胰岛素抵抗（均数差0.30 [95%CI 0.18至0.42]）、糖耐量受损（均数差1.31 [0.37至2.25]）以及糖耐量受损患者数量（比值比5.44 [2.63至11.27]）有关，但与空腹血糖无关（均数差0.03 mmol/L [-0.04至0.09]）。
我们的研究结果表明糖尿病前期标志物，特别是糖耐量受损和胰岛素抵抗，与首次发作精神病之间存在潜在联系。然而，我们无法确定因果关系，且纳入本综述的研究存在一定偏倚风险。尽管如此，这些发现可能有助于解释精神分裂症患者中2型糖尿病患病率的增加，并可能对精神分裂症患者的管理产生影响。
无。
