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      Influence of the use of atypical antipsychotics in metabolic syndrome Translated title: Apoyo social percibido, resiliencia y consumo de sustancias psicoactivas en internas en establecimientos penitenciarios

      review-article
      Revista Española de Sanidad Penitenciaria
      Sociedad Española de Sanidad Penitenciaria
      metabolic syndrome, antipsychotics, schizophrenia, bipolar disorder, prolactin, prisons, prisiones, mujeres, bebidas alcohólicas, drogas ilícitas, apoyo social

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          ABSTRACT

          Objectives

          To describe the possible relationship between the use of antipsychotic drugs and the presence of metabolic syndrome. Other objectives are to list the main side effects of antipsychotic treatment, and to determine if there is any pharmacological treatment that can contribute towards counteracting metabolic syndrome.

          Material and method

          A narrative bibliographic review was carried out of the following databases: PubMed, Cochrane, CINAHL, IBECS, LILACS and HealthCare. Preference in the selection process was given to clinical trials and systematic review articles or review articles and some articles that were considered relevant because of their content. The time period was limited to between January 2014 and November 2019. The languages were English and Spanish. Repeated articles and those that were not related to the objectives were rejected. The search criteria were: “antipsychotic AND metabolic syndrome”; “schizophrenia AND metabolic syndrome”; “bipolar disorder AND metabolic syndrome”; “metabolic syndrome AND suicide NOT disorder”; “metabolic syndrome AND prisons”; “metabolic syndrome AND prolactin”.

          Results

          24 articles were selected out of the 510 that were consulted. The relationship between atypical antipsychotics and metabolic syndrome was evident. Other anticholinergic, antidopaminergic effects, extrapyramidal syndromes, neuroleptic malignant syndrome, hypotension, arrhythmias, sedation, hypovitaminosis D, increased prolactin, sexual dysfunction, sleep disturbances, etc. are also highlighted. Pharmacological associations with other drugs were also found.

          Discussion

          There is a relationship between the use of atypical antipsychotics and weight gain, lipid disorders, glucose and high blood pressure. There are some associated drugs that decrease some symptoms (ranitidine, topiramate, metformin, melatonin, modafinil). Patients taking this type of medication should be monitored and encouraged to lead healthy lifestyles.

          RESUMEN

          Objetivos

          Determinar la influencia del apoyo social percibido y la resiliencia en el consumo de alcohol y otras drogas en mujeres privadas de libertad.

          Material y método

          Estudio transversal con 174 internas en dos establecimientos penitenciarios de la Región de Murcia. Se utilizó un cuestionario autosuministrado incluyendo variables sociodemográficas, penitenciarias, consumo de alcohol y otras drogas, apoyo social percibido y resiliencia.

          Resultados

          El 28,2% de las internas consumió al menos una de las sustancias analizadas (alcohol, cannabis, cocaína, heroína y/o tranquilizantes sin receta médica) en prisión. Las internas consumidoras mostraban significativamente menor nivel de apoyo social percibido y de resiliencia, respecto a aquellas que no consumían en prisión.

          Discusión

          Los resultados reflejan cómo el apoyo social percibido y la resiliencia son factores de protección ante el consumo en prisión, pudiendo ser incorporados estos en futuros programas de prevención de consumo de alcohol y otras drogas durante la pena privativa de libertad.

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          Most cited references28

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Antipsychotics, Metabolic Adverse Effects, and Cognitive Function in Schizophrenia

            Cognitive impairment is a core symptom domain of schizophrenia. The effect of antipsychotics, the cornerstone of treatment in schizophrenia, on this domain is not fully clear. There is some evidence suggesting that antipsychotics may partially improve cognitive function, and that this improvement may vary depending on the specific cognitive domain. However, this research is confounded by various factors, such as age, duration/stage of illness, medication adherence, and extrapyramidal side effects that complicate the relationship between antipsychotics and cognitive improvement. Furthermore, antipsychotics—particularly the second generation, or “atypical” antipsychotics—can induce serious metabolic side effects, such as obesity, dyslipidemia and type 2 diabetes, illnesses which themselves have been linked to impairments in cognition. Thus, the inter-relationships between cognition and metabolic side effects are complex, and this review aims to examine them in the context of schizophrenia and antipsychotic treatment. The review also speculates on potential mechanisms underlying cognitive functioning and metabolic risk in schizophrenia. We conclude that the available literature examining the inter-section of antipsychotics, cognition, and metabolic effects in schizophrenia is sparse, but suggests a relationship between metabolic comorbidity and worse cognitive function in patients with schizophrenia. Further research is required to determine if there is a causal connection between the well-recognized metabolic adverse effects of antipsychotics and cognitive deficits over the course of the illness of schizophrenia, as well as, to determine underlying mechanisms. In addition, findings from this review highlight the importance of monitoring metabolic disturbances in parallel with cognition, as well as, the importance of interventions to minimize metabolic abnormalities for both physical and cognitive health.
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              Metformin for Clozapine Associated Obesity: A Systematic Review and Meta-Analysis

              Background Although clozapine is the gold-standard for treatment refractory schizophrenia, it has the worst metabolic profile of all antipsychotics. This is partly mediated by clozapine’s impact on glucagon-like peptide (GLP-1). There is an absence of robust evidence for effective treatments for clozapine associated weight gain and metabolic syndrome. Metformin, with its role in increasing GLP-1 may aid weight loss among people on clozapine. Methods We conducted a systematic-review and meta-analysis of metformin versus placebo for change in weight and metabolic syndrome for people on clozapine without diabetes mellitus. We searched the Cochrane Schizophrenia Group’s trial register, Pubmed and Embase, as well as the following Chinese databases: the Chinese Biomedical Literature Service System and China Knowledge Resource Integrated Database. This was supplemented by hand searches of key papers. Results Eight studies, of which three were from Chinese databases, with 478 participants were included. We found that metformin was superior to placebo in terms of weight loss (-3.12kg, 95%CI -4.88kg to -1.37kg) and BMI (-1.18kg/m2, 95%CI -1.76kg/m2 to -0.61kg/m2). Metformin significantly improved three of the five components of metabolic syndrome; waist circumference, fasting glucose and triglycerides. Sensitivity analysis on study quality and duration did not greatly impact results. Conclusions Metformin led to clinically meaningful weight loss among people on clozapine, and may reduce the rates of metabolic syndrome. Inclusion of metformin into the treatment protocols of people on clozapine, as tolerated, should be considered. Trial Registration PROSPERO registration number: CRD42015029723
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                Author and article information

                Journal
                Rev Esp Sanid Penit
                Rev Esp Sanid Penit
                sanipe
                Revista Española de Sanidad Penitenciaria
                Sociedad Española de Sanidad Penitenciaria
                1575-0620
                2013-6463
                May-Aug 2020
                10 July 2020
                : 22
                : 2
                : 80-86
                Affiliations
                [1] originalUniversitat Jaume I. Castelló de la Plana. Castelló. orgnameUniversitat Jaume I Castelló de la Plana. Castelló,
                Author notes
                Correspondence: Patricia Doménech-Matamoros. E-mail: al377102@ 123456uji.es
                Article
                10.18176/resp.00014
                7537359
                32697278
                6797df47-0254-4c24-90a5-6d7c977a0cad

                This is an open-access article distributed under the terms of the Creative Commons Attribution License

                History
                : 17 March 2020
                : 17 April 2020
                Page count
                Figures: 1, Tables: 2, Equations: 0, References: 30, Pages: 07
                Categories
                Review

                metabolic syndrome,antipsychotics,schizophrenia,bipolar disorder,prolactin,prisons,prisiones,mujeres,bebidas alcohólicas,drogas ilícitas,apoyo social

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