Polymorphism A118G of opioid receptor mu 1 (OPRM1) is associated with emergence of suicidal ideation at antidepressant onset in a large naturalistic cohort of depressed outpatients.

Antidepressants have been the object of an international controversy for about thirty years. Some patients are inclined to develop suicidal ideation (SI) at antidepressant onset; this phenomenon is known as Treatment Emergent Suicidal Ideation (TESI), and it has conducted regulatory bodies to prompt warnings on antidepressants. Since, few studies have explored the pharmacogenomics of TESI. Given the growing body of evidence connecting the opioidergic system with suicidal behavior (particularly mu opioid receptor (MOR)), we decided to examine the relationship between two genetic polymorphisms (SNPs) in the opioidergic system and TESI in a sample of 3566 adult depressed outpatients. General practitioners and psychiatrists throughout France followed participants for 6 weeks after an initial prescription of tianeptine, an antidepressant treatment with mu agonism. Suicidal ideation was assessed with the item 10 of the Montgomery-Asberg Depression Rating Scale (item dedicated to SI) at baseline, and after 2 weeks, 4 weeks and 6 weeks. We analysed rs1799971 from the OPRM1 gene and rs105660 from the OPRK1 gene. Within the sample, 112 patients reported TESI while 384 did not. We found a significant association between AA genotype of rs1799971 and TESI even after adjustment for potential cofounders (OR = 1.93, 95% CI = [1.07; 3.49]; p-value = 0.03). On the other hand there were no significant association between rs1799971 and rs105560 with worsening of suicidal ideation or lifetime suicide attempts. Nevertheless, our results suggest a possible involvement of opioidergic system in TESI.

[Mental retardation as a risk factor to develop a psychotic disease]. / Retraso mental como factor de riesgo para el desarrollo de un trastorno psicótico.

INTRODUCTION: One of the main aims of research on schizophrenia has been to pinpoint the early symptoms and signals of the disease before its appearance. OBJECTIVES: We have examined the diagnoses previously given to patients before they were diagnosed of schizophrenia. METHOD: This is a case-control study in which we used a data register including the fields of minimum basic data set (MBDS) whose time period included 1999 to 2005. RESULTS: In our study, there was a 3.6% frequency of mental retardation and 2.1% one of behavioral and emotional disorders with onset usually occurring in childhood and adolescence, both diagnosed previously. The estimated odds ratio for a mentally retarded patient to suffer adult onset psychosis is 4.6 (95%CI [3.43-6.26]), schizophrenia 5.8 (95% CI [4.20-7.88]), paranoid schizophrenia 4.8 (95% CI [3.39 -6.93]), residual schizophrenia 7.0 (95% CI [4.81 -10.09]) and persistent delusional disorder 2.7 (95% CI [1.57 -4.73]). CONCLUSIONS: It can be concluded from our study that there is an increased frequency of mental retardation among the pathological records of subjects who will be diagnosed with paranoid schizophrenia and residual schizophrenia in the future. This fact supports the etiological thesis of schizophrenia involving neurodevelopment disorders.