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The aim of this study is to investigate possible associations between a set of single-nucleotide polymorphisms (SNPs) within 10 genes with Schizophrenia (SCZ) and response to antipsychotics in Korean in-patients treated with antipsychotics. Two hundred and twenty-one SCZ in-patients and 170 psychiatrically healthy controls were genotyped for 42 SNPs within ABCB1, ABCB4, TAP2, CLOCK, CPLX1, CPLX2, SYN2, NRG1, 5HTR1A and GPRIN2. Baseline and final clinical measures, including the Positive and Negative Symptoms Scale (PANSS), were recorded. Rs10042486 within 5HTR1A was associated with both SCZ and clinical improvement on PANSS total scores as well as on PANSS positive and PANSS negative scores. The haplotype analyses focusing on the four, three and two blocks' haplotypes within 5HTR1A confirmed such findings as well. We did not observe any significant association between the remaining genetic variants under investigation in this study and clinical outcomes. Our preliminary findings suggest that rs10042486 within 5HTR1A promoter region could be associated with SCZ and with clinical improvement on PANSS total, positive and negative scores in Korean patients with SCZ. However, taking into account the several limitations of our study, further research is needed to draw more definitive conclusions.

Background and Aims: Time of onset of antipsychotic action is still a debated matter. We aimed to replicate and extend previous findings that early response can predict subsequent non-response. Methods: 86 acutely psychotic patients treated with haloperidol were studied. Results: A PANSS reduction ≤16% at 1 week predicts non-response at 3 weeks of treatment (specificity 92%, sensitivity 82%). Conversely, a PANSS reduction ≥23% at 1 week of treatment predicts response at 3 weeks, with a specificity of 84% and a sensitivity of 86%. Conclusion: Our results confirm that an early response to antipsychotic treatment accurately predicts the treatment effectiveness and extends it to a prediction performed as early as 1 week.

ObjectiveThe present study aimed to explore whether 4 single nucleotide polymorphisms (SNPs) within the AHI1 gene could be associated with major depressive disorder (MD) and bipolar disorder (BD), and whether they could predict clinical outcomes in mood disorders.MethodsOne hundred and eighty-four (184) patients with MD, 170 patients with BD and 170 healthy controls were genotyped for 4 AHI1 SNPs (rs11154801, rs7750586, rs9647635 and rs9321501). Baseline and final clinical measures for MD patients were assessed through the Hamilton Rating Scale for Depression (HAM-D). Allelic and genotypic frequencies in MD and BD subjects were compared with those of each disorder and healthy group using the χ2 statistics. Repeated measures ANOVA was used to test possible influences of SNPs on treatment efficacy.ResultsThe rs9647635 A/A was more represented in subjects with BD as compared with MD and healthy subjects together. The rs9647635 A/A was also more presented in patients with MD than in healthy subjects. With regard to the allelic analysis, rs9647635 A allele was more represented in subjects with BD compared with healthy subjects, while it was not observed between patients with MD and healthy subjects.ConclusionOur findings provide potential evidence of an association between some variants of AHI1 and mood disorders susceptibility but not with clinical outcomes. However, we will need to do more adequately-powered and advanced association studies to draw any conclusion due to clear limitations.

A 71-year-old man developed coma with severe respiratory failure, hypotension, and tachycardia induced by the intentional ingestion of quetiapine fumarate extended release (XR) 20 g. At the time, he had been treated for bipolar depression with venlafaxine 75 mg/day, lamotrigine 100 mg/day, pregabalin 75 mg/day, and quetiapine XR 400 mg/day for approximately 1 year. Comorbidities were hypertension treated with metoprolol, diabetes mellitus type 2 treated with metformin, and benign prostatic hyperplasia treated with silodosin. In the emergency room, about 4 h after ingestion of quetiapine fumarate XR, the presenting symptomatology was characterized by coma (Glasgow Coma Scale score 3), hypotension (blood pressure [BP] 90/60 mmHg), tachycardia (electrocardiogram [ECG] showed sinus tachycardia with heart rate 120 beats per minute and a QTc of 499 ms). A gastric lavage was performed and activated charcoal 50 g and magnesium sulfate 30 g was administered. About 6 h after ingestion, he developed marked desaturation and underwent mechanical ventilation; 13 h after ingestion, a severe hypotensive episode followed (BP 70/40), which was treated with an infusion of ringer lactate 500 cc. On the 3rd day after intentional overdose, an episode of agitation occurred; 4 days after ingestion, the quetiapine plasma level was found to be 42 ng/ml (within therapeutic range). At 5 days after ingestion, the patient developed septicemia caused by staphylococci (probably originating from the central vein catheter), which was treated with antibiotic therapy. On days 10 and 18 after the suicide attempt, two episodes of paroxysmal supraventricular tachycardia (PSVT) occurred and were successfully treated with intravenous adenosine triphosphate. The patient recovered completely without residual symptoms. In line with literature data, in this case report, symptoms of quetiapine overdose were tachycardia, agitation, hypotension, QT interval prolongation, and coma. A causal relationship between PSVT and quetiapine intoxication seems quite unlikely due to the drug level.