Background High level of comorbidity between bipolar disorder or schizophrenia and cardiovascular diseases (CVD) in clinical practice may contribute to drug-drug interactions between medications used in these conditions. The aim of this study was to evaluate harmful interactions between antipsychotics and medications used in treatment of CVD. Methods The analysis of 52 cases of adverse reactions with a clinical picture indicates that they were the result of the combination of antipsychotic with cardiovascular medications. Results The highest number of interactions with antipsychotics was recorded among beta-blockers (n = 13, 25% of all cases), including cardiac arrhythmias [atrial fibrillation (n = 1): risperidone plus atenolol; bradycardia (n = 1): perphenazine with metoprolol; ventricular arrhythmias: sertindole with metoprolol (n = 1) and ziprasidone with sotalol (n = 3)] and hypotension [chlorprotixene with nebivolol or metoprolol (n = 2)]. 12 cases concerned statins-myalgia, myopathy, or creatine kinase elevation appeared after combination of atorvastatin with haloperidol (n = 1), quetiapine (n = 3) or risperidone (n = 1), and simvastatin with quetiapine (n = 5) or risperidone (n = 2). There were also cases of interactions observed for the use of antipsychotics with anti-arrhythmic drugs (amiodarone, flecainide, propafenone) (n = 11), calcium channel blockers (n = 6), and other cardiac medications: clonidine, dabigatran, doxazosin, ivabradine, and losartan (n = 10). Conclusions Due to a high risk of interactions and related adverse effects, particular attention should be paid while using cardiovascular medications with antipsychotics. Clinical decisions should be preceded by a detailed analysis of safety, riskbenefit ratio to search for, as safe as possible, drug combinations.
Cel pracyOcena występowania niekorzystnych interakcji leków przeciwdepresyjnych (LPD) z lekami stosowanymi w chorobach układu krążenia (leki krążeniowe - LK)MetodaAnaliza 66 przypadków wystąpienia objawów niepożądanych, o obrazie klinicznym wskazującym w stopniu prawdopodobnym lub pewnym, że były one skutkiem połączenia LPD z LKWynikiNajczęstszym niepożądanym efektem (n=25 – tj. 37.9%) było wystąpienie bradykardii (i innych działań niepożądanych betablokerów) w następstwie dołączenia metoprololu lub propranololu do leku z grupy SSRI lub bupropionu. W jednym przypadku połączenie fluoksetyny z propranololem skutkowało zatrzymaniem krążenia. Zanotowano 8 przypadków nasilenia działań niepożądanych amlodypiny (obrzęki kończyn dolnych, bóle głowy) po połączeniu z: fluoksetyną, sertraliną lub paroksetyną, oraz wystąpienie mialgii, elewacji aminotransferaz, wielomoczu i hipotensji w połaczeniu lerkarnidypiny niektórymi SSRI. Stwierdzono też m.in: pogorszenie tolerancji propafenonu o połączeniu z wenlafaksyną lub bupropionem, 2 przypadki granulopenii związane z kombinacją duloksetyna -propafenon, 2 przypadki powikłań krwotocznych związanych z kombinacją wortioksetyna- warfaryna, 1 przypadek hiponatremii związany z połączeniem wortioksetyny i chydrochlorotiazydu, a także antagonizowanie dziłania hipotensyjnego klonidyny przez mirtazapinę i zakrzepicę obwodową w następstwie połączenia warfaryny z trazodonem.WnioskiZe względu na wysokie ryzyko interakcji i związanych z nimi efektów niepożądanych, zwłaszcza u pacjentów w starszym wieku, każda decyzja dotycząca połączenia określonego LPD i LK powinna być poprzedzona szczegółową analizą bezpieczeństwa oraz bilansu korzyści i ryzyka a także powinna wiązać się z poszukiwaniem najbardziej bezpiecznych, alternatywnych kombinacji ww leków.
These are the preliminary results of a 12-week non-randomized, open-label, non-inferiority study comparing the effectiveness of trazodone in an extended-release formulation (XR) versus SSRIs in the treatment of major depressive disorder (MDD). Participants (n = 76) were recruited, and 42 were assigned to the trazodone XR group and 34 to the SSRIs group. The choice of drug was based on clinical presentation and relied upon the attending physician. Assessments were made at five observation time points, at the following weeks: 0, and after 2, 4, 8, and 12 weeks. The evaluations included: symptoms of depression (MADRS, QIDS-clinician, and self-rated versions-primary study endpoints), anhedonia (SHAPS), anxiety (HAM-A), insomnia (AIS), psychosocial functioning (SDS), and therapeutic efficacy (CGI). At baseline, the trazodone group had significantly more severe depressive, anxiety, and insomnia symptoms and worse psychosocial functioning compared to the SSRIs group. After 12 weeks, trazodone XR was more effective than SSRIs in reducing the severity of insomnia and depression. There were no differences between the groups in the frequencies of therapeutic response and remission, which indicated the non-inferiority of the trazodone XR treatment. In conclusion, our results showed that in a “real world” setting, trazodone XR is effective in the treatment of patients with MDD.
Lurasidone is an atypical antipsychotic approved for the treatment of schizophrenia and bipolar depression. It seems to have a favorable metabolic profile and low risk of causing adverse interactions. Here we present a case of a 25-year old female patient with treatment-resistant ultra-rapid cycling bipolar disorder, obesity, hypothyroidism, and epilepsy. Because of predominant depressive symptoms, occasional occurrence of brief psychotic symptoms and patient's somatic comorbidities, treatment with lurasidone was initiated. Clinical improvement was observed 3 weeks and cessation of ultra-rapid cycling course of the disease 8 weeks after the beginning of lurasidone treatment. The patient's level of functioning improved and body mass significantly decreased, with good tolerance of the pharmacotherapy. Lurasidone seems to be a promising treatment option in patients with treatment-resistant rapid cycling bipolar disorder.
What is new?Fibromyalgia (FM) patients are heterogenous in metabolic status. Contrary to the previously published data our study shows that only a subgroup of FM patients is characterized by insulin resistance. FM patients who are responsive to SNRI (serotonin and noradrenalin reuptake inhibitors) treatment have similar levels of fasting glucose, insulin, insulin resistance, BMI compared to healthy controls. However, FM patients who are not responsive to treatment with SNRI are characterized by higher fasting glucose, fasting insulin, insulin resistance, BMI compared to healthy controls and to FM patients responsive to SNRI. FM patients who are not responsive to treatment with SNRI present higher prevalence of depression, anxiety and personality disorders than those responsive to SNRI. Insulin resistance, depression, anxiety and personality disorders are predictors of the lack of response to treatment with SNRI in fibromyalgia.
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