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Piotr Boguta, Dariusz Juchnowicz, Paulina Wróbel-Knybel, Agnieszka Biała-Kędra and Hanna Karakuła-Juchnowicz

Abstract

Introduction: Warfarin has been considered as a “gold standard” in the prevention and treatment of thromboembolic events since 1954. Since the introduction of direct oral anticoagulants in the last few years (NOAC-Non-Vitamin K antagonist Oral Anticoagulants) prescriptions volume for apixaban, edoxaban, dabigatran and rivaroxaban have been gradually surpassing warfarin. The benefits include: anticoagulation from day one, fixed daily dosing, elimination for the need of international normalised ratio (INR) monitoring, fewer interactions with food and co-administered medicines with reduced risk of bleeding and better overall life quality.

Objectives: Assessing evidence for the safe use of Non-vitamin K Oral Anticoagulants (NOAC) with Selective Serotonin Reuptake Inhibitors (SSRI) and Serotonin and Noradrenaline Reuptake Inhibitors (SNRI).

Method: Review of literature published between 2014 and 2016 was made using the key words: Selective Serotonin Reuptake Inhibitor, Serotonin and Noradrenaline Reuptake Inhibitors, apixaban, dabigatran, edoxaban, rivaroxaban, bleeding, interaction, depression with time description from 2014 to 2018. Evidence within the literature was then compared with guidelines from the National Institute for Health and Care Excellence (UK), British National Formulary (UK), Clinical Excellence Commission (Australia), Thrombophilia and Anticoagulation Clinic (USA) and Summaries of Product Characteristics (SPC).

Results: 1. Serotonin plays a critical role in maintaining homeostasis. Use of SSRI/SNRI compromises its platelet reuptake increasing risk of bleeding.

2. Increased tolerability and safety of NOAC over Warfarin, although caution is advised when NOAC is used with SSRI/SNRI with less evidence suggesting pharmacodynamic interactions.

3. It is not recommended to use NOAC with strong CYP and P-gp inhibitors.

Conclusions: With limited literature evidence, caution is advised when co-prescribed NOACs with SSRI/SNRI, especially with other cofactors and interacting medicines further increasing risk of bleeding.

Open access

Jakub Siembida and Kaja Karakuła

Abstract

Introduction: Gamma-hydroxybutyric acid (GHB) is commonly known as a recreation drug or the so-called “date rape drug”. It is also used in medicine to treat narcolepsy and alcohol addiction. GHB has an affinity for two types of receptors: GABAB and the relatively recently discovered GHB receptors. GHB receptors were first cloned in 2003 in mice and then in 2007 in humans. So far, evidence has been presented for their impact on dopaminergic transmission, which may imply that they play a role in the pathogenesis of diseases such as schizophrenia. At the same time, it has been demonstrated that benzamide antipsychotic drugs have an affinity for GHB receptors, which is why it is postulated that some of the effects of these drugs may result precisely from this affinity.

Aim: The study presents the current state of knowledge about GHB receptors and their potential role in the pathogenesis of schizophrenia, and discusses drugs which show an affinity for this receptor.

Material and method: The literature review was based on a search of articles indexed between 1965 and 2018 in Medline, Google Scholar, ScienceDirect and Research Gate databases. The following search terms were used: GHB receptor, GHB, sulpiride, and amisulpride.

Result and discussion: 1. It is possible that GHB receptors are involved in the pathogenesis of schizophrenia, although more research is needed in this area.

2. Part of the effects of some benzamide antipsychotic drugs (such as amisulpride) may be due to their affinity for GHB receptors.

Open access

Karolina Mielko, Ewelina Soroka, Karolina Sprawka and Marcin Olajossy

Abstract

Introduction. The authors present an overview of current views on the treatment of obsessive-compulsive disorder refractory to pharmacological and psychological treatment.

Aim: To review the mechanisms of stimulation of deep brain structures and to evaluate the effectiveness of therapy in obsessive-compulsive disorder.

Method: Review and analysis of the Polish and foreign scientific articles from the years 1999-2016.

Conclusions: According to the literature considered, in half of the examined patients there was an improvement of over 35% on the Y-BOCS scale, in some patients even a reduction of symptoms reaching 81-83% was described. Previous studies have been carried out on small groups of patients. Since 2009, the method of invasive treatment with deep brain stimulation of the obsessive-compulsive syndrome is registered in the EU. In spite of the above, additional studies are necessary on a larger group of patients in order to precisely estimate the effectiveness of the procedure and elaborate the criteria for qualifying patients for inclusion in the procedure.

Open access

Karolina Dańko, Piotr Dańko, Ewelina Soroka, Véronique Petit and Marcin Olajossy

Abstract

The progress of medicine in the recent decades has strongly improved perinatal care, especially its somatic-related aspects. Pregnancy and childbirth have become much safer, but the mental strain and stress have remained the same. The models of motherhood and the number of children in a family have changed, giving rise to significant requirements concerning the quality of life of the offspring. These changes have brought about new psychological challenge for women and a team of psychiatrists and gynaecologists – obstetricians. The aim of this study is to look at the affective disorders affecting women during pregnancy and postpartum: the postpartum depression and so-called baby blues, which were both compiled in the form of a table in the final part of this work to illustrate the differences between these two mental disorders.

Open access

Nazli Khajehnasiri, Homayoun Khazali, Farzam Sheikhzadeh and Mahnaz Ghowsi

Abstract

Objective. The hypothalamic arcuate nucleus proopiomelanocortin (POMC) and neuropeptide Y (NPY) circuitries are involved in the inhibition and stimulation of the appetite, respectively. The aim of this study was to investigate the effects of one-month lasting high-intensity exercise on the POMC mRNA and NPY mRNA expression in the above-mentioned brain structure and appetite and food intake levels.

Methods. Fourteen male Wistar rats (250±50 g) were used and kept in the well-controlled conditions (22±2 °C, 50±5% humidity, and 12 h dark/light cycle) with food and water ad libitum. The rats were divided into two groups (n=7): 1) control group (C, these rats served as controls) and 2) exercised group (RIE, these rats performed a high-intensity exercise for one month (5 days per week) 40 min daily with speed 35 m/min. The total exercise time was 60 min. The body weight and food intake were recorded continuously during the experiments.

Results. The results showed relative mRNA expression of POMC and NPY estimated in the hypothalamic arcuate nucleus. There were no significant differences in the NPY and POMC mRNAs expression levels and food intake between C and RIE groups.

Conclusions. The present data indicate that one-month regular intensive exercise did not alter the levels of NPY and POMC mRNAs expression (as two important factors in the regulation of appetite) in the hypothalamic arcuate nucleus and food intake suggesting that this type of exercise itself is not an appropriate procedure for the body weight reduction.

Open access

Hisham El Falougy, Barbora Filova, Daniela Ostatnikova, Zuzana Bacova and Jan Bakos

Abstract

Current understanding of the neuroanatomical abnormalities in autism includes gross anatomical changes in several brain areas and microstructural alterations in neuronal cells as well. There are many controversies in the interpretation of the imaging data, evaluation of volume and size of particular brain areas, and their functional translation into a broad autism phenotype. Critical questions of neuronal pathology in autism include the concept of the reversible plasticity of morphological changes, volume alterations of brain areas, and both short- and long-term consequences of adverse events present during the brain development. At the cellular level, remodeling of the actin cytoskeleton is considered as one of the critical factors associated with the autism spectrum disorders. Alterations in the composition of the neuronal cytoskeleton, in particular abnormalities in the polymerization of actin filaments and their associated proteins underlie the functional consequences in behavior resulting in symptoms and clinical correlates of autism spectrum disorder. In the present review, a special attention is devoted to the role of oxytocin in experimental models of neurodevelopmental disorders manifesting alterations in neuronal morphology.

Open access

Camile Wunsch, Thais Fernanda Dornelles, Pricila Girardi, Marcelo Emilio Arndt, Julia Pasqualini Genro and Veronica Contini

Abstract

Objective. Genetic variants in the transcription factor 7-like 2 (TCF7L2) gene have been described as the most noteworthy ones regarding the type 2 diabetes mellitus (T2DM) liability. This work is aimed to evaluate the association between rs12255372 and rs7903146 polymorphisms and T2DM in patients with cardiovascular disease (CAD) risk.

Methods. A sample of six hundred and forty-seven patients that underwent the coronary angiography in a Cardiac Catheterization Lab was evaluated. The patients were investigated for the presence of T2DM and coronary stenosis. The TCF7L2 polymorphisms were genotyped by real-time PCR and the haplotype analysis was performed with the MLOCUS software. All genetic tests were carried out by considering the haplotype combinations in patients divided into three groups: 0 – carrying none disease risk allele, 1 – carrying one or two risk alleles and 2 – carrying three or four risk alleles.

Results. No significant associations between TCF7L2 risk haplotypes and the presence of T2DM or CAD were detected.

Conclusions. Our results indicate that the TCF7L2 rs12255372 and rs7903146 polymorphisms do not influence T2DM in Brazilian patients with the high risk for CAD. Therefore, we assume that these variants may only be relevant for a specific subgroup of T2DM patients or some particular human population.

Open access

Dmytro O. Minchenko, Dariia O. Tsymbal, Vadim V. Davydov and Oleksandr H. Minchenko

Abstract

Objective. The development of obesity and its metabolic complications is associated with dys-regulation of various intrinsic mechanisms, which control basic metabolic processes via changes in the expression of numerous regulatory genes. The main goal of this work was to study the association between the expression of insulin-like growth factors (IGF1 and IGF2) and IGF-binding proteins and insulin resistance in obese adolescents for evaluation of possible contribution of these genes in development of insulin resistance.

Methods. The expression of IGF1, IGF2, and IGFBPs mRNA was measured in blood of obese adolescents with normal insulin sensitivity and insulin resistance in comparison with the normal (control) individuals.

Results. In the blood of obese adolescents with normal insulin sensitivity the expression of IGFBP4, IGFBP5 and HTRA1 genes was down-regulated, but IGFBP2 and IGFBP7 genes up-regulated as compared to control (normal) group. At the same time, no significant changes in IGF1 and IGF2 gene expressions in this group of obese adolescents were found. Insulin resistance in obese adolescents led to up-regulation of IGF2, IGFBP2, and IGFBP7 gene expressions as well as to down-regulation of the expression of IGF1, IGFBP5 and HTRA1 genes in the blood in comparison with the obese patients, which have normal insulin sensitivity. Furthermore, the level of IGFBP4 gene expression was similar in both groups of obese adolescents.

Conclusions. Results of this investigation provide evidence that insulin resistance in obese adolescents is associated with gene specific changes in the expression of IGF1, IGF2, IGFBP2, IGFBP5, IGFBP7, and HTRA1 genes and these changes possibly contribute to the development of glucose intolerance and insulin resistance.

Open access

Hajar Oghbaei, Mohammad Reza Alipour, Gisou Mohaddes, Gholam Reza Hamidian and Rana Keyhanmanesh

Abstract

Objective. Diabetes induces sensory symptoms of neuropathy as positive (hyperalgesia), negative (hypoalgesia), or both.

Methods. In the present study, fifty male Wistar rats were allocated to five groups: control, control+nitrate, diabetes, diabetes+insulin, and diabetes+nitrate. Thirty days after diabetes confirmation, insulin (2–4 U/day) was injected subcutaneously in diabetes+insulin group and nitrate (100 mg/l) was added into drinking water of the control+nitrate and diabetes+nitrate groups for a period of 2 months. In order to assess the mechanical and thermal algesia, tail immersion, hot plate, and von Frey tests were performed. The serum insulin levels were determined with insulin ELISA Kit. Serum level of NOx was determined by the Griess method.

Results. Both thermal and mechanical nociceptive thresholds showed a significant decrease (p<0.05) which was followed by a significant increase (p<0.01) in the thermal nociceptive threshold in the diabetes group. Chronic nitrate or insulin treatment led to a significant decrease (p<0.01) in blood glucose levels, as well as a significant (p<0.05) increase in the body weight and serum NOx. Moreover, nitrate treatment significantly increased serum insulin levels (p<0.001) compared to the other groups.

Conclusion. Chronic nitrate treatment modified the thermal and mechanical sensitivities in diabetic animals.

Open access

Heba A. Abdel-Hamid, Mona M. I. Abdalla, Nagwa M. Zenhom and Rasha F. Ahmed

Abstract

Objective. The aim of the present study was to assess the effect of the PYY3–36, as a potential therapy for the type 2 diabetes mellitus (T2DM), induced by high fat diet (HFD) and an intraperitoneal (i.p.) administration of streptozotocin (STZ) in albino rats.

Methods. Forty adult male albino Wistar rats were divided into: 1) control group (C, in which the rats were fed with a standard diet and received vehicle; 2) diabetic group (D, in which T2DM was induced by feeding the rats with HFD for four weeks followed by a single i.p. injection of 35 mg/kg STZ, this group was also allowed to have HFD till the end of the study; and 3) D+PYY3–36 group (in which the diabetic rats were treated with 50 µg/kg i.p. PYY3–36 twice a day for one week). Food intake, water intake, body weight (b.w.), visceral fat weight (VFW), liver glycogen content, serum levels of glucose, insulin, and interleukin-6 (IL-6), were measured. Homeostatic-model assessment of insulin resistance (HOMA-IR) was estimated. The gene expression of the hypothalamic neuropeptide Y (NPY) and visceral nuclear factor kappa B (NF-κB) were assessed by a reverse transcription polymerase chain reaction (RT-PCR).

Results. The PYY3–36 administration to the diabetic group of rats significantly increased the serum insulin levels and liver glycogen content, decreased the body weight, VFW, food intake, water intake, serum levels of the glucose, IL-6, and HOMA-IR. It also decreased the expression of both the hypothalamic NPY and the visceral fat NF-κB.

Conclusion. With respect to the fact of improved insulin release and enhanced insulin sensitivity (an effect that may be mediated via suppressing accumulation of visceral fat and inflammatory markers), in the rats treated with PYY3–36, the PYY3–36 might be considered for the future as a promising therapeutic tool in T2DM.