Search

Patients with serious mental illness are a high-risk category of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Patients with schizophrenia are not participatory and have increased mortality and morbidity, patients with dementia cannot be cared for while depression, anxiety, bipolar tubing are associated with low immune status. Social stress is amplified by social isolation, amplifying depression and the mechanisms of decreased immunity. Hygiene measures and prophylactic behavior are impossible to put into practice in conditions of chronic mental illness. In coronavirus disease 2019 (COVID-19), the risk for severe development is associated with the presence of comorbidities and immune system deficiency. Prothrombotic status, cytokine storm and alveolar destruction are mechanisms that aggravate the evolution of patients, especially in the context in which they have dysfunction of the autonomic system. The activity of proinflammatory cytokines is accentuated by hyperglutamatergia, which potentiates oxidative stress and triggers the mechanisms of neural apoptosis by stimulating microglial activation. Activation of M1-type microglia has an important role in pathogenesis of major psychiatric disorders, such as major depression, schizophrenia or bipolar disorder, and may associate hippocampal atrophy and disconnection of cognitive structures. Memantine and Amantadine, N-methyl-D-aspartate (NMDA) glutamate receptor inhibitors, have demonstrated, through their pharmacological profile, psychotropic effects but also antiviral properties. In the conditions of the COVID-19 pandemic, based on these arguments, we suggest that they can be associated with the therapy with the basic psychotropics, Memantine or Amantadine, for the control of neuropsychiatric symptoms but also as adjuvants with antiviral action.

Holoprosencephaly (HPE) is a dramatic human brain malformation sequence with an extreme variable phenotypic spectrum and genetic heterogeneity, variable degree of severity and unknown etiology, in many cases. HPE is classified into syndromic, chromosomal, and non-syndromic, non-chromosomal. The most cases of HPE are syndromic. We present an atypical case of syndromic alobar HPE associated with digynic triploidy fetus, prenatally diagnosed, early at 18 weeks of gestation, by ultrasound (US) and complex genetic investigations. The US examination was performed with a specialized US machine, General Electric Voluson E10 OLED BT18, using two-dimensional (2D) scanning, three-dimensional (3D) image reconstruction, four-dimensional (4D) spatiotemporal image methodology and the highest power Doppler US technology. A detailed US examination of the fetus revealed several major abnormalities of the fetal head and severe facial malformations. Based on the antenatal US findings, the fetus was diagnosed with alobar HPE. After a careful examination and genetic counseling, additional cytogenetic investigations and molecular genetic analyses were performed, which revealed an abnormal number of 69 chromosomes, digynic triploidy (69,XXY). Two days later, the parents choose to interrupt the current gestation because of major fetal malformations. The pathological examination of the embryo reaffirmed the antenatal diagnostics.

Background: Type 2 diabetes mellitus (T2DM) is associated with increased mortality and morbidity, including cardiovascular diseases and obstructive sleep apnea (OSA). The aim of this study was to assess the associations between cardiovascular risk, chronic diabetes complications and the risk of OSA in adult patients with T2DM. Methods: The study included 529 patients with T2DM in whom moderate-to-severe OSA risk was assessed using the STOP-Bang questionnaire, dividing the subjects into two groups: group 1: STOP-Bang score

Objective. To identify qualitative and quantitative changes involving coagulation factors engaged in maternal and fetal complications, to determine the level of correlation between them, and to highlight the involvement of hereditary thrombophilia among pregnant women. Material and method. The article is based on 92 publications from 1995 to 2017, including a total of 49,127 thrombophilic patients, of whom 1272 were controls, with inclusion criteria as preeclampsia, intrauterine growth retardation, or early or late pregnancy loss. Results. 31 studies based on preeclampsia- demonstrate the involvement of G1691A factor V Leiden gene mutation, G20210A Prothrombin gene mutation and/or C677T and A1298C MTHFR gene mutation as the main factors in the development of this complication. 10 studies focuses on the intrauterine growth restriction place G20210A Factor V Leiden gene mutation, G20210A Prothrombin gene mutation, C677T and A1298C MTHFR gene mutation, protein C and protein S deficiency as the main factors involved. Another 32 studies cite the involvement of factor V Leiden mutation, Prothrombin mutation and MTHFR mutation in the development of early or late pregnancy losses. Conclusion. Based on 92 rigorously selected publications, we were able to demonstrate the relationship between medium/increased risk thrombophilia and pregnancy outcome, especially due to the presence of factor V Leiden gene mutation, Prothrombin gene mutation but also MTHFR gene mutation homozygous status.

Obiectiv. Identificarea modificărilor calitative şi cantitative ale mutaţiile factorilor de coagulare implicate în complicaţii materne şi fetale, determinarea nivelului de corelaţie dintre acestea şi gradul de implicare al trombofiliei ereditare în rândul femeilor însărcinate. Material şi metodă. Articolul se bazează pe 92 de publicaţii din 1995 până în 2017, incluzând 49.127 de paciente cu trombofilie, dintre care 1.272 au fost martori, având drept criterii de includere în studiu prezenţa preeclampsiei, retardul de creştere intrauterină sau pierderea timpurie sau tardivă a sarcinii. Rezultate. 31 studii bazate pe preeclampsie demonstrează implicarea mutaţiei genei G1691A factor V Leiden, a mutaţiei genei G20210A a protrombinei şi a mutaţiei genei C677T şi A1298C MTHFR ca factori principali în dezvoltarea acestei complicaţii. 10 studii se concentrează asupra gradului de restricţie de creştere intrauterine, iar mutaţia genei G20210A a factorului V Leiden, mutaţia genei G20210A a protrombinei, mutaţia genei C677T şi A1298C MTHFR, deficitul de proteina C şi proteină S fiind principalii factori implicaţi. Alte 32 de studii citează implicarea mutaţiei factorului V Leiden, a mutaţiei protrombinei şi a mutaţiei MTHFR în dezvoltarea pierderilor de sarcină precoce sau tardive. Concluzii. Pe baza a 92 de publicaţii riguros selectate, am putut demonstra relaţia dintre trombofilia cu risc mediu/crescut şi rezultatul sarcinii, în special din cauza prezenţei mutaţiei genei factor V Leiden, a mutaţiei genei protrombinei, dar şi a statusului homozigot al mutaţiei genei MTHFR.