Liver involvement in Coronavirus Disease 2019 (COVID-19) has been widely documented. However, data regarding liver-related prognosis are scarce and heterogeneous. The current study aims to evaluate the role of abnormal liver tests and incidental elevations of non-invasive fibrosis estimators on the prognosis of hospitalized COVID-19 patients. We conducted a retrospective cohort study to investigate the impact of elevated liver tests, non-invasive fibrosis estimators (the Fibrosis-4 (FIB-4), Forns, APRI scores, and aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio), and the presence of computed tomography (CT)-documented liver steatosis on mortality in patients with moderate and severe COVID-19, with no prior liver disease history. A total of 370 consecutive patients were included, of which 289 patients (72.9%) had abnormal liver biochemistry on admission. Non-survivors had significantly higher FIB-4, Forns, APRI scores, and a higher AST/ALT ratio. On multivariate analysis, severe FIB-4 (exceeding 3.25) and elevated AST were independently associated with mortality. Severe FIB-4 had an area under the receiver operating characteristic (AUROC) of 0.73 for predicting survival. The presence of steatosis was not associated with a worse outcome. Patients with abnormal liver biochemistry on arrival might be susceptible to a worse disease outcome. An FIB-4 score above the threshold of 3.25, suggestive of the presence of fibrosis, is associated with higher mortality in hospitalized COVID-19 patients.

A growing body of evidence points to links between internalizing symptoms and various executive functioning deficits, and especially to inhibition and set-shifting difficulties. However, there is limited developmental research regarding the impact of internalizing symptoms on the shifting function, particularly during middle childhood. The current study investigated attention shifting in a sample of 108 early school age children (7-11 years) using a task-switching paradigm which required participants to alternate between emotional and nonemotional judgments. Results indicated that higher levels of internalizing symptoms (anxiety and depression) had a detrimental effect on performance efficiency (measured by response times) but not on response accuracy. This effect was only observed on emotional (and not on nonemotional) repetition trials and did not affect switching trials; moreover, it was only present when feedback was presented to participants. The findings partially support the predictions of the Attentional Control Theory in a developmental sample and suggest that individual differences in internalizing symptoms play a role in children's ability to flexibly alternate between emotional judgments.

The celiac disease is an immune chronic condition with genetic transmission, caused by the intolerance to gluten. Gluten is a protein from cereals containing the following soluble proteins: gliadine, which is the most toxic, and the prolamins. The average prevalence is about 1% in USA and Europe, but high in Africa: 5.6% in West Sahara. In the pathogenesis several factors are involved: gluten as external trigger, genetic predisposition (HLA, MYO9B), viral infections, abnormal immune reaction to gluten. Severity is correlated with the number of intraepithelial lymphocytes, cryptic hyperplasia and villous atrophy, as well as with the length of intestinal involvement. The severity is assessed according to the Marsh–Oberhuber staging. Diagnostic criteria are: positive serological tests, intestinal biopsy, the reversal after gluten free diet (GFD). Beside refractory forms, new conditions have been described, like the non celiac gluten intolerance. In a time when more and more people adhere to GFD for nonscientific reasons, practitioners should be updated with the progress in celiac disease knowledge.

Background/Aim: The renin-angiotensinaldosterone system (RAAS) may be implicated in carotid atheromatosis (CA) development. We aimed to assess the relationship of M235T-angiotensinogen (AGT) and insertion/deletion of angiotensin conversion enzyme (I/D-ACE) genotypes with CA in patients with essential hypertension (EHT). Patients and Methods: We determined the M235T-AGT and I/D-ACE genotypes, using PCR-RFLP methods, in 162 hypertensive subjects from three tertiary regional medical centers. The relationship between the studied RAAS gene polymorphisms and CA was assessed by multiple logistic regressions. Results: Hypertensive patients carrying the MT/TT235-AGT and MT235-AGT genotypes had a 2.17-fold (p=0.033) and 2.24-fold (p=0.036) increased risk to develop CA, respectively. These genotypes, MT/TT 235-AGT (OR=2.17, p=0.033) and MT235-AGT (OR=2.24, p=0.036), remain independent risk factors for CA in hypertensive patients according to the multivariate model. Conclusion: There is a statistically significant association between M235T-AGT and CA, when adjusting for several confounders and controlling for hypertension. Essential hypertension (EHT) is associated with cardiovascular risk factors, such as carotid atheromatosis (CA), dyslipidemia, obesity, left ventricular hypertrophy (LVH), and presents a high risk for ischemic coronary and cerebrovascular events (1-4). According to the World Health Organization (WHO), ischemic cardiovascular diseases are responsible for 31% of all deaths worldwide. Stroke and myocardial infarction (MI) represent 80% of all deaths of ischemic vascular cause (5). CA and the increase in carotid intima-media thickness (cIMT) in the carotid-vertebral axis are manifestations of atherosclerotic disease and diagnostic markers for ischemic heart disease (IHD) and ischemic cerebrovascular disease (6, 7). The genetic polymorphisms of the renin-angiotensinaldosterone system (RAAS) are associated with uncontrolled EHT (8, 9). RAAS influences atherosclerosis (ATS) through oxidative stress, an increase in NADPH activity, reactive oxygen species production and low-density lipoprotein cholesterol (LDL-C) peroxidation (10, 11). The components of RAAS are angiotensinogen (AGT), angiotensin-converting enzyme (ACE), angiotensin I (AngI), angiotensin II (AngII), angiotensin II type 1 receptor (AngII R1) and angiotensin II type 2 receptor (AngII R2) (12). AGT is secreted by the liver and is converted to AngI upon the action of renin (REN). ACE converts AngI to AngII, This article is freely accessible online.

Hypertensive cardiac remodeling is illustrated by increased left ventricular (LV) mass index values and/or relative wall thickness (RWT) values >0.42, and functionally by isolated alteration of LV diastole (abnormal relaxation). The aim of the present study was to establish differentiated models of anatomical and functional adaptation to essential hypertension (EHT), in relation to the genetic variants of genes involved in the Renin-Angiotensin-Aldosterone System (RAAS). The M235T-AGT, I/D-ACE, A1166C-R1AngII, A3123C-R2AngII and G83A-REN genotypes were determined using PCR-Restriction Fragment Length Polymorphism in 139 hypertensive subjects. The relationship between the studied RAAS gene polymorphisms with morphological and functional cardiac remodeling was assessed by multiple logistic regression analysis. Patients carrying the C/C, A/C genotypes (A3123C-R2AngII polymorphism) had a 2.72-fold (P=0.033) increased risk of exhibiting an RWT value <0.42; in the multivariate model the risk was 4.02-fold higher (P=0.008). Analysis of LV diastolic dysfunction (LVDD) revealed that hypertensive patients carrying the T/T, M/T genotypes (M235T-AGT polymorphism) had a 2.24-fold (P=0.037) increased risk of developing LVDD and a 2.42-fold increased risk (P=0.039) after adjustment for confounders. Similarly, carriers of the G/G, A/G genotypes (G83A-REN) had a 2.32-fold (P=0.021) increased risk of developing LVDD, and this remained an independent risk factor based on the multivariate model (P=0.033). The results of the present study showed that no particular gene was associated with increased LV mass, but the A3123C-R2AngII polymorphism was associated with a non-concentric type of cardiac response in hypertensive patients. Conversely, the M235T-AGT and G83A-REN polymorphisms were found to be statistically significantly associated with LVDD when assessing abnormal relaxation.