Brugada Syndrome and Right Ventricle Morphofunctional Abnormalities on Echocardiography in Young Male with Family Anamnesis of Sudden Cardiac Death

First presented by Brugada and Brugada in 1992, Brugada Syndrome (BrS) is a primary electrical disease of the heart that causes sudden cardiac death or life-threatening ventricular arrhythmias. This disease is hereditary autosomic dominant transmitted and genetically determined. The syndrome has been linked to mutations in SCN5A, the gene encoding for the α-subunit of the sodium channel. Electrocardiogram (ECG) abnormalities indicating Brugada syndrome, include repolarization and depolarization abnormalities in the absence of identifiable structural cardiac abnormalities or other conditions or agents known to lead to ST-segment elevation in the right precordial leads (V1-V3). Intravenous administration of sodium channel blocking drugs may modify the ECG pattern. Ajmaline, flecainide, procainamide and propafenone exaggerate the ST-segment elevation or unmask it when it is initially absent. An implantable cardioverter-defibrillator (ICD) is the only proven effective device treatment for the disease. Although BrS is primary electrical disease, some authors have suggested the presence of morphological and functional abnormalities mainly located in the right ventricle (RV), notably in the outflow tract (RVOT). In this short report we will present a young male, with predisposition and positive family history of sudden cardiac death, with complete diagnostic procedure including propafenon testing unmasking Brugada syndrome. An echosonography revealed dilated apical right ventricle, suggesting BrS is not only electrical disorder, but may include morphofunctional abnormalities, described in previous reports. In addition, we reviewed the possible connection between Brugada syndrome and morphological abnormalities in RV

Hypothyroidism and Nonalcoholic Fatty Liver Disease: Pathophysiological Associations and Therapeutic Implications

Nonalcoholic fatty liver disease (NAFLD) is a complex clinical entity which can be secondary to many other diseases including hypothyroidism, characterized by lowering of thyroid hormones and increased thyroid stimulating hormone (TSH). A lot of emerging data published recently advocates the hypothesis that hypothyroid induced NAFLD could be a separate clinical entity, even suggesting possible treatment options for NAFLD involving substitution therapy for hypothyroidism along with lifestyle modifications. In addition, a whole new field of research is focused on thyromimetics in NAFLD/NASH treatment, currently in phase 3 clinical trials. In this critical review we summarized epidemiological and pathophysiological evidence linking these two clinical entities and described specific treatment options with the accent on promising new agents in NAFLD treatment, specifically thyroid hormone receptor (THR) agonist and its metabolites

Visualizing levels of osteoblast differentiation by a two-color promoter-GFP strategy: Type I collagen-GFPcyan and osteocalcin-GFPtpz

A 3.9 kb DNA fragment of human osteocalcin promoter and 3.6 kb DNA fragment of the rat collagen type1a1 promoter linked with visually distinguishable GFP isomers, topaz and cyan, were used for multiplex analysis of osteoblast lineage progression. Three patterns of dual transgene, expression can be appreciated in primary bone cell cultures derived from the transgenic mice and by histology of their corresponding bones. Our data support the interpretation that strong pOBCol3.6GFPcyan alone is found in newly formed osteoblasts, while strong pOBCol3.6GFPcyan and hOC-GFPtpz are present in osteoblasts actively making a new matrix. Osteoblasts expressing strong hOC-GFPtpz and weak pOBCol3.6GF-Pcyan are also present and may or may not be producing mineralized matrix. This multiplex approach reveals the heterogeneity within the mature osteoblast population that cannot be appreciated by current histological methods. It should be useful to identify and isolate populations of cells within an osteoblast lineage as they progress through stages of differentiation

Are We Compensating for the Lack of Physical Activity in Our Diabetic Patients with Treatment Intensification?

Background: We studied the association between leisure time physical activity (LTPA) and glycemic control, body mass index (BMI), and hypoglycemic incidents in type 1 (T1DM) and type 2 diabetes patients (T2DM). Methods: This is a cross-sectional study of 198 diabetic patients (60 with type 1 diabetes, 138 with type 2 diabetes). LTPA was assessed by a validated 12-month questionnaire. Patients were grouped as sedentary and moderately to vigorously active. Outcome measures were Hemoglobin A1c (HbA1c), BMI, and hypoglycemic episodes. Results: LTPA effect on the HbA1c reduction was present in diabetes type 1 patients. Patients who were involved in the moderate to vigorous-intensity physical activity had a greater decrease in the HbA1c (p = 0.048) than patients with low physical activity (p = 0.085). Level of LTPA was neither associated with increased number of hypoglycemic episodes, nor BMI. After an average of 4 years of diabetes, the number of patients requiring more than one antidiabetic agent increased, although the observed difference did not correlate with LTPA level. Conclusions: LTPA has an influence on the regulation of diabetes type 1, and intensification of medical treatment is compensating for the lack of lifestyle change—especially in type 2 diabetics

Psoriasis Severity—A Risk Factor of Insulin Resistance Independent of Metabolic Syndrome

Background: It is still debatable whether psoriasis increases cardiovascular risk indirectly since it is associated with metabolic syndrome or is an independent cardiovascular risk factor. The aim of this study was to evaluate psoriasis severity as an independent predictor of insulin resistance (IR) irrespective of the presence of metabolic syndrome (MetS). Methods: This was a case control study including 128 patients stratified into two groups: patients with psoriasis and metabolic syndrome vs. patients with psoriasis and no metabolic syndrome. MetS was diagnosed according to ATP III criteria with homeostatic model assessment of insulin resistance (HOMA-IR), as well as a homeostatic model assessment of beta cell function (HOMA-β) were calculated. Results: Compared to subjects without metabolic syndrome, patients with metabolic syndrome had a significantly higher Psoriasis Area Severity Index (PASI) values (p < 0.001). The strongest correlation was established for HOMA-IR and the PASI index (p < 0.001), even after adjustment for body mass index (BMI) in regression analysis model. In patients without MetS and severe forms of disease, the HOMA-IR and HOMA-β values were significantly higher compared to mild forms of disease (p < 0.001 for all) while in subjects with MetS no difference was established for HOMA-IR or HOMA-β based on disease severity. Conclusions: Psoriasis severity is an independent risk factor of HOMA-IR, the strongest association being present in the non-MetS group, who still had preserved beta cell function suggesting direct promotion of atherosclerosis via insulin resistance depending on the disease severity, but irrespective of the presence of metabolic syndrome

Flash Glucose Monitoring in Croatia: The Optimal Number of Scans per Day to Achieve Good Glycemic Control in Type 1 Diabetes

Background and Objectives: The purpose of this study is to determine the optimal number of scans per day required for attaining good glycemic regulation. Materials and Methods: The association of scanning frequency and glucometrics was analyzed according to bins of scanning frequency and bins of time in range (TIR) in the Croatian population of type 1 diabetes (T1DM) patients. Results: Intermittently scanned continuous glucose monitoring (isCGM) Libre users in Croatia performed on average 13 ± 7.4 scans per day. According to bins of scanning frequency, bin 5 with 11.2 ± 02 daily scans was sufficient for achieving meaningful improvements in glycemic regulation, while decreasing severe hypoglycemia required an increasing number of scans up to bin 10 (31 ± 0.9), yet with no effect on TIR improvement. When data were analyzed according to bins of TIR, an average of 16.3 ± 10.5 scans daily was associated with a TIR of 94.09 ± 3.49% and a coefficient of variation (CV) of 22.97 ± 4.94%. Improvement was shown between each successive bin of TIR but, of notice, the number of scans performed per day was 16.3 ± 10.5 according to TIR-based analysis and 31.9 ± 13.5 in bin 10 according to scan frequency analysis. Conclusions: In conclusion, an optimal average number of scans per day is 16.3 in order to achieve glucose stability and to minimize the burden associated with over-scanning

Thyroid Stimulating Hormone as a Possible Additional COVID-19 Outcome Marker

Background and Objectives: The interaction between thyroid and SARS-CoV-2 is complex and not yet fully understood. This study aimed to identify a predictive value of serum TSH levels on the short-term and middle-term outcomes of patients hospitalized for COVID-19. Materials and Methods: We retrospectively analyzed electronic records (ERs) data for hospitalized COVID-19 patients between March 2020 and June 2021 and their ERs during outpatient visits, 6–8 weeks post-discharge, in cases of known serum TSH levels and no previous thyroid disorder. The short-term (length of hospital stay, MSCT findings of lung involvement, required level of oxygen supplementation, admission to the ICU, and death) and middle-term outcomes after 6 to 8 weeks post-discharge (MSCT findings of lung involvement) were analyzed. Results: There were 580 patients included: 302 males and 278 females, average age of 66.39 ± 13.31 years, with no known thyroid disease (TSH mean 1.16 ± 1.8; median 0.80; no value higher than 6.0 mIU/L were included). Higher TSH was observed in patients with less severe outcomes and was associated with significantly higher SpO2 during hospitalization. Patients who required overall more oxygen supplementation or HFOT, mechanical ventilation, and patients who were more frequently admitted to the ICU or were more often treated with corticosteroids had lower TSH than those who did not show these indicators of disease severity. Lower TSH was also present in non-survivors when compared to survivors (all p p = 0.028). In the post-COVID-19 period, there was an overall, statistically significant increase in the TSH levels when compared to TSH during hospitalization (p Conclusions: Low/suppressed serum TSH levels during acute COVID-19 may be an additional laboratory test that should be included in the prediction of unfavorable short- and middle-term outcomes

Long-Term Effectiveness of Liraglutide in Association with Patients’ Baseline Characteristics in Real-Life Setting in Croatia: An Observational, Retrospective, Multicenter Study

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