Acute coronary syndrome in diclofenac sodium-induced type I hypersensitivity reaction : Kounis syndrome

Drug-induced type I hypersensitivity reactions are frequent. Sometimes, acute coronary syndrome (ACS) can be registered in such patients, which may have a serious impact on the course and management of the allergic reaction. Because of potentially atypical ACS clinical presentations, the ECG is an obligatory diagnostic tool in any allergic reaction. Coronary artery spasm is the pathophysiological basis of ACS, triggered by the action of potent vasoactive mediators (histamine, neutral proteases, arachidonic acid products) released from the cells involved in type I hypersensitivity. Allergic angina and allergic myocardial infarction are referred to as Kounis Syndrome. We describe herein a case of ACS in a patient with registered systemic immediate hypersensitivity reaction which developed following the muscular administration of diclofenac sodium.peer-reviewe

Impaired Insulin sensitivity and Insulin secretion in Haemodialysis patients with and without Secondary Hyperparathyroidism

The aim of our study was to investigate insulin sensitivity and beta cell function in hemodialysis (HD) patients without diabetes. We hypothesized that parathyroid gland function was a determinant of insulin sensitivity and/or beta cell function. The study was a randomized, cross-sectional one and patients were divided into two groups (total 27 patients), Gp.1 being those with relative hypoparathyroidism (iPTH<200 pg/ml) ­ 9 (33.3%), Gp.2 those with hyperparathyroidism (iPTH200 pg/ml) ­ 18 (66.6%) with Gp.3 (consisting of 43 healthy subjects acting as controls). Insulin resistance and insulin secretion were calculated from fasting serum insulin and glucose concentrations by the Homeostatic Model Assessment score (HOMA IR and HOMA BETA). The value of HOMA IR (3.28±1.3 for Gp.1, 4.80±2.4 for Gp.2, 1.70±0.8 for Gp.3) as well as the glucose level (5.0±1.0mmol/l in Gp.1, 5.2±0.8mmol/ l in Gp.2, 4.6±0.4mmol/l in Gp.3) was significantly higher in HD patients than in control subjects. Excessive insulin secretion was present in HD patients (as assessed by HOMA BETA) significantly higher only in Gp.1 (p=0.02).peer-reviewe

Autophagy and diabetes

The current literature findings on autophagy’s beneficial and detrimental roles in diabetes mellitus (DM) and diabetes-related comorbidities were reviewed. The effects of oral hypoglycaemic medicines and autophagy in DM. Autophagy plays an important function in cellular homeostasis by promoting cell survival or initiating cell death in physiological settings was also assessed. Although autophagy protects insulin-target tissues, organelle failure caused by autophagy malfunction influences DM and other metabolic diseases. Endoplasmic reticulum and oxidative stress enhance autophagy levels, making it easier to regulate stress-induced intracellular changes. Evidence suggests that autophagy-caused cell death can occur when autophagy is overstimulated and constitutively activated, which might prevent or develop DM. Even though the precise role of autophagy in DM complications is uncertain, deregulation of the autophagic machinery is strongly linked to beta cell destruction and the aetiology of DM. Thus, improving autophagy dysfunction is a possible therapeutic objective in treating DM and other metabolic disorders

Nitric oxide, thyroglobulin, and calcitonin: unraveling the nature of thyroid nodules

BackgroundThyroid nodules (TN) are localized morphological changes in the thyroid gland and can be benign or malignant.ObjectiveThe present study investigates the relationships between biochemical markers in serum (s) and their homologs in washout (w) after fine-needle aspiration biopsy (FNAB) of the TN of interest and their correlation with cytology specimen findings.MethodsWe investigated the relationships between serum biochemical markers nitric oxide (NO), thyroglobulin (TG), and calcitonin (CT), their homologs in washout after FNAB of the TN of interest, and cytology findings of biopsy samples classified according to the Bethesda system for thyroid cytopathology in this study, which included 86 subjects.ResultsWashout TG (TGw) level positively correlates with the cytology finding of the biopsy. A higher level of TGw correlates with higher categories of the Bethesda classification and indicates a higher malignant potential. The levels of serum NO (NOs), serum TG (TGs), serum CT (CTs), and washout CT (CTw) do not correlate with the cytology finding of the biopsy, and the higher levels of washout NO (NOw) correspond to the more suspicious ultrasound findings.ConclusionThe findings of our study suggest that TGw and NOw could be used as potential predictors of malignancy in TN

Atherosclerosis linked to aberrant amino acid metabolism and immunosuppressive amino acid catabolizing enzymes

This work is part of the collaboration between the Laboratory of Radiobiology and Molecular Genetics, Vinca Institute of Nuclear Sciences, University of Belgrade, Belgrade, Serbia, and King Abdullah University of Science and Technology (KAUST), Computational Bioscience Research Center (CBRC), Thuwal, Saudi Arabia. The research was funded by the Ministry of Education, Science and Technological Development of the Republic of Serbia and by the KAUST grant OSR#4129 (E.R.I I TG). T.G. was supported by the KAUST Base Research Funds BAS/1/1059-01-01, respectively, while M.E. was supported by the KAUST Office of Sponsored Research (OSR) grant no. FCC/1/1976-17-01.Cardiovascular disease is the leading global health concern and responsible for more deaths worldwide than any other type of disorder. Atherosclerosis is a chronic inflammatory disease in the arterial wall, which underpins several types of cardiovascular disease. It has emerged that a strong relationship exists between alterations in amino acid (AA) metabolism and the development of atherosclerosis. Recent studies have reported positive correlations between levels of branched-chain amino acids (BCAAs) such as leucine, valine, and isoleucine in plasma and the occurrence of metabolic disturbances. Elevated serum levels of BCAAs indicate a high cardiometabolic risk. Thus, BCAAs may also impact atherosclerosis prevention and offer a novel therapeutic strategy for specific individuals at risk of coronary events. The metabolism of AAs, such as L-arginine, homoarginine, and L-tryptophan, is recognized as a critical regulator of vascular homeostasis. Dietary intake of homoarginine, taurine, and glycine can improve atherosclerosis by endothelium remodeling. Available data also suggest that the regulation of AA metabolism by indoleamine 2,3-dioxygenase (IDO) and arginases (1 and 2) are mediated through various immunological signals and that immunosuppressive AA metabolizing enzymes are promising therapeutic targets against atherosclerosis. Further clinical studies and basic studies that make use of animal models are required. Here we review recent data examining links between AA metabolism and the development of atherosclerosis.Publisher PDFPeer reviewe

A quality of life assessment and the correlation between generic and disease-specific questionnaires scores in outpatients with chronic liver disease-pilot study

Introduction. Chronic liver diseases (CLD) are an important cause of morbidity and mortality in general population. The aim of this study was to analyze potential differences between patients with CLD and healthy control group, and to estimate the severity of CLD by using simple questionnaires: general health questionnaire (GHQ-12) and chronic liver disease questionnaire (CLDQ). Methods. A cross-sectional pilot study was performed in Zemun Clinical Hospital during years 2014 and 2015. Sixty participants were divided into 4 groups (15 per group): chronic alcoholic hepatitis, other chronic hepatitis, liver cirrhosis, and healthy control group. Entire study population chose one of four offered answers of structured questionnaires GHQ-12 and CLDQ, based on which mean model of end-stage liver disease (MELD) and Child-Turcotte-Pugh (CTP) scores were calculated. Results. Mean GHQ12 and CLDQ scores were 10.5 and 5.21 ± 1.11 respectively. Regarding certain CLDQ domain scores, a significant difference between alcoholic and non-alcoholic hepatitis groups in the worry domain was observed. Mean MELD score was 7.42 ± 2.89 and did not differ between chronic hepatitis groups, while mean CTP score was 5.73 ± 0.88. A statistically significant correlation was observed between GHQ12 and CLDQ scores (ρ = -0.404, p < 0.01), but not between subjective and objective scores. Conclusions. Mean GHQ12 and CLDQ scores pointed out to general psychological no-distress condition of the studied participants, as well as scarcely expressed CLD-specific complaints. Mean MELD and CTP scores indicated stable chronic liver diseases, with low three-month mortality rates in the cases of chronic hepatitis, as well as determination to Child A group in the case of liver cirrhosis

Chronic Hepatitis C, Insulin Resistance and Vascular Disease

The role of hepatitis C virus (HCV) infection in the development of vascular disease is controversial. Insulin resistance (IR) is a recognized risk factor for cardiovascular disease (CVD) and is associated with chronic hepatitis C (CHC). Thus, IR may promote atherosclerosis and vascular disease in CHC patients. HCV-associated IR may also cause hepatic steatosis and resistance to antiviral treatment. In addition, HCV may contribute a direct, proatherogenetic action on the vascular wall. This review considers the impact of IR on interferon-based therapy of HCV infection and the role of insulin-sensitizing agents on the response to antiviral treatment and prevention of IR complications, including CVD

Levothyroxine treatment and the risk of cardiac arrhythmias – focus on the patient submitted to thyroid surgery

This work is part of a collaboration between the Department of Radiobiology and Molecular Genetics "VINCA" Institute in Nuclear Sciences - National Institute of the Republic of Serbia, Belgrade, Serbia, and Computational Bioscience Reserach Center (CBRC) at King Abdullah University of Science and Technology (KAUST). This work was funded by the MInistry of Education, Science and Technological Development of the Republic of Serbia (Contract No: 451-03-9/2021-14/200017) and KAUST grant OSR No. 4129 (awarded to E.R.I. and V.B.B.), which also supported M.O. M.E. has been supported by the KAUST Office of Sponsored Research (OSR) Award No. FCC/1/1976-17-01, and T.G. by the King Abdullah University of Science and Technology (KAUST) Base Reserach Fund (BAS/1/1059-01-01).Levothyroxine (LT4) is used to treat frequently encountered endocrinopathies such as thyroid diseases. It is regularly used in clinical (overt) hypothyroidism cases and subclinical (latent) hypothyroidism cases in the last decade. Suppressive LT4 therapy is also part of the medical regimen used to manage thyroid malignancies after a thyroidectomy. LT4 treatment possesses dual effects: substituting new-onset thyroid hormone deficiency and suppressing the local and distant malignancy spreading in cancer. It is the practice to administer LT4 in less-than-high suppressive doses for growth control of thyroid nodules and goiter, even in patients with preserved thyroid function. Despite its approved safety for clinical use, LT4 can sometimes induce side-effects, more often recorded with patients under treatment with LT4 suppressive doses than in unintentionally LT4-overdosed patients. Cardiac arrhythmias and the deterioration of osteoporosis are the most frequently documented side-effects of LT4 therapy. It also lowers the threshold for the onset or aggravation of cardiac arrhythmias for patients with pre-existing heart diseases. To improve the quality of life in LT4-substituted patients, clinicians often prescribe higher doses of LT4 to reach low normal TSH levels to achieve cellular euthyroidism. In such circumstances, the risk of cardiac arrhythmias, particularly atrial fibrillation, increases, and the combined use of LT4 and triiodothyronine further complicates such risk. This review summarizes the relevant available data related to LT4 suppressive treatment and the associated risk of cardiac arrhythmia.Publisher PDFPeer reviewe

Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS

An altered hepatic lipid metabolism involves multifactorial pathologies such as hepatic inflammation, insulin resistance and oxidative stress. Immunity has an essential role in the regulation of glucose and lipid metabolism in the liver. Inducible nitric oxide (NO) synthase (iNOS) has been proposed as an important factor that interplays between immunity and energy metabolism and also in the pathogenesis of obesity-linked insulin resistance. In the liver, locally produced NO plays a protective role during inflammation, and the balance of NO protective and cytotoxic effects is very important. This review is focused on understanding the molecular mechanisms of iNOS regulation in the state of altered hepatic lipid metabolism, which is critical for developing new strategies for treatment of hepatic disorders