Exploring free amino acid profiles in CCHF patients: Implications for disease progression.

This study investigated the intricate interplay between Crimean-Congo hemorrhagic fever virus (CCHFV) infection and alterations in amino acid metabolism. Our primary aim is to elucidate the impact of Crimean-Congo hemorrhagic fever (CCHF) on specific amino acid concentrations and identify potential metabolic markers associated with viral infection. One hundred ninety individuals participated in this study, comprising 115 CCHF patients, 30 CCHF negative patients, and 45 healthy controls. Liquid chromatography-tandem mass spectrometry techniques were employed to quantify amino acid concentrations. The amino acid metabolic profiles in CCHF patients exhibit substantial distinctions from those in the control group. Patients highlight distinct metabolic reprogramming, notably characterized by arginine, histidine, taurine, glutamic acid, and glutamine metabolism shifts. These changes have been associated with the underlying molecular mechanisms of the disease. Exploring novel therapeutic and diagnostic strategies addressing specific amino acids may offer potential means to mitigate the severity of the disease.

Exploring free amino acid profiles in Crimean-Congo hemorrhagic fever patients: Implications for disease progression.

This study investigated the intricate interplay between Crimean-Congo hemorrhagic fever virus infection and alterations in amino acid metabolism. The primary aim is to elucidate the impact of Crimean-Congo hemorrhagic fever (CCHF) on specific amino acid concentrations and identify potential metabolic markers associated with viral infection. One hundred ninety individuals participated in this study, comprising 115 CCHF patients, 30 CCHF negative patients, and 45 healthy controls. Liquid chromatography-tandem mass spectrometry techniques were employed to quantify amino acid concentrations. The amino acid metabolic profiles in CCHF patients exhibit substantial distinctions from those in the control group. Patients highlight distinct metabolic reprogramming, notably characterized by arginine, histidine, taurine, glutamic acid, and glutamine metabolism shifts. These changes have been associated with the underlying molecular mechanisms of the disease. Exploring novel therapeutic and diagnostic strategies addressing specific amino acids may offer potential means to mitigate the severity of the disease.

Deciphering the host genetic factors conferring susceptibility to severe COVID-19 using exome sequencing.

The COVID-19 pandemic remains a significant public health concern despite the new vaccines and therapeutics. The clinical course of acute SARS-CoV-2 infection is highly variable and influenced by several factors related to the virus and the host. Numerous genetic studies, including candidate gene, exome, and genome sequencing studies, genome-wide association studies, and other omics efforts, have proposed various Mendelian and non-Mendelian associations with COVID-19 course. In this study, we conducted whole-exome sequencing on 90 unvaccinated patients from Turkey with no known comorbidities associated with severe COVID-19. Of these patients, 30 had severe, 30 had moderate, and 30 had mild/asymptomatic disease. We identified rare variants in genes associated with SARS-CoV-2 susceptibility and pathogenesis, with an emphasis on genes related to the regulation of inflammation, and discussed these in the context of the clinical course of the patients. In addition, we compared the frequencies of common variants between each group. Even though no variant remained statistically significant after correction for multiple testing, we observed that certain previously associated genes and variants showed significant associations before correction. Our study contributes to the existing literature regarding the genetic susceptibility to SARS-CoV-2. Future studies would be beneficial characterizing the host genetic properties in different populations.

Concordance of LDL-C Estimating Equations with Direct Enzymatic Measurement in Diabetic and Prediabetic Subjects.

Low-density lipoprotein cholesterol (LDL-C) is a well-established biomarker in the management of dyslipidemia. Therefore, we aimed to evaluate the concordance of LDL-C-estimating equations with direct enzymatic measurement in diabetic and prediabetic populations. The data of 31,031 subjects included in the study were divided into prediabetic, diabetic, and control groups according to HbA1c values. LDL-C was measured by direct homogenous enzymatic assay and calculated by Martin-Hopkins, Martin-Hopkins extended, Friedewald, and Sampson equations. The concordance statistics between the direct measurements and estimations obtained by the equations were evaluated. All equations evaluated in the study had lower concordance with direct enzymatic measurement in diabetic and prediabetic groups compared to the non-diabetic group. Even so, the Martin-Hopkins extended approach demonstrated the highest concordance statistic in diabetic and prediabetic patients. Further, Martin-Hopkins extended was found to have the highest correlation with direct measurement compared with other equations. Over the 190 mg/dL LDL-C concentrations, the equation with the highest concordance was again Martin-Hopkins extended. In most scenarios, the Martin-Hopkins extended performed best in prediabetic and diabetic groups. Additionally, direct assay methods can be used at low values of the non-HDL-C/TG ratio (<2.4), as the performance of the equations in LDL-C estimation decreases as non-HDL-C/TG decreases.

Validation of low-density lipoprotein cholesterol equations in pediatric population.

Several studies have shown a high prevalence of dyslipidemia in children. Since childhood lipid concentrations continue into adulthood, recognition of lipid abnormalities in the early period is crucial to prevent the development of future coronary heart disease (CHD). Low density lipoprotein cholesterol (LDL-C) is one of the most used parameters in the initiation and follow-up of treatment in patients with dyslipidemia. It is a well known fact that LDL-C lowering therapy reduces the risk of future CHD. Therefore, accurate determination of the LDL-C levels is so important for the management of lipid abnormalities. This study aimed to validate different LDL-C estimating equations in the Turkish population, composed of children and adolescents. A total of 3,908 children below 18 years old at Sivas Cumhuriyet University Hospital (Sivas, Turkey) were included in this study. LDL-C was directly measured by direct homogeneous assays, i.e., Roche, Beckman, Siemens and estimated by Friedewald's, Martin/Hopkins', extended Martin-Hopkins' and Sampson's formulas. The concordances between the estimations obtained by the formulas and the direct measurements were evaluated both overall and separately for the LDL-C, triglycerides (TG) and non-high-density lipoprotein cholesterol (non-HDL-C) sublevels. Linear regression analysis was performed and residual error plots were generated between each estimation and direct measurement method. Coefficient of determination (R 2) and mean absolute deviations were also evaluated. The overall concordance of Friedewald, Sampson, Martin-Hopkins and the extended Martin-Hopkins formula were 64.6%, 69.9%, 69.4%, and 84.3% for the Roche direct assay, 69.8%, 71.6%, 73.6% and 80.4% for the Siemens direct assay, 66.5%, 68.8%, 68.9% and 82.1% for the Beckman direct assay, respectively. The extended Martin-Hopkins formula had the highest concordance coefficient in both overall and all sublevels of LDL-C, non-HDL-C, and TG. When estimating the LDL-C categories, the highest underestimation degrees were obtained with the Friedewald formula. Our analysis, conducted in a large pediatric population, showed that the extended Martin-Hopkins equation gives more reliable results in estimation of LDL-C compared to other equations.

Validation of Friedewald, Martin-Hopkins and Sampson low-density lipoprotein cholesterol equations.

BACKGROUND: Low-density lipoprotein cholesterol (LDL-C) is an important biomarker for determining cardiovascular risk and regulating lipid lowering therapy. Therefore, the accurate estimation of LDL-C concentration is essential in cardiovascular disease diagnosis and prognosis. Sampson recently proposed a new formula for the estimation of LDL-C. However, little is known regarding the validation of this formula. OBJECTIVES: This study aimed to validate this new formula with other well-known formulas in Turkish population, composed of adults. METHODS: A total of 88,943 participants above 18 years old at Sivas Cumhuriyet University Hospital (Sivas, Turkey) were included to this study. LDL-C was directly measured by homogeneous assays, i.e., Roche, Beckman and Siemens and estimated by Friedewald's, Martin-Hopkins', extended Martin-Hopkins' and Sampson's formulas. The concordances between the estimations obtained by the formulas and the direct measurements were evaluated both in general and separately for the LDL-C, TG and non-HDL-C sublevels. Linear regression analysis was applied and residual error plots were generated between each estimation and direct measurement method. Coefficient of determination (R2) and mean absolute deviations were also calculated. RESULTS: The results showed that the extended Martin-Hopkins approach provided the most concordant results with the direct assays for LDL-C estimation. The results also showed that the highest concordances were obtained between the direct assays with the extended Martin-Hopkins formula calculated with the median statistics obtained from our own population. On the other hand, it was observed that the results of the methods may differ in different assays. The extended Martin-Hopkins approach, calculated from the median statistics of our population, gave the most concordant results in patients with "low LDL-C level (LDL-C levels < 70 mg/dL) or hypertriglyceridemia (TG levels ≥ 400 mg/dL)". CONCLUSIONS: Although the results of the formulas in different assays may vary, the extended Martin-Hopkins approach was the best one with the highest overall concordances. The validity of the Martin Hopkins' and Sampson's formulas has to be further investigated in different populations.

Survival of biological therapeutics in psoriasis: retrospective analysis of 3-years data in a Turkish registry, PSORTAKSIS.

BACKGROUND: TPSORTAKSIS is a psoriasis registry, which is used for follow-up of patients in Kayseri City Education and Research Hospital, Dermatology Clinic since 2016 in Turkey. PSORTAKSIS includes demographic data, follow-up clinical findings, laboratory output, and treatment information of patients. Here, drug survivals of biologic therapeutics (BT) according to three-year data of PSORTAKSIS will be presented. METHODS: Drug survival of BT in PSORTAKSIS was analyzed from 2016 to March 2019. RESULTS: 158 patients (111 of them BT-naive) with psoriasis under BT were enrolled in the current study. Drug survival analysis of patients with ongoing BT (158 treatment periods) revealed mean survival time as 15.49 months for ustekinumab, 15.37 months for adalimumab, 14.00 months for etanercept, 5 months for infliximab, and 4.59 months for secukinumab. The differences between drug survivals of BT were statistically significant (log-rank test, χ2 = 79.915, p < 0.0001).