It seems that during SARS-CoV-2 infection, total cholesterol, LDL-C, and HDL-C values decrease and lipids could play a fundamental role in viral replication. Moreover, it has been shown that SARS-CoV-2 infection could influence thyroid function. We performed a retrospective analysis of 118 hospitalized patients with COVID-19, comparing pre-infection lipid profile (53 patients) and thyroid-stimulating hormone (TSH) values (45 patients) to those measured on admission. Our aim was to evaluate whether SARS-CoV-2 infection could be involved in thyroid and lipid profile alterations and study possible correlations with disease severity and clinical outcome. Median baseline values at the admission time were: total cholesterol at 136.89 ± 42.73 mg/dL, LDL-C 81.53 ± 30.35 mg/dL, and HDL-C 32.36 ± 15.13 mg/dL; and triglycerides at 115.00 ± 40.45 mg/dL, non-HDL-C 104.53 ± 32.63 md/dL, and TSH 1.15 ± 1.08 μUI/mL. Median values of pre-infection total cholesterol, HDL-C, and TSH were significantly higher than those measured at the admission time (p value < 0.05). The C-reactive protein (CRP) negatively correlated with LDL-C (p = 0.013) and HDL-C (p = 0.05). Our data underline a possible impact of SARS-CoV-2 infection on thyroid function. Moreover it suggests a possible relation between COVID-19 and the lipid profile with a negative correlation between CRP, LDL-C, and HDL-C values, proposing the hypothesis that lipid lowering could follow the rising of the COVID-19 inflammatory state.

Background The Dutch Lipid Clinic Network Score (DLCN) is a useful score to guide the physician to the diagnosis of familial hypercholesterolemia (FH). However, some concerns have been pointed out about its diagnostic accuracy in pediatric population; so, other scores such as Simon Broome (SB) and US MedPed Program have been tested and currently used. Aim To test the different diagnostic and predictive accuracy between those three scores (DLCN, SM and MedPed) in relation to positivity of genetic test. Methods We enrolled 25 pediatric patients aged &lt;18 yo referred to our Chieti and Rome lipid clinics for the clinical suspicion of FH. We performed the genetic analysis for searching pathogenetic mutations for FH (NGS by Lipid in Code, LIPIGEN study). Differently from the others, DLCN provides a numerical data as a diagnostic score; thus, to uniform the three scores, we chose to define subjects with a DLCN score ≥6 as likely FH, while subjects with a lower value were defined as unlikely FH. Furthermore, we calculated the SB and the MedPed score, as previously demonstrated, defining the subjects as likely or unlikely FH. Therefore, we analyzed the diagnostic accuracy of those scores in relation to FH mutation data (positive or negative). Results We recruited 25 patients, 13 males (52%), mean age of 11.8 years. Sixteen patients (64%) resulted positive for the genetic mutation The DLCN showed a sensitivity of 43%, specificity of 66%, a positive predictive value (PPV) of 0.7 and a negative predictive value (NPV) of 0.4. SB showed a sensitivity of 68%, specificity of 55%, a PPV of 0.73 and NPV of 0.5. The MedPed score showed a sensitivity of 68%, specificity of 44%, a PPV of 0.68 and NPV of 0.44. Furthermore, we elaborated a ROC curve of low-density lipoprotein cholesterol (LDL-C) values with respect to the positivity of the FH genetic test: the value that showed the best diagnostic accuracy was 190 mg / dL (sensitivity 68.8% and specificity 75%), while the value of 116.5 mg/dL demonstrated a sensitivity of 100% but with a specificity of 11%. Conclusions Our work demonstrates that none of the three scores tested has an optimal diagnostic accuracy with respect to the diagnosis of FH in the pediatric population. By comparison, SB demonstrates the best sensitivity and the best specificity. In addition, the LDL-C value of 190 mg / dL provides the best diagnostic accuracy against the diagnosis of FH in the pediatric population. Further data and studies will be needed to improve the diagnostic performance of these scores, in order to refer pediatric patients to the genetic test, for an early confirmation in order to refer pediatric patients to the genetic test, for an early FH diagnosis confirmation. Funding Acknowledgement Type of funding source: None

Background: Several studies have shown that high plasma concentrations of asymmetric dimethylarginine (ADMA), a known endogenous competitive inhibitor of endothelial nitric oxide synthase (eNOS), correlate with the severity of coronary artery disease (CAD), with worsening of cardiac ischemia/reperfusion (I/R) injury and coronary atherosclerosis. It is believed that it may be an important risk factor for myocardial infarction. ADMA, when in high concentrations, can determine a significant decrease in the synthesis and bioavailability of NO (Nitric oxide) and therefore alter the mechanisms of regulation of coronary vasodilation and vasomotor function of epicardial coronary arteries. Higher serum ADMA concentration is associated with worsening of post-ischemic remodeling since coronary angiogenesis, vasculogenesis, and collateral coronary growth are seriously impaired. In addition, there are reasons to believe that elevated plasma ADMA levels are related to the development of diseases affecting coronary microcirculation, such as ischemic non-obstructive coronary artery disease (INOCA). Methods: Methods: With the aim of providing the pharmacologist engaged in the design and discovery of new ADMA-lowering drugs with a complete examination of the subject, in this review, we discuss the most important studies related to the correlations between serum ADMA levels and cardiovascular diseases mentioned above. In addition, we critically discuss the main aspects of enzymology, synthesis, and metabolism of ADMA as a prerequisite for understanding the molecular mechanisms through which high concentrations of ADMA could contribute to promoting cardiovascular diseases. Results and Conclusion: ADMA represents a new target for pharmacological modulation of cardiovascular endothelial function and therefore, there is a possibility of using selective pharmacological ADMA lowering drugs in cardiovascular disease with endothelial dysfunction and high plasma ADMA levels.

No abstract

No abstract