RESUMEN
AIMS -: As people with type 1 diabetes have increased risk of cardiovascular morbi-mortality, management of cardiovascular risk factors is of crucial importance. We assessed the prevalence and factors associated with LDL-cholesterol (LDL-c) target achievement in patients with type 1 diabetes at high and very-high cardiovascular risk. METHODS -: In this observational multicenter study, we included hospitalized patients with type 1 diabetes who had a fasting blood lipid analysis at admission. Cardiovascular risk level and LDL-c target values were defined according to ESC/EAS guidelines into force at admission: LDL-c target for very-high risk (VHR) and high risk (HR) patients was 1.4 and 1.8 mmol/l respectively for patients included from September 2019 (2019 guidelines) and 1.8 and 2.6 mmol/l respectively for patients included in 2016-2019 (2016 guidelines). LDL-c target attainment was assessed in HR and VHR patients, and factors associated with attainment were identified with multivariable analysis. RESULTS -: We included 85 HR patients (median age 37y [interquartile range: 27;45], 64% females) and 356 VHR patients (49 [35;61] years, 42% females). In HR patients, 7% were treated with statins, and 35.3% achieved the LDL-c target. Increasing age (odds ratio 0.58 [95% confidence interval: 0.38;0.89]), body mass index (0.86 [0.75;0.98]), and HbA1c (0.69 [0.50;0.94]) were independently associated with lower odds of attaining LDL-c target. In VHR patients, 36% were treated with statins, and 17.4% achieved LDL-c target. Statin treatment (2.33 [1.22;4.43]), secondary prevention (2.33 [1.21;4.48]) and chronic renal failure (2.82 [1.42;5.61]) were associated with higher odds of attaining LDL-c target. CONCLUSION -: Control of LDL-c is highly insufficient in both HR and VHR patients. Cardiovascular risk evaluation and better control of risk factors may help decrease cardiovascular morbi-mortality in patients with type 1 diabetes. REGISTRATION NUMBER: NCT03449784.
RESUMEN
An increase of pyroglutamic acid, or 5-oxoproline plasmatic concentration was reported in metabolic acidosis observed after chronic intake of some drugs, as acetaminophen. We developed a simple, fast and reproducible method by capillary zone electrophoresis using a commercial Anion Analysis Kit® to quantify pyroglutamic acid, in plasma after acetonitrile precipitation, and after simple dilution in urines. Fumaric acid was used as internal standard in both. In less than 7 min, the method separates pyroglutamic acid from other organic and inorganic anions. The method is linear between 0.25 and 10 mmol/L in plasma, and 0.15 and 10 mmol/L in urines. The quantification limits are 0.25 mmol/L and 0.15 mmol/L for plasma and urines, respectively. For repeatability and intermediate precision, the variation coefficients are less than 15% and the bias values are between ± 10%. For the 2 matrices, the recoveries are between 88% and 101%. The method does not interfere with physiological organic and inorganic anions. Pyroglutamic acid concentrations measured in 9 children were between 0.45 and 3.96 mmol/L in the plasma and between 0.15 and 3.2 mmol/L in the urine. No correlation between pyroglutamic acid and acetaminophen concentrations were found, regardless of the biological media. In conclusion, our method measures pathophysiological concentrations of pyroglutamic acid and highlights the increase in other organic acids that may explain metabolic acidosis due to chronic acetaminophen intake.