Concentration of Lp-PLA 2 in stable patients in secondary prevention after STEMI and dose-effect of statins on its values [Koncentrace Lp-PLA 2 u stabilních pacientů v sekundární prevenci po STEMI a vliv dávky statinů na její hodnoty]
Parenicova I.,Interni kardiologicka klinika |
Prymusova K.,Kardiologicke Oddeleni |
Benovska M.,Oddeleni klinicke biochemie a hematologie |
Babusikova L.,Oddeleni klinicke biochemie a hematologie |
And 9 more authors.
Cor et Vasa
Background and aim: Phospholipase A 2 associated with lipoprotein (Lp-PLA 2) is a biomarker specific for a vascular inflammation. Lp-PLA 2 hydrolyzes oxidized phosphatidylcholine and produces an effective pro-inflammatory mediators that facilitate formation of atherosclerotic plaque instability. Previous works demonstrated that elevated Lp-PLA 2 > 200-235 μg/L is an independent predictor of increased cardiovascular risk even after adjustment for traditional risk factors. The goal of our work was to determine levels of Lp-PLA 2 in a group of stable patients after STEMI and to assess the effect of increased doses of statins on levels of Lp-PLA 2 in a part of the patients with its elevated value. Methods: 186 stable patients after acute myocardial infarction were examined. The lipid spectrum and levels of Lp-PLA 2 were evaluated. The statin therapy was intensified in the patients with Lp-PLA 2 > 200 μg/L, and after 3 months the control of lipids and Lp-PLA 2 was performed. Results: 12 months after acute MI in the group of 186 patients there was achieved a total cholesterol < 4 mmol/L in 45% of the patients, LDL cholesterol < 2 mmol/L in 50% of the patients. The average value of Lp-PLA 2 was 166±86 μg/L. The patients with LDL < 2 mmol/L had significantly lower levels of Lp-PLA 2 (151±75 vs. 178±92 μg/L; P = 0.02). Total 20% of the patients had Lp-PLA 2 > 200 μg/L, and in the group of patients with LDL-cholesterol < 2 mmol/L there were 14% of patients with high level of Lp-PLA 2. There was found a significant decline in both total and LDL cholesterol and levels of Lp-PLA 2 (286 vs. 229 μg/L; P = 0.02) after the increased dose of statins. Conclusions: About 7% of stable patients after STEMI had elevated levels of Lp-PLA 2, despite well-controlled LDL cholesterol. More intensive statin therapy led to a significant reduction in Lp-PLA 2 in these patients. Source
Comparison of results of monoclonal free immunoglobulin light chains quantification in the serum in clinical laboratories in the Czech Republic [Mezilaboratorní studie stanovení volných monoklonálních lehkých řetězců imunoglobulinů]
Vavrova J.,UKBD |
Tichy M.,UKBD |
Friedecky B.,UKBD |
Maisnar V.,II. Interni Klinika |
And 15 more authors.
Klinicka Biochemie a Metabolismus
Free monoclonal immunoglobulin light chains (FLC) quantification is recommended for diagnosis assessment and monitoring therapy for patients with monoclonal gammopathy. But there are numerous uncertainties regarding the detection, interpretation and FLC quantification. Our interlaboratory study showed that kappa/lambda ratio is strongly influenced by measurement errors and therefore we recommended the preferential use of FLC concentration values. Unified protocols are needed to minimise interlaboratory variability introduced by manual dilution or volume augmentation of clinical sample. Source
Malaskova L.,Oddeleni klinicke biochemie a hematologie |
Malaskova L.,Katedra laboratornich metod Lekarske |
Winterova J.,Interni Hematoonkologicka Klinika |
Dastych M.,Oddeleni klinicke biochemie a hematologie |
And 6 more authors.
Voriconazole and posaconazole are azole broadspectrum pharmaceuticals used in treatment and prophylaxis of invasive fungal infections. Determination of both the antifungals in blood plasma in the course of treatment makes it possible to achieve optimal dosing. Our aim was to integrate voriconazole and posaconazole monitoring in the treatment of fungal infections in hematooncological patients. At present the simple and rapid ultra performance liquid chromatography (UPLC) monitoring of both the antifungals is a part of daily routine. Source