scholarly journals Gamma-glutamyl transferase and oxidised high-density lipoprotein: a pilot study

2020 ◽  
Vol 5 (1) ◽  
pp. 43-44
Author(s):  
Kazuhiko Kotani ◽  
Kouichi Miura
Keyword(s):  
Pilot Study ◽  
High Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Gamma Glutamyl Transferase ◽  
Lipoprotein A ◽  
Gamma Glutamyl ◽  
Glutamyl Transferase

A magasvérnyomás-betegség előfordulása és kezelése frissen diagnosztizált familiáris hypercholesterinaemiás betegekben

2021 ◽  
Vol 25 (1) ◽  
pp. 7-11
Author(s):  
Bíborka Nádró ◽  
Ágnes Diószegi ◽  
Beáta Kovács ◽  
György Paragh ◽  
Dénes Páll ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Low Density ◽  
Lipoprotein A

A familiáris hypercholesterinaemia (FH) a koleszterin-anyagcsere veleszületett zavarával járó kórkép, amelyet jelentősen emelkedett összkoleszterinszint (TC) és low density lipoprotein koleszterinszint (LDL-C), ennek következtében a szív- és érrendszeri betegségek korai megjelenése jellemez. A magas vérnyomás előfordulási gyakorisága FH-s betegekben nem tisztázott, de jelenléte független kockázati tényezője a cardiovascularis betegség kialakulásának. Megfelelő terápiája ezért kiemelt fontosságú ebben a nagy kockázatú betegcsoportban.Célul tűztük ki 86, szakrendelésünkön először megjelent, frissen diagnosztizált, lipidcsökkentő kezelésben még nem részesülő heterozigóta FH-s beteg (27 férfi, 59 nő, átlagéletkoruk 53,6±13,4 év) esetén a lipidszintek, valamint a dokumentáció alapján a magas vérnyomás előfordulásának és kezelésének értékelését. Az FH diagnózisát a Dutch Lipid Network kritériumrendszer alkalmazásával állítottuk fel.A betegek átlagos TC-szintje 8,49±1,7 mmol/l, átlagos LDL-C-szintje 6,11±1,5 mmol/l, átlagos high density lipoprotein koleszterin (HDL-C) szintje 1,62±0,5 mmol/l, míg a lipoprotein-(a)-szint mediánja 301 mg/l volt. Mindössze 33 beteg esetén diagnosztizáltak korábban magas vérnyomást (38,4%). Béta-blokkolót 23, ACE-gátlót 13, ARB-t 12, kalciumcsatorna-blokkolót 9, HCT-t 11 beteg kapott. 11 beteg részesült monoterápiában, 10 beteg kettős, 11 beteg hármas, míg 1 beteg négyes kombinált kezelést kapott.Az eredmények alapján a magasvérnyomás-betegség ebben a betegcsoportban valószínűleg aluldiagnosztizált, a javasolt kezelés pedig sem az alkalmazott szer típusát, sem annak módját tekintve nem felelt meg az aktuális terápiás irányelveknek. A magasvérnyomás-betegség szűrése és korszerű kezelése, tekintettel az FH esetén kialakuló korai érelmeszesedésre, jóval nagyobb figyelmet érdemel ebben a kiemelt kockázatú betegcsoportban.

Biological variability of cholesterol, triglyceride, low- and high-density lipoprotein cholesterol, lipoprotein(a), and apolipoproteins A-I and B

1994 ◽  
Vol 40 (4) ◽  
pp. 574-578 ◽  
Author(s):  
S M Marcovina ◽  
V P Gaur ◽  
J J Albers
Keyword(s):  
High Density Lipoprotein ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
Biological Variability ◽  
Apo B ◽  
Lipoprotein A ◽  
The Individual

Abstract Biological variability is a major contributor to the inaccuracy of cardiovascular risk assessments based on measurement of lipids, lipoproteins, or apolipoproteins. We obtained estimates of biological variation (CVb) for 20 healthy adults and calculated the percentiles of CVb as an expression of the variability of CVb among individuals for cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein (apo) A-I, apo B, and lipoprotein(a) [Lp(a)] by four biweekly measurements of these analytes. The CVb for the group was approximately 6-7% for cholesterol, HDL cholesterol, apo A-I, and apo B; approximately 9% for LDL cholesterol; and 28% for triglyceride. However, for each analyte, there was a considerable variation of CVb among individuals. For all analytes except Lp(a), there was no relation between the individual's CVb and the analyte concentration. Lp(a) was inversely related to CVb, and there was a very wide variation in the CVb for Lp(a) among the participants, ranging from 1% to 51%. The number of independent analyses to perform to accurately assess an individual's risk for coronary artery disease should be determined on the basis of the individual CVb for a given analyte rather than the average CVb.

Fetal and Maternal Lipoprotein Metabolism in Human Pregnancy

1995 ◽  
Vol 88 (3) ◽  
pp. 311-318 ◽  
Author(s):  
Richard H. Neary ◽  
Mark D. Kilby ◽  
Padma Kumpatula ◽  
Francis L. Game ◽  
Deepak Bhatnagar ◽  
...  
Keyword(s):  
Caesarean Section ◽  
High Density Lipoprotein ◽  
Cholesteryl Ester ◽  
Free Cholesterol ◽  
Cholesterol Metabolism ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Lipoprotein A ◽  
Lipid Enrichment

1. Lipid, apolipoprotein concentration and composition were determined in maternal venous and umbilical arterial and venous blood at delivery by elective Caesarean section in 13 full-term pregnancies and in 25 healthy non-pregnant females. The indications of Caesarean section were a previous Caesarean section or breech presentation. None of the women was in labour and there were no other complications of pregnancy or fetal distress. 2. The objectives of the study were to establish whether the placenta has a role in feto-maternal cholesterol metabolism through either synthesis or transplacental cholesterol flux. The potential for free cholesterol diffusion between mother and fetus and rates of cholesterol esterification and transfer between lipoproteins were determined and related to the differences in composition between fetal and maternal lipoproteins. 3. Pregnant women had raised levels of all lipid and lipoprotein fractions compared with control subjects. The greatest increases were in free cholesterol and triacylglycerol (P < 0.0001). Lipoprotein (a) levels were significantly greater in the pregnant women [112(12.2) mg/l] than in the control women [50 (10.0) mg/l]. 4. The only significant correlation between maternal and fetal lipoprotein concentrations was in lipoprotein (a) levels (r = 0.791, P = 0.002). In both umbilical venous and arterial blood, concentrations of very-low- and low-density lipoproteins, particularly apolipoprotein B, cholesteryl ester and triacylglycerol, were lower than in maternal blood (P < 0.0001), but high-density lipoprotein levels were similar. 5. There was no umbilical arteriovenous differences in lipoprotein concentration or composition. This suggests that cholesterol synthesis or free cholesterol diffusion does not occur in the placenta. The relative concentrations of free cholesterol to phospholipid in maternal and fetal lipoproteins do not indicate the existence of a concentration gradient favouring free cholesterol diffusion across the placenta. 6. The esterification of free cholesterol was significantly reduced in maternal [17.7 (2.4) μmol h−1 l−1, P < 0.001] and fetal [6.7 (3.5) μmol h−1 l−1, P < 0.0001] compared with control [40.9 (13.2) μmol h−1 l−1] blood. 7. In fetal compared with maternal high-density lipoproteins the ratios cholesteryl ester/apoliproprotein A-I [0.84 (0.35) versus 0.40 (0.05), P < 0.01] and phospholipid/apolipoprotein A-I [1.66 (0.14) versus 0.58 (0.10), P < 0.0001] indicated lipid enrichment of these particles in the fetus. 8. Lipid enrichment of high-density lipoprotein is due in part to a marked reduction in transfer of cholesteryl ester in the fetus [1.0 (0.6) μmol h−1 l−1] compared with maternal [6.15 (1.3) μmol h−1 l−1, P = 0.004] and control [17.3 (7.2) μmol h−1 l−1, P < 0.0001] blood. 9. In conclusion, there was no evidence for involvement of the placenta in cholesterol metabolism during pregnancy. In fetal life high-density lipoproteins are lipid rich, partly because of a reduction in transfer of esterified cholesterol to other particles. Maternal and fetal lipoprotein levels are not correlated, although the results suggested that lipoprotein (a) levels may be related.

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