All analyses were conducted with Stata/IC, version 14.2 (StataCorp LP) or SAS, version 9.4 (SAS Institute). in undertreatment of high-risk patients. A novel method (Martin/Hopkins) using a patient-specific conversion factor provides more accurate LDL-C levels. However, this method has not been tested in proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitorCtreated patients. Objective To investigate accuracy of 2 different methods for estimating LDL-C levels (Martin/Hopkins and Friedewald) compared with gold standard preparative Parathyroid Hormone 1-34, Human ultracentrifugation (PUC) in patients with low LDL-C levels in the Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Patients With Elevated Risk (FOURIER) trial. Design, Setting, and Participants The FOURIER trial was a randomized clinical trial of evolocumab vs placebo added to statin therapy in 27?564 patients with stable atherosclerotic cardiovascular disease. The patients LDL-C levels were assessed at baseline, 4 weeks, 12 weeks, 24 weeks, and every 24 weeks thereafter, and measured directly by PUC when the level was less than 40 mg/dL per the Friedewald method (calculated as nonCHDL-C level ? triglycerides/5). In the Martin/Hopkins method, patient-specific ratios of triglycerides to very low-density lipoprotein cholesterol (VLDL-C) ratios were determined and used to estimate VLDL-C, which was subtracted from the nonCHDL-C level to obtain the LDL-C level. Main Outcomes and Measures Low-density lipoprotein cholesterol calculated by the Friedewald and Martin/Hopkins methods, with PUC Parathyroid Hormone 1-34, Human as the reference method. Results For this analysis, the mean (SD) age was 62.7 (9.0) years; 2885 of the 12 742 patients were women (22.6%). A total of 56?624 observations from 12?742 patients had Friedewald, Martin/Hopkins, and PUC LDL-C measurements. The median difference from PUC LDL-C levels for Martin/Hopkins LDL-C levels was ?2 mg/dL (interquartile range [IQR], ?4 to 1 1 mg/dL) and for Friedewald LDL-C levels was ?4 mg/dL (IQR, ?8 to ?1 mg/dL; transformations. All analyses were conducted with Stata/IC, version 14.2 (StataCorp LP) or SAS, version 9.4 (SAS Institute). Values of ValueValueValueValueValueValue /th th valign=”top” colspan=”1″ align=”left” scope=”colgroup” rowspan=”1″ Martin/Hopkins /th th valign=”top” align=”left” scope=”col” rowspan=”1″ colspan=”1″ Friedewald /th th valign=”top” colspan=”1″ align=”left” scope=”colgroup” rowspan=”1″ Martin/Hopkins /th th valign=”top” align=”left” Rabbit polyclonal to XPO7.Exportin 7 is also known as RanBP16 (ran-binding protein 16) or XPO7 and is a 1,087 aminoacid protein. Exportin 7 is primarily expressed in testis, thyroid and bone marrow, but is alsoexpressed in lung, liver and small intestine. Exportin 7 translocates proteins and large RNAsthrough the nuclear pore complex (NPC) and is localized to the cytoplasm and nucleus. Exportin 7has two types of receptors, designated importins and exportins, both of which recognize proteinsthat contain nuclear localization signals (NLSs) and are targeted for transport either in or out of thenucleus via the NPC. Additionally, the nucleocytoplasmic RanGTP gradient regulates Exportin 7distribution, and enables Exportin 7 to bind and release proteins and large RNAs before and aftertheir transportation. Exportin 7 is thought to play a role in erythroid differentiation and may alsointeract with cancer-associated proteins, suggesting a role for Exportin 7 in tumorigenesis scope=”col” rowspan=”1″ colspan=”1″ Friedewald /th th valign=”top” colspan=”1″ align=”left” scope=”colgroup” rowspan=”1″ Martin/Hopkins /th th valign=”top” align=”left” scope=”col” rowspan=”1″ colspan=”1″ Friedewald /th /thead 577.1 (23.2/53.9)59.9 (13.0/46.9) .00168.0 (35.0/33.0)17.2 (2.2/15.1) .00179.5 (20.0/59.5)71.3 (15.9/55.4) .001 5-1020.3 (5.2/15.1)26.8 (0.8/26.1)21.9 (17.1/4.9)32.5 (0.4/32.1)19.9 (2.1/17.8)25.3 (0.8/24.5) 10-202.3 (1.9/0.4)11.7 (0.1/11.7)8.4 (8.3/0.2)43.0 (0.3/42.7)0.6 (0.2/0.5)3.4 (0.04/3.3) 20-300.3 (0.3/ 0.01)1.4 (0.02/1.4)1.3 (1.3/ 0.01)6.6 (0.1/6.5)0.01 (0.01/ 0.01)0.01 ( 0.01/0.01) 300.1 (0.1/ 0.01)0.1 ( 0.01/0.1)0.3 (0.3/ 0.01)0.7 ( 0.01/0.7) 0.01 ( 0.01/ 0.01) 0.01 ( 0.01/ 0.01) Open in a separate window Abbreviations: FOURIER, Further Cardiovascular Outcomes Research With Parathyroid Hormone 1-34, Human PCSK9 Inhibition in Patients With Elevated Risk; LDL-C, low-density lipoprotein cholesterol; TG, triglycerides. SI conversion factors: To convert cholesterol to millimoles per liter, multiply by 0.0259; triglycerides to millomoles per liter, multiply by 0.0113. In scatterplots of estimated vs PUC LDL-C levels, Martin/Hopkins LDL-C levels were more evenly distributed around the regression line than Friedewald values were (Figure). The Spearman correlation coefficient with PUC LDL-C levels was significantly higher for Martin/Hopkins vs Friedewald LDL-C levels (Martin/Hopkins: , 0.918 [95% CI, 0.916-0.919] vs Friedewald: , 0.867 [95% Parathyroid Hormone 1-34, Human CI, 0.865-0.869]; em P /em ? ?.001) and Martin/Hopkins LDL-C levels deviated less from observed values (Martin/Hopkins: root mean square [RMS] error, 4.32 [95% CI, 4.25-4.39] vs Friedewald: RMS error, 5.41 [95% CI, 5.34-5.48] mg/dL). Open in a separate window Figure. Scatterplots Parathyroid Hormone 1-34, Human of Estimated Low-Density Lipoprotein Cholesterol (LDL-C) vs Preparative Ultracentrifugation Measured LDL-CA line of unity (solid line) and regression line (dashed line) are shown. Note that the study population was defined by Friedewald LDL-C estimations less than 40 mg/dL, whereas Martin/Hopkins and preparative.
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