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Effect of directly acting antivirals for hepatitis C virus infection on proprotein convertase subtilisin/kexin type 9 level
Author(s) -
Torti Carlo,
Scaglione Vincenzo,
Cesana Bruno Mario,
Costa Chiara,
Marascio Nadia,
Schiaroli Elisabetta,
Busti Chiara,
Bastianelli Sabrina,
Mazzitelli Maria,
Trecarichi Enrico Maria,
Francisci Daniela
Publication year - 2021
Publication title -
health science reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.462
H-Index - 7
ISSN - 2398-8835
DOI - 10.1002/hsr2.273
Subject(s) - pcsk9 , kexin , medicine , proprotein convertase , hepatitis c virus , subtilisin , gastroenterology , immunology , ldl receptor , cholesterol , lipoprotein , virus , biology , biochemistry , enzyme
Background and aims Eradication of the hepatitis C virus (HCV) may affect proprotein convertase subtilisin/kexin type 9 (PCSK9) levels and cardiovascular risk. However, information regarding PCSK9 level after HCV eradication is lacking. Hence, in this case‐control retrospective study, we aimed to evaluate PCSK9 level from pretherapy baseline up to sustained virological response (SVR). Methods Eighty‐four patients treated with directly acting antivirals (DAAs) between July 2015 and May 2018 were enrolled. Differences in baseline PCSK9 level due to absence/presence of recorded baseline characteristics (covariates) were evaluated. Changes in PCSK9 levels from pretherapy to SVR (ΔPCSK9) and their correlations with the covariates were assessed. The repeated measures analysis of variance was used to investigate the differences in PCSK9 level from the baseline to the achievement of SVR due to absence/presence of any covariate. Results The mean age of the patients was 67.6 ± 11 years, and 53.6% were males. Baseline PCSK9 levels were statistically lower in patients using statins than in those not using statins (mean, 70.3 ± 43.1 ng/mL vs 271.8 ± 252.2 ng/mL; P = .017). PCSK9 level decreased significantly from baseline to the time of SVR (255 ± 248 ng/mL vs 169 ± 188 ng/mL; P < .001). PCSK9 levels were statistically higher in the HCV‐infected patients at baseline than in the control group (255 ± 248 vs 166.3 ± 120.2 ng/mL; P = .020); however, this difference was lost after achieving SVR (mean, 169 ± 188 vs 166.3 ± 120.2 ng/mL; P = .464). Changes in PCSK9 level was not statistically related to any of the recorded covariates. The PCSK9 mean level did not differ significantly with absence/presence of any covariate from pretherapy to SVR. Conclusions The reduction in mean PCSK9 level from baseline pretherapy to after HCV eradication was statistically significant. Whether PCSK9 is a new biomarker for cardiovascular risk in these patients remains to be ascertained.

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