The effect of hepatitis C virologic clearance on cardiovascular disease biomarkers in human immunodeficiency virus/hepatitis C virus coinfection.
BACKGROUND
Successful hepatitis C virus (HCV) treatment may reduce cardiovascular disease (CVD) risk and improve levels of CVD biomarkers produced outside the liver (nonhepatic biomarkers).


METHODS
Stored serum or plasma from before and 24 weeks after end of HCV treatment (EOT) from human immunodeficiency virus (HIV)/HCV-coinfected subjects who received up to 72 weeks of peginterferon/ribavirin, 27 with and 27 without sustained virologic response (SVR) matched by race, ethnicity and sex, were tested for nonhepatic (soluble intercellular adhesion molecule-1 [sICAM-1], soluble P-selectin [sP-selectin], interleukin [IL]-6, d-dimer, and lipoprotein-associated phospholipase A2 [Lp-PLA2]) and hepatic (cholesterol and high-sensitivity C-reactive protein) CVD and macrophage activation markers (soluble CD163 [sCD163] and soluble CD14). Changes in biomarkers and their association with SVR were examined by t tests or Wilcoxon tests and regression models.


RESULTS
Of the 54 subjects, 30 were white, 24 were black, and 44 were male. Pretreatment levels of nonhepatic biomarkers were high: sICAM-1 overall median, 439.2 ng/mL (interquartile range [IQR], 365.6-592.8]; sP-selectin, 146.7 ng/mL (IQR, 94.1-209.9), and IL-6, 2.32 pg/mL (IQR, 1.61-3.49). Thirty-seven of 52 (71%) subjects had Lp-PLA2 >235 ng/mL. Sustained virologic response was associated with decrease in sICAM-1 (P = .033) and sCD163 (P = .042); this result was attenuated after controlling for changes in the alanine aminotransferase level. At 24 weeks after EOT, 17 (63%) SVRs had Lp-PLA2 >235 ng/mL vs 25 (93%) non-SVRs (P = .021).


CONCLUSIONS
Hepatitis C virus clearance may reduce hepatic and, subsequently, systemic inflammation and CVD risk in HIV/HCV coinfection.
Department of Medicine , David Geffen School of Medicine at University of California, Los Angeles.
Kara W
KW
Chew
Department of Biostatistics , Harvard School of Public Health , Boston, Massachusetts.
Lei
L
Hua
Department of Medicine , David Geffen School of Medicine at University of California, Los Angeles.
Debika
D
Bhattacharya
Department of Medicine , University of Pittsburgh School of Medicine , Pennsylvania ; Sheikh Khalifa Medical City , Abu Dhabi , United Arab Emirates.
Adeel A
AA
Butt
Department of Medicine , David Geffen School of Medicine at University of California, Los Angeles.
Lorelei
L
Bornfleth
Department of Medicine , Harvard Medical School and Massachusetts General Hospital.
Raymond T
RT
Chung
Center for Biostatistics in AIDS Research , Harvard School of Public Health , Boston, Massachusetts.
Janet W
JW
Andersen
Department of Medicine , David Geffen School of Medicine at University of California, Los Angeles.
Judith S
JS
Currier
HIV/HCV coinfection; cholesterol; macrophage activation; sustained virologic response; vascular adhesion molecules