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Publications (3)9.85 Total impact

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    ABSTRACT: Noninvasive markers of liver fibrosis have not been extensively studied in patients with chronic hepatitis B virus (HBV) infection. Our aim was to evaluate the capacity of FibroSURE, one of the two noninvasive fibrosis indices commercially available in the United States, to identify HBV infected patients with moderate to severe fibrosis.
    BMC Gastroenterology 07/2014; 14(1):118. · 2.11 Impact Factor
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    ABSTRACT: OBJECTIVE:: We sought to develop a score to predict sustained virological response (SVR) in racially diverse HIV/HCV co- and HCV mono-infected pegylated interferon (PEG-IFN)/ribavirin (RBV) treated patients. METHODS:: We retrospectively evaluated 374 patients (259 mono-, 115 co-infected) treated at a single tertiary care center. IL28B rs12979860 SNP genotyping was performed in 335 and plasma CXCL10 levels were measured by ELISA in 171 patients. RESULTS:: 64.9% of patients were Caucasian, 17.2% were African-American, 76.5% were HCV genotype 1-infected, and 49.3% had advanced fibrosis. SVR was achieved by 151 (40.4%) patients, 106 (40.9%) mono- and 45 (39.1%) co-infected. Patients with IL28B C/C genotype were significantly more likely to achieve an SVR compared to non-C/C genotype patients, but only if they were infected with HCV genotypes 1/4 (59.1% vs. 21.1%, p<0.0001). No significant differences existed in IL28B predictive capacity between co- and mono-infected patients. Pretreatment CXCL10 levels were significantly higher in non-responders, both mono- and co-infected, compared to SVR patients (p=0.0018). Co-infected patients had higher CXCL10 levels compared to mono-infected patients (p=0.03). The combination of IL28B genotype, pretreatment CXCL10 and HCV RNA levels, and HCV genotype had the best ability to predict treatment response in both patient groups (AUROC=0.85). Among all patients, a cutoff score ≥-0.94 had sensitivity of 0.93 and specificity of 0.59. In co-infected patients, a score ≥-0.55 had sensitivity of 0.81 and specificity of 0.80. CONCLUSIONS:: IL28B genotype, pretreatment CXCL10 and HCV RNA levels have very good capacity to predict PEG-IFN/RBV treatment outcome in both HIV/HCV co- and HCV mono-infected patients.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 12/2012; · 4.65 Impact Factor
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    ABSTRACT: Noninjection drug use, although recognized as an emerging risk factor for acquisition of other blood-born pathogens, is still unconfirmed as a route of hepatitis C virus (HCV) transmission. Our goal was to measure HCV exposure and prevalence in noninjection drug users (NIDUs). Fifty-seven NIDUs were screened by extensive questionnaire to exclude prior injection drug use and evaluated for HCV-specific serologic and cellular immune responses. HCV-specific T-cell responses were measured using interferon-gamma (IFN-γ) enzyme-linked immunospot (ELISpot) assay with overlapping HCV peptides covering the entire HCV genome. Fifteen individuals who never used illicit drugs served as negative controls. Eleven people with no history of injecting drug use (19.3%) were HCV seropositive: seven with chronic HCV infection and four with previously resolved infection. Of 51 NIDUs with ELISpot results, HCV-specific cellular immunity was detected in 5 (9.8%). These responses were relatively weak and narrow. We did not find significant associations between HCV-specific immune responses and noninjection drug use practices. Subjects with HCV-specific immunity, however, were significantly more likely to have bought sex in the past 6 months, to have had more casual partners of the opposite sex in the last 6 months, and those partners were more likely to have ever injected drugs compared to subjects without HCV-specific immunity. In summary, we found serologic or cellular HCV-specific immune responses in 27.5% of NIDUs. Our results suggest that sexual behaviour associated with noninjection drug use might be a risk factor for HCV acquisition. Additional studies are needed to precisely determine the practices that lead to HCV exposure among this population.
    Journal of Viral Hepatitis 08/2012; 19(8):554-9. · 3.08 Impact Factor