Browsing by Subject "Hepatitis C"
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Item Healthcare costs and resource utilization in treated versus untreated chronically infected hepatitis C patients(2014-08) Kim, Yoona Amy; Rascati, Karen L.; Wilson, James P.Successful treatment of chronic hepatitis C virus (HCV) leads to significant benefits in both hepatic and extrahepatic morbidity and mortality. However, treatment is costly and onerous. The purpose of this study was to evaluate the resource utilization and healthcare costs of chronic HCV patients who are treated versus those who are not treated. Patients eligible for this study were Texas Medicaid patients ≥18 and ≤63 years who had evidence of chronic HCV during the identification period (1/1/07-9/30/11) and continuous enrollment throughout the analysis period. High dimensional propensity scoring techniques were used to match treated vs. untreated patients (1:2 ratio). Unadjusted and adjusted analyses compared the healthcare costs and utilization between patient cohorts at 6 and 18 months. For those treated, adherence was measured by proportion of days covered and persistence was evaluated as a gap in medication (of one fill) as determined by refill records. There were a total of 24,032 patients identified with chronic HCV. After high dimensional propensity scoring, there were no significant differences in key clinical and demographic characteristics between treated (n=939) and untreated (n=1878) cohorts. Over 97% of patients had evidence of end stage liver disease at baseline. Based on adjusted analyses of total costs using a generalized linear regression model, the mean difference in costs between the treated vs. untreated patients was $13,960 (SE $458, p<0.001). At 18 months of follow-up, the adjusted mean all-cause costs were $20,834 higher for treated patients (n=456) compared to those untreated (n=849) (p<0.001); however, mean outpatient costs were $1,894 (SE $274) less in treated vs. untreated patients. For those treated, the average HCV medication PDC was 71%, and by the end of 24 weeks, only 42.3% of patients remained on HCV therapy. This study did not show short-term cost offsets, but the sub-analysis following patients for 18 months showed trends in downstream cost offsets. Most patients had advanced liver disease, reducing the chances of successful treatment and averting liver disease sequelae. Earlier identification and treatment could bend the cost curve before these patients reached the more advanced stages seen in this costly cohort.Item Impact of surveillance and early-stage versus late-stage hepatocellular carcinoma (HCC) detection on patient overall survival(2018-08) Bui, Cat Nguyen; Rascati, Karen L.; Gordon, Stuart; Lawson, Kenneth A; Wilson, JamesThis study investigated the impact of surveillance and early-stage versus late-stage hepatocellular carcinoma (HCC) detection on patients’ overall survival using a national US health plan database (1/1/2007 through 12/31/2012). Eligible Medicare patients were included in this two-phase study. Phase A assessed cirrhotic patients with surveillance versus no-surveillance from the cirrhosis diagnosis index date. Phase B assessed HCC patients with early-stage versus late-stage HCC detection from the HCC diagnosis index date. Phase A included 6,131 cirrhotic patients (surveillance N=3,376, no-surveillance N=2,755); 73% (N=4,443) decompensated and 27% (N=1,688) compensated patients; 145 (2.4%) with HCC; and 814 (13.3%) deaths. Among all cirrhotic patients, the surveillance cohort had a 28% higher risk of death compared to the no-surveillance cohort (adjusted hazard ratio [HR]=1.28; 95% CI=1.10-1.49; P<0.001); a non-statistically significant reduced risk among the subgroup of compensated-only patients (adjusted HR=0.68; 95% CI=0.46-1.02; P=0.06); a non-significant increased risk among cirrhotic patients with HCC (adjusted HR=1.18; 95% CI=0.70-1.98; P=0.54). The surveillance cohort had no significant difference in the odds of early-stage HCC detection compared to the no-surveillance cohort (adjusted odds ratio [OR]=1.77; 95% CI=0.80-3.91; P=0.16). Decompensated cirrhotic patients had higher odds of early-stage HCC detection compared to compensated patients (adjusted OR=5.12; 95% CI=1.12-23.35; P=0.03). Phase B (HCC) patients included 580 early-stage and 1,173 late-stage diagnoses; half (N=886) had cirrhosis pre-HCC index diagnosis (compensated: 13.0%, N=115; decompensated: 87.0%, N=771); 10% (N=181) received one regular surveillance a year pre-HCC index; 36 % (N=636) received HCC treatment (82.1%; N=522/636 received systemic chemotherapy); and 587 (33.5%) patients died. Patients with late-stage HCC diagnoses had a 60% higher risk of death compared to early-stage HCC diagnoses (adjusted HR=1.60; 95% CI=1.23-2.09; P=0.001). Patients with one regular surveillance a year pre-HCC diagnosis had a 29% lower risk of death compared to patients without regular surveillance (adjusted HR=0.71; 95% CI=0.51-0.97; P=0.03). This study found that surveillance had no survival benefit among all cirrhotic patients; however, surveillance reduced the risk of death among compensated cirrhotic patients, although non-significant. HCC patients with at least one regular surveillance a year pre-HCC diagnosis had a lower risk of death. Surveillance should be provided to patients before HCC diagnosis.Item Substrates and Regulation of the RNA Phosphatase DUSP11(2017) Lam, Victor; Sullivan, ChrisDUSP11 (Dual-specificity phosphatase 11) is an understudied human RNA phosphatase with an unclear function. DUSP11 converts 5′ triphosphates on RNAs into 5′ monophosphates, and it is required for the efficient biogenesis of some bovine leukemia virus-encoded microRNAs1. However, there is little understanding of DUSP11 substrates and the biochemical pathways it participates in. Here, I test the activity of DUSP11 on potential viral and transposon RNA substrates as well as the potential regulation of DUSP11 via its C terminus phosphorylation. My in vitro experiments show that DUSP11 can act on triphosphorylated viral and Alu RNAs and render them susceptible to XRN-1-mediated degradation. In contrast, knockout of the DUSP11 homolog PIR-1 in C. elegans did not lead to the accumulation of RNAs derived from the transposable element CELE45, implying possibly different functionality for the phosphatase in worms and mammals. My work also shows that mutations of individual phosphorylation sites of the DUSP11 C terminus do not substantially alter activity in a mammalian cell-based assay.