Sa1083 Association of Low Density Lipoprotein and Sustained Virologic Response in Genotypes 2 and 3...
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AASLD Abstracts *Average (Standard Deviation) **Other Race: Hispanic (3, 7%), Middle Eastern (1, 2%) Treatment Outcomes, Frequency of Adverse Events and Change in Key Lab Parameters by Week of Therapy *N (%) *Average (Standard Deviation) Δ p-value comparing baseline to week 4 or week 12 <0.0001, paired t-test γ p-value comparing baseline to week 4 or week 12 <0.05, paired t-test Sa1081 Therapeutic Dose Effects of the Cyclophilin Inhibitor Alisporivir (ALV) on Circulating Bilirubin Concentrations in Healthy Subjects Steven J. Kovacs, June Ke, Kristina Dabovic, Avantika Barve, Daniel Stein Background: A transient hyperbilirubinemia associated with ALV has been observed in healthy subjects and CHC patients. Reversible drug-related hyperbilirubinemia is known to occur for several drugs by inhibition of BILI transport and/or conjugation. In Vitro, ALV inhibits the uptake transporters OATP1B1 and OATP1B3 (IC50 0.7 μM) and the efflux transporter MRP2 (Ki 5.9 μM) but does not inhibit the conjugating enzyme UGT1A1, all involved in the normal handling of BILI. Since ribavirin-associated hemolysis contributes to BILI changes that are evident in CHC patients, the time course of changes in BILI associated with the highest intended therapeutic exposure to ALV was investigated in healthy subjects to characterize the specific effect of ALV. The effect of ALV on the OATP1B1, 1B3, and MRP2 substrate valsartan was also investigated. Methods: ALV 600 mg BID was administered for 7 days followed by 600 mg QD for 1, 2, or 3 days to three groups of 16 healthy subjects (48 total) in 3 different drug-drug interaction studies. One group received 40 mg valsartan before and after ALV. Subjects known or suspected to have any inherited BILI disorder were excluded. Laboratory tests performed at baseline, on days 4, 7, 9, 10 /11, and end-of-study (14±1 days after the last dose). Results: All subjects completed the study and tolerated ALV well. Mean age 31 yrs; mean BMI 25.5 kg/m2. 47 male, 43 Caucasian. The most commonly reported AEs included headache, nausea, dry mouth, dizziness. Mean change from baseline increases of 9.9-11.3 μM (0.6-0.7 mg/dL; median 2.3-fold) in total BILI occurred between days 7 and 9 without coincident changes in other LFTs. Maximum total BILI concentration was 46 μM (2.7 mg/dL), observed on Day 9 in a 21 yo male whose baseline was 15 μM (0.9 mg/dL). All BILI increases were asymptomatic and reversible. Total BILI exceeded the ULN in 4 subjects (8.3%) and an increase in unconjugated (indirect) BILI predominated. Valsartan exposure increased ~6-fold. Conclusions: ALV inhibits OATP1B1, OATP1B3, and S-964 AASLD Abstracts MRP2 In Vivo causing increases in total BILI and valsartan. The smaller effect on BILI relative to valsartan suggests transport or clearance of BILI via additional pathways. Sa1082 Effect of Telaprevir on the Pharmacokinetics of Sirolimus in Two Post-Liver Transplant Recurrent HCV Patients Matthew Lincoln, Alex De La Vega, Madhavi Rudraraju Hepatitis C virus (HCV) is the most common etiology for liver transplantation with approxim- ately 30% of HCV infected liver transplant recipients dying, losing their allograft, or develop- ing cirrhosis due to HCV recurrence. Telaprevir is an inhibitor of the cytochrome P4503A pathway which is responsible for the metabolism of many pharmacologic agents including immunosuppressive agents in transplant recipients. A recent study showed significantly increased blood concentrations of cyclosporine and tacrolimus with concomitant use of telaprevir. Currently there is no published data on the effect of telaprevir on sirolimus pharmacokinetics in the liver transplant population. We present two cases of post-transplant recurrent HCV patients who remained on sirolimus while undergoing HCV treatment with telaprevir. Methods: The patients were admitted for close observation during the initiation of treatment and titration of immunosuppression. Telaprevir was given as a standard dose of 750mg orally q8h with a 20g fatty meal. Sirolimus was given daily at 0700. Patients had blood sirolimus levels drawn pre-telaprevir dose @ 0, 0.5h,1h,1.5h,2h,3h,4h,6h,8h,12h, and 20h with subsequent post telaprevir doses at the same intervals. The linear trapezoidal method was used to calculate Area Under Curve (AUC) of sirolimus post telaprevir doses. Sirolimus levels continued to be drawn daily for 1 week followed by twice a week levels thereafter. Results: For patient 1, outpatient dose of 2mg and 1mg alternating was reduced to 1mg daily on the day of admission. This patient received 1mg of sirolimus on days 1 and 2 and 0.5mg on day 7. After just 24 hours of starting telaprevir, sirolimus AUC(0-∞)= 400ng-h/mL, which is approximately 2 fold higher than the mean AUC concentration that had been reported in adult renal transplant patients who were on 2 mg a day. Sirolimus levels remained supratherapeutic on day 19. Immunosuppression was switched to cyclosporine after sirolimus was decreased to sub-therapeutic levels. As for patient 2, outpatient sirolimus dose was reduced from 1mg daily to 0.5mg on day of admission. 24 hours after the initiation of telaprevir, sirolimus AUC(0-∞)=236ng-h/mL. There was also 2 fold increase in “trough” concentrations over a period of 2 days. With a dose of 0.5mg twice a week, we were able to obtain therapeutic levels. Conclusions: Telaprevir significantly increases the blood concentration of sirolimus which could lead to serious or life-threatening adverse events. Although sirolimus steady state concentrations may not have been reached initially, our AUC approximations do establish an exponential increase in sirolimus concentrations after the initiation of telaprevir. The new protease inhibitors offer tempting treatment options in post-liver transplant recurrent HCV infection however they should be used with extreme caution and intense monitoring. Sa1083 Association of Low Density Lipoprotein and Sustained Virologic Response in Genotypes 2 and 3 Chronic Hepatitis C Patients Treated With Peginterferon and Ribavirin, a Single Center Study Payam Afshar, Anders H. Nyberg, Raoul J. Burchette, Lisa M. Nyberg Introduction: The entry of the hepatitis C virus (HCV) into the hepatocyte is initiated by host low-density lipoprotein (LDL) receptors. Subsequently, HCV exploits the lipid metabolism of the hepatocyte for its replication and assembly process based on cell culture studies. Recent retrospective data have identified a correlation of pretreatment elevated LDL, low HDL, statin use, and increased likelihood of sustained virologic response (SVR) in genotype 1 HCV patients treated with peginterferon (PEG-IFN) and ribavirin therapy, yet studies were underpowered to make this correlation for genotypes 2 and 3 HCV patients. This study was designed to identify if these pre-treatment parameters correlate with SVR in genotypes 2 and 3 HCV based on a retrospective analysis of a large database from Kaiser Permanente, San Diego. Methods: A total of 189 genotype 2 and 197 genotype 3-infected patients were identified in the system between March 2000 and February 2010. Included were 129 genotype 2 and 132 genotype 3 patients in the study based on the presence of lipid profiles being identified within 24 months prior to initiation of peginterferon and ribavirin therapy. Other pre-treatment patient parameters included calculated BMI, age, comprehensive meta- bolic panel, complete blood counts, INR, HCV RNA levels, and statin use. Results: Overall SVR for genotype 2 was 85% and for genotype 3 was 71%. Mean, median and standard deviation LDL for genotypes 2 and 3 are listed in the first table. Using students t-test for analysis of continuous variables, LDL was significantly higher in the genotype 2 SVR group compared to the genotype 2 non-SVR group (p=0.02); while there was no significant difference in genotype 3. Using our local lab cut-off for normal LDL as <100, there was a highly significant correlation between SVR and high LDL (>100) for genotype 2 but not genotype 3 (chi square, p<0.005). LDL levels did not correlate with markers for severity of liver disease including platelet, INR, albumin, or bilirubin (correlation coefficients range: -0.06 to 0.28). No significant difference was noted in BMI of SVR vs. non-SVR in either genotype. There was no correlation of BMI and presence or absence lipid profile in our patient population of either genotype. There were too few patients with concomitant statin use in this study to assess a correlation with SVR in either genotype. Conclusion: In accordance with prior HCV genotype 1 data, HCV genotype 2 SVR correlates significantly with higher pre-treatment LDL levels in comparison to HCV genotype 2 non-SVR patients. This correla- tion was not noted in HCV genotype 3 patients and could be due to under-powering of this study or a genotype difference in lipid metabolism. Further investigation is ongoing with Kaiser Permanente Los Angeles and Northern California to accumulate more patients in this retrospective study. HCV genotype, virologic response, and LDL levels
Transcript of Sa1083 Association of Low Density Lipoprotein and Sustained Virologic Response in Genotypes 2 and 3...
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*Average (Standard Deviation) **Other Race: Hispanic (3, 7%), Middle Eastern (1, 2%)Treatment Outcomes, Frequency of Adverse Events and Change in Key Lab Parametersby Week of Therapy
*N (%) *Average (Standard Deviation) Δ p-value comparing baseline to week 4 or week12 <0.0001, paired t-test γ p-value comparing baseline to week 4 or week 12 <0.05, pairedt-test
Sa1081
Therapeutic Dose Effects of the Cyclophilin Inhibitor Alisporivir (ALV) onCirculating Bilirubin Concentrations in Healthy SubjectsSteven J. Kovacs, June Ke, Kristina Dabovic, Avantika Barve, Daniel Stein
Background: A transient hyperbilirubinemia associated with ALV has been observed inhealthy subjects and CHC patients. Reversible drug-related hyperbilirubinemia is known tooccur for several drugs by inhibition of BILI transport and/or conjugation. In Vitro, ALVinhibits the uptake transporters OATP1B1 and OATP1B3 (IC50 0.7 μM) and the effluxtransporter MRP2 (Ki 5.9 μM) but does not inhibit the conjugating enzyme UGT1A1, allinvolved in the normal handling of BILI. Since ribavirin-associated hemolysis contributesto BILI changes that are evident in CHC patients, the time course of changes in BILI associatedwith the highest intended therapeutic exposure to ALV was investigated in healthy subjectsto characterize the specific effect of ALV. The effect of ALV on the OATP1B1, 1B3, andMRP2 substrate valsartan was also investigated. Methods: ALV 600 mg BID was administeredfor 7 days followed by 600 mg QD for 1, 2, or 3 days to three groups of 16 healthy subjects(48 total) in 3 different drug-drug interaction studies. One group received 40 mg valsartanbefore and after ALV. Subjects known or suspected to have any inherited BILI disorder wereexcluded. Laboratory tests performed at baseline, on days 4, 7, 9, 10 /11, and end-of-study(14±1 days after the last dose). Results: All subjects completed the study and tolerated ALVwell. Mean age 31 yrs; mean BMI 25.5 kg/m2. 47 male, 43 Caucasian. The most commonlyreported AEs included headache, nausea, dry mouth, dizziness. Mean change from baselineincreases of 9.9-11.3 μM (0.6-0.7 mg/dL; median 2.3-fold) in total BILI occurred betweendays 7 and 9 without coincident changes in other LFTs. Maximum total BILI concentrationwas 46 μM (2.7 mg/dL), observed on Day 9 in a 21 yo male whose baseline was 15 μM(0.9 mg/dL). All BILI increases were asymptomatic and reversible. Total BILI exceeded theULN in 4 subjects (8.3%) and an increase in unconjugated (indirect) BILI predominated.Valsartan exposure increased ~6-fold. Conclusions: ALV inhibits OATP1B1, OATP1B3, and
S-964AASLD Abstracts
MRP2 In Vivo causing increases in total BILI and valsartan. The smaller effect on BILI relativeto valsartan suggests transport or clearance of BILI via additional pathways.
Sa1082
Effect of Telaprevir on the Pharmacokinetics of Sirolimus in Two Post-LiverTransplant Recurrent HCV PatientsMatthew Lincoln, Alex De La Vega, Madhavi Rudraraju
Hepatitis C virus (HCV) is the most common etiology for liver transplantation with approxim-ately 30% of HCV infected liver transplant recipients dying, losing their allograft, or develop-ing cirrhosis due to HCV recurrence. Telaprevir is an inhibitor of the cytochrome P4503Apathway which is responsible for the metabolism of many pharmacologic agents includingimmunosuppressive agents in transplant recipients. A recent study showed significantlyincreased blood concentrations of cyclosporine and tacrolimus with concomitant use oftelaprevir. Currently there is no published data on the effect of telaprevir on sirolimuspharmacokinetics in the liver transplant population. We present two cases of post-transplantrecurrent HCV patients who remained on sirolimus while undergoing HCV treatment withtelaprevir. Methods: The patients were admitted for close observation during the initiationof treatment and titration of immunosuppression. Telaprevir was given as a standard doseof 750mg orally q8h with a 20g fatty meal. Sirolimus was given daily at 0700. Patients hadblood sirolimus levels drawn pre-telaprevir dose @ 0, 0.5h,1h,1.5h,2h,3h,4h,6h,8h,12h,and 20h with subsequent post telaprevir doses at the same intervals. The linear trapezoidalmethod was used to calculate Area Under Curve (AUC) of sirolimus post telaprevir doses.Sirolimus levels continued to be drawn daily for 1 week followed by twice a week levelsthereafter. Results: For patient 1, outpatient dose of 2mg and 1mg alternating was reducedto 1mg daily on the day of admission. This patient received 1mg of sirolimus on days 1and 2 and 0.5mg on day 7. After just 24 hours of starting telaprevir, sirolimus AUC(0-∞)=400ng-h/mL, which is approximately 2 fold higher than the mean AUC concentration thathad been reported in adult renal transplant patients who were on 2 mg a day. Sirolimus levelsremained supratherapeutic on day 19. Immunosuppressionwas switched to cyclosporine aftersirolimus was decreased to sub-therapeutic levels. As for patient 2, outpatient sirolimus dosewas reduced from 1mg daily to 0.5mg on day of admission. 24 hours after the initiation oftelaprevir, sirolimus AUC(0-∞)=236ng-h/mL. There was also 2 fold increase in “trough”concentrations over a period of 2 days. With a dose of 0.5mg twice a week, we wereable to obtain therapeutic levels. Conclusions: Telaprevir significantly increases the bloodconcentration of sirolimus which could lead to serious or life-threatening adverse events.Although sirolimus steady state concentrations may not have been reached initially, ourAUC approximations do establish an exponential increase in sirolimus concentrations afterthe initiation of telaprevir. The new protease inhibitors offer tempting treatment options inpost-liver transplant recurrent HCV infection however they should be used with extremecaution and intense monitoring.
Sa1083
Association of Low Density Lipoprotein and Sustained Virologic Response inGenotypes 2 and 3 Chronic Hepatitis C Patients Treated With Peginterferonand Ribavirin, a Single Center StudyPayam Afshar, Anders H. Nyberg, Raoul J. Burchette, Lisa M. Nyberg
Introduction: The entry of the hepatitis C virus (HCV) into the hepatocyte is initiated by hostlow-density lipoprotein (LDL) receptors. Subsequently, HCV exploits the lipid metabolism ofthe hepatocyte for its replication and assembly process based on cell culture studies. Recentretrospective data have identified a correlation of pretreatment elevated LDL, low HDL,statin use, and increased likelihood of sustained virologic response (SVR) in genotype 1HCV patients treated with peginterferon (PEG-IFN) and ribavirin therapy, yet studies wereunderpowered to make this correlation for genotypes 2 and 3 HCV patients. This study wasdesigned to identify if these pre-treatment parameters correlate with SVR in genotypes 2and 3 HCV based on a retrospective analysis of a large database from Kaiser Permanente,San Diego. Methods: A total of 189 genotype 2 and 197 genotype 3-infected patients wereidentified in the system between March 2000 and February 2010. Included were 129genotype 2 and 132 genotype 3 patients in the study based on the presence of lipid profilesbeing identified within 24 months prior to initiation of peginterferon and ribavirin therapy.Other pre-treatment patient parameters included calculated BMI, age, comprehensive meta-bolic panel, complete blood counts, INR, HCV RNA levels, and statin use. Results: OverallSVR for genotype 2 was 85% and for genotype 3 was 71%. Mean, median and standarddeviation LDL for genotypes 2 and 3 are listed in the first table. Using students t-test foranalysis of continuous variables, LDL was significantly higher in the genotype 2 SVR groupcompared to the genotype 2 non-SVR group (p=0.02); while there was no significantdifference in genotype 3. Using our local lab cut-off for normal LDL as <100, there was ahighly significant correlation between SVR and high LDL (>100) for genotype 2 but notgenotype 3 (chi square, p<0.005). LDL levels did not correlate with markers for severity ofliver disease including platelet, INR, albumin, or bilirubin (correlation coefficients range:-0.06 to 0.28). No significant difference was noted in BMI of SVR vs. non-SVR in eithergenotype. There was no correlation of BMI and presence or absence lipid profile in ourpatient population of either genotype. There were too few patients with concomitant statinuse in this study to assess a correlationwith SVR in either genotype. Conclusion: In accordancewith prior HCV genotype 1 data, HCV genotype 2 SVR correlates significantly with higherpre-treatment LDL levels in comparison to HCV genotype 2 non-SVR patients. This correla-tion was not noted in HCV genotype 3 patients and could be due to under-powering ofthis study or a genotype difference in lipid metabolism. Further investigation is ongoingwith Kaiser Permanente Los Angeles and Northern California to accumulate more patientsin this retrospective study.HCV genotype, virologic response, and LDL levels
Mean BMI (standard deviation) and Correlation with Lipid Profile Presence or Absence
Sa1084
Current and Future Disease Progression of HCV-Infected Patients AmongDifferent Age CohortsMartin Zalesak, Kevin Francis, Ann Kwong, Hong Li, Derek Martyn, Leslie S. Orne,Amanda Smith, Kyle Hvidsten
BACKGROUND: In 2008, the estimated U.S. prevalence of patients with anti-HCV antibodywas 3.6 million, with 1.1- and 1.6-million individuals estimated to be diagnosed andundiagnosed with chronic HCV-infection, respectively. Chronic HCV can lead to advancedliver disease (ALD), including cirrhosis, decompensated cirrhosis, and liver cancer/trans-plantation. We aimed to determine annual ALD progression rates within the HCV-infectedpopulation by age cohort, and to project ALD prevalence in U.S. HCV-infected patientsthrough 2015, assuming lack of treatment.METHODS: Two claims databases, PharMetrics (representative US commercial payers; IMSLifeLink: Health Plan Claims Database, IMS Health Incorporated, all rights reserved) andMedicare (100% inpatient/outpatient claims, 5% carrier data), were analyzed to determineALD progression rate by identifying the number of HCV patients with and without ALDusing ICD-9 codes. Future ALD prevalence was projected using progression and mortalityrate trends from these databases.RESULTS: The number of patients diagnosed with ALD was tallied over a 3-year interval.1.1-million diagnosed chronic HCV-infected patients (2008) were apportioned between agecohorts: 16-44 (16.1%), 45-54 (38.8%), 55-64 (36.4%) and 65+ (8.6%). The proportionof diagnosed HCV patients with ALD increased with age: the 16-44, 45-54 and 55-64cohorts had 9.1%, 17.1% and 22.4% of patients with ALD, respectively. An exception tothis trend, 19.2% of patients 65+ had ALD, as all-cause mortality outpaced ALD progression.Among the most populous cohort (45-64), 4.4% of non-ALD HCV-infected patients pro-gressed to ALD annually; 11.5% of cirrhotics progressed to decompensated cirrhosis; 3.2%to liver cancer and/or transplant. Without treatment, pre-2009 diagnosed HCV patientswith ALD is projected to rise from 198,000 (2008) to 304,000 (2015). Applying identicalprogression rates, ~299,000 undiagnosed patients are estimated to progress to ALD between2008 and 2015 without treatment.CONCLUSIONS: In 2008, 45-64-year-old patients diagnosed with HCV represented themajority of HCV-infections. A significant proportion are expected to progress to ALD annu-ally, indicating an urgency to diagnose and treat before costly and irreversible complicationsdevelop. Without treatment, the number of ALD patients is expected to triple from 198,000in 2008 to 603,000 in 2015.
FIGURE: Projected HCV patients with ALD by diagnosis state
Sa1085
Burden of Illness in Treatment NaïVE Hepatitis C (HCV) Patients in the USAntoine El Khoury, Girish Prajapati, Jeffrey Vietri
Background: Mortality and morbidity related to existing HCV infection is expected to increasein coming decades. The objective of this study was to assess productivity loss, healthcareresource utilization, and health related quality of life (HRQoL) in treatment naive HCVpatients in the US. Methods: Data were analyzed from the 2010 wave of US National Healthand Wellness Survey (NHWS) conducted by Kantar Health. Among patients' ≥18 years
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without HBV or HIV infection, treatment naïve HCV patients were matched using propensityscore matching methodology with those without HCV on age, gender, race, education, sexualorientation, marital status, current alcohol, smoking and exercise status, and comorbidities(excluding liver disease). The two groups were compared on work productivity [percentageof work time missed (absenteeism) and percentage of impairment experienced while at work(presenteeism) because of one's health in past seven days] and activity impairment; indirectcosts [annual lost wages due to absenteeism and presenteeism]; healthcare resource utilization[outpatient and ER visits, hospitalization in past 6 months] and related direct costs; andHRQoL [Medical Outcomes Study 12-Item Short Form Survey Instrument based Physicaland Mental Component Summary (PCS and MCS), and Health Utility score]. Comparisonswere made using chi-square for categorical, and independent samples t-tests and Mann-Whitney-U non-parametric tests for continuous outcomes. Results: Of 74,149 eligible subjectsfrom NHWS database, 306 treatment naïve HCV infected patients and 306 matched non-HCV individuals were analyzed. The mean age of HCV patients was 52.6 years and 64%were male. Non-HCV individuals were, on average, 54.3 years old and 60 % were male.HCV patients reported higher presenteeism (23.16% vs. 13.06%), overall work impairment(26.16% vs. 14.91%), activity impairment (42.16% vs. 27.29%), and greater mean indirectcosts ($10,316 vs. $5468.56) than non-HCV subjects (all P<0.001). On average, outpatient(12.24 vs. 8.22; P<0.001) and ER (0.76 vs. 0.54; P=0.023) visits, total healthcare relateddirect costs ($22,818.48 vs. $15,361.64; P=0.001) were higher and poorer HRQoL (PCS40.20 vs. 44.89; MCS 43.72 vs. 48.62; SF6D utility score 0.65 vs. 0.73; all P<0.001) wasreported in HCV patients, when compared to non-HCV subjects. Differences in absenteeismand hospitalizations for the two groups were not statistically significant. Conclusion: Treat-ment naïve HCV patients were associated with higher productivity loss, more healthcareresource utilization and costs, and poorer HRQoL when compared to non-HCV individuals.
Sa1086
Characterization of a Cohort of Incident Hepatitis C Patients in the US (2005-2010): Comorbidities, use of Medications and Diagnostic TestsSalil D. Sheth, Montserrat Vera-Llonch, Joseph P. Lynch, Winifred Werther, RaymondRubin
Objective. To describe the clinical characteristics of an incident cohort of patients withchronic hepatitis C (HCV) virus infection in the US, including prevalence of comorbidities anduse of medication and diagnostic tests. Methods. Data from the American GastroenterologicalAssociation Digestive Health Outcomes Registry (AGA-Registry) and the MedAssurant Med-ical Outcomes Research on Economics and Effectiveness (MORE2) Registry (2005-2010)were analyzed. Incident cases of chronic HCV infection (CHC) were identified based on: a)≥2 ICD-9-CM diagnosis codes for CHC or ≥1 codes for acute HCV infection with ≥1codes for CHC (the earliest of such claims was designated the “index date”); b) no evidenceof HCV infection or treatment prior to index date; c) at least 12 months of continuousenrollment before and after index date; and d) age ≥ 18 years. CHC treatment was basedon pharmacy claims for pegylated interferon or ribavirin post-index date. Co-morbiditiesand medication use were ascertained based on ICD-9 CM and NDC codes, while use ofdiagnostic tests for anti-HCV antibody, qualitative, or quantitative RNA was identified basedon procedure codes. Results. 32,194 patients met study criteria. Mean (SD) age was 53(±13) years, and 52% of patients were male; insurance source was Medicaid for 51.3% ofpatients. Mean (SD) follow-up was 27 (±12) months. Pre-existing comorbidities included:hypertension (35%), mental health disease (anxiety, depression, schizophrenia or bipolardisorder) (29%), diabetes (27%), coronary heart disease (16%), alcohol dependence (14%),drug dependence (14%), cirrhosis (8%), and heart failure (8%). Common medications pre-index date included calcium-channel blockers (15%), benzodiazepines (13%), statins (13%),and oral antihypergycemics (12%). While 65% (n=20,944) of patients had evidence of anti-HCV antibody, RNA testing (qualitative or quantitative) in the 60-days prior to diagnosisor any time thereafter, only 48.3% had a quantitative RNA test. Median time (Inter QuartileRange, IQR) from diagnosis to first HCV test was 3 (-1-33) weeks. Overall, 9% (n=2,845)of patients had evidence of CHC treatment which varied by insurance (15% [Commercial],8% [Medicaid], and 5% [Medicare]). Median (IQR) time from diagnosis to treatment initiationwas 22 (11-47) weeks. 75% (n=2,131) of treated patients had evidence of RNA quantitativetesting in the six-months prior to treatment initiation; corresponding estimate post-treatmentinitiation was 67% and median (IQR) time to quantitative RNA test was 9 (5-15) weeks.Conclusion. In a cohort of HCV-infected patients (2005-2010) with predominantly Medicaidinsurance, the prevalence of comorbidities was high and few (9%) patients were treated.Findings also suggest opportunities for quality improvement with respect to use of diagnostictests and treatment in this patient population.
Sa1087
Less Established Risk Factors are Common in Asian Americans With HepatitisC Virus: A Case-Control StudyKevin C. Kin, Brian Lin, Kevin T. Chaung, Nghiem B. Ha, Huy N. Trinh, Ruel T. Garcia,Huy A. Nguyen, Khanh K. Nguyen, Brian S. Levitt, Eduardo B. da Silveira, Mindie H.Nguyen
Purpose: The Center for Disease Control recommends screening for hepatitis C virus (HCV)in those who have had illicit injected drug use, clotting factors prior to 1987, or bloodtransfusion or organ transplant prior to 1992; however, this data is derived primarily fromnon-Hispanic White, non-Hispanic Black, and Hispanic populations. The purpose of thisstudy was to examine both traditional and non-traditional risk factors for HCV in AsianAmericans. Methods: This was a case control study with the cases being 437 consecutivepatients assessed for chronic hepatitis C between 1/2001 and 12/2008 at two U.S. gastroenter-ology clinics. Controls included 437 patients with negative HCV antibody test between 1/2001 and 2/2011 referred for non-liver related reasons at the same clinics. Controls werematched at a one to one ratio for sex, age (±5 years), and ethnicity. We determined relevantpatient history and risk factors via treating physicians' encounter note at patients' first clinicvisit. Results: Cases and controls were well matched with similar median age (50 years),proportion of male patients (67%), and Asians (88%). Established risk factors were elicitedat routine clinical visits in the majority (71%) of non-Asian patients with positive anti-HCV
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