Ali Hariri

Takeda California, Inc., San Diego, California, United States

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Publications (10)28.37 Total impact

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    ABSTRACT: The objective of this study was to assess the utility of hyperuricemia as a marker for diabetes and prediabetes (impaired fasting glucose) and insulin resistance in young adults. Using Cox proportional hazards regression models, the authors analyzed 15-year follow-up data on 5,012 persons in 4 US cities who were aged 18-30 years and diabetes-free at the time of enrollment. At baseline (1986), 88% of participants had a body mass index (weight (kg)/height (m)(2)) less than 30. During the follow-up period (through 2001), the incidence rates of diabetes and prediabetes (insulin resistance and impaired fasting glucose) were higher among persons with greater serum urate concentrations. In multivariable Cox regression analyses that adjusted for age, gender, race, body mass index, family history of diabetes, diastolic blood pressure, total cholesterol, smoking, and alcohol use, the hazard ratios for diabetes, insulin resistance, and prediabetes among persons with hyperuricemia (serum urate level >7 mg/dL vs. ≤7.0 mg/dL) were 1.87 (95% confidence interval (CI): 1.33, 2.62), 1.36 (95% CI: 1.23, 1.51), and 1.25 (95% CI: 1.04, 1.52), respectively. This observation was generally consistent across subgroups. The authors conclude that hyperuricemia in the midtwenties is an independent marker for predicting diabetes and prediabetes among young adults in the subsequent 15 years.
    American journal of epidemiology 07/2012; 176(2):108-16. DOI:10.1093/aje/kws002 · 4.98 Impact Factor
  • Alex Yang · Will Harrison · Ali Hariri
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    ABSTRACT: On average ESRD patients are hospitalized twice yearly for 12 days a year (USRDS 2011 Ann. Report). Hb levels decline immediately post-hospitalization, requiring extended periods for recovery and elevated ESA dosing for >1 year (Solid et al. Hemodial Int. 2007). We evaluated post-hospitalization anemia trends and ESA use in ESRD.Data from an LDO (N=273,877 pts; Q1 2008–Q1 2011) were evaluated for post-hosp Hb change (difference, pre- and post-hosp Hb measurement), time to Hb recovery (time from discharge to when Hb levels ≥ pre-hosp level), time to ESA recovery (time from discharge until 3 consecutive non-zero epoetin doses ≤ pre-hosp dose) and incremental ESA (sum of all differences from last pre-hosp dose until ESA recovery, 6 months if no recovery, or end of follow-up for long-term follow-up population).62% of all hospitalizations were associated with declining Hb (mean, -1.29 g/dL; Figure); 54% of these never returned to pre-hosp levels. Among hospitalizations that experienced a Hb drop and eventually recovered Hb (mean recovery time, 42 days), 73% used a mean 56K U of incremental epoetin until recovery; dose was recovered within 68 days on average. For the remaining 27% who never returned to pre-hosp ESA dose, an additional 266K U of epoetin were utilized.The majority of hospitalizations (∼2/3) had considerable post-hosp Hb drops (mean >1 g/dL), with >50% permanently reduced. ∼1.5 months were needed to recover Hb, with elevated ESA doses for >2 months. ESA dose was permanently elevated in 27% of hospitalizations that recovered Hb. Strategies to address post-hosp anemia may mitigate the protracted recovery time and increased ESA use.
    06/2012; 31(2):A94. DOI:10.1016/j.krcp.2012.04.629
  • Alex Yang · Ali Hariri · Will Harrison · Jay Wish
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    ABSTRACT: Recent post hoc analyses of large randomized clinical trials have suggested an association between high ESA dose and cardiovascular events (Szczech et al. 2008 KI 74:791). In 2011, implementation of CMS ESRD bundled payment and FDA-mandated ESA label changes that target lower hemoglobin (Hb) created further downward pressure on ESA doses. Long-term safety of intravenous (IV) iron is poorly understood. This study evaluated temporal changes in the ratio of IV iron-to-epoetin use across patients (N=200,170) from a large dialysis organization from 2008 through 2011.Mean IV iron use was normalized to mg/month. Mean epoetin was normalized to U/month. The IV iron-to-epoetin ratio was calculated by taking the mean IV iron value relative to mean epoetin (per 1000U/month) for Q1 2008 – Q4 2011.Although mean epoetin utilization has fallen since start of Q3 2010, mean IV iron utilization has remained fairly stable. From Q1 2008 to Q3 2010, the ratio of IV iron-to-epoetin was constant (2.5 mg/month for every 1000 U per month), but has risen 46% from Q3 2010 to Q4 2011, while hemoglobin levels have fallen 0.9 g/dL (11.5 to 10.6 g/dL).While ESA doses decreased, iron doses remained constant, resulting in a shift toward a higher ratio of iron-to-ESA use from Q3 2010 through Q4 2011. Further analyses are warranted to understand the appropriate balance between iron and ESA use with regards to efficacy and safety
    06/2012; 31(2):A93. DOI:10.1016/j.krcp.2012.04.628
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    ABSTRACT: Peginesatide (P) is a synthetic, pegylated, peptide-based ESA approved for treatment of anemia due to chronic kidney disease in adult patients (pts) on dialysis. P demonstrated noninferiority to epoetin (E) in maintenance of Hb levels in hemodialysis (HD) pts in two Phase 3 randomized, active-controlled, open-label trials (EMERALD 1,2). A large dialysis organization (LDO) recently reported an ESA dose adjustment rate of 12.1/pt-year (Bond et al, ISPOR 2012). This post hoc analysis evaluated dosing practices for maintaining Hb with P vs E.Pooled data from the two trials compared P (1x monthly; N=1066) with E (1-3x wkly; N=542) in HD pts previously on stable doses of E. Hb was measured during screening, at baseline and wkly (evaluation period, wks 29-36) or every 2 wks (all other periods). Dose adjustments were not to be made more frequently than every 4 wks, unless required for safety purposes. Dose adjustments (defined as change >±20% from last dose) were evaluated during the titration (wks 0-28), evaluation, and long-term follow-up (LT, wks 36-52) periods. Dose postponements were defined as >35d for P; for E, they were >4d, 6d, or 9d for TIW, BIW, and QW, respectively.Across the entire study period, P doses were adjusted ∼3 times less frequently and held ∼8 times less than P (Table). P (per pt-year)E (per pt-year)E/P ratioTotal Dose Adjustments3.510.32.9Dose Increases1.75.33.0Dose Decreases1.85.02.8Dost Postponements0.65.08.3Within each treatment arm, dose adjustment and postponement rates (including corresponding E/P ratios) were similar across titration, evaluation, and LT periods.E dose adjustment rate was similar to that of real world practice in an LDO. E doses were adjusted and held more frequently than P despite similar protocol specifications for dose alteration and Hb maintenance.
    06/2012; 31(2):A93. DOI:10.1016/j.krcp.2012.04.627
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    ABSTRACT: Few studies have investigated the association between hyperuricemia and subclinical myocardial dysfunction. The authors analyzed the relationship between serum uric acid and subclinical markers of heart failure in participants in the Framingham Offspring Cohort (N=2169, mean age 57.3 years, 55.4% women). Cardiac dysfunction was assessed through echocardiographic measurements of left ventricular (LV) mass and thickness, end-diastolic LV thickness, and LV fractional shortening at the sixth visit, approximately 24 years after study onset. Participants in the highest serum uric acid quartile (≥ 6.2 mg/dL serum uric acid) had a significantly greater frequency of echocardiographic abnormalities compared with those in the lowest quartile (<4.3 mg/dL). Those in the highest quartile had multivariable-adjusted odds ratios of 9.013 (95% confidence interval, 2.051-39.604) for abnormal LV ejection fraction and 4.584 (95% confidence interval, 1.951-10.768) for LV systolic dysfunction compared with those in the lowest quartile. Hyperuricemia in young adults can be a marker for subsequent heart failure.
    Congestive Heart Failure 05/2012; 18(3):138-43. DOI:10.1111/j.1751-7133.2011.00259.x
  • Jay Wish · Ali Hariri · Will Harrison · Alex Yang
    Spring Clinical Meeting of the National-Kidney-Foundation; 04/2012
  • Spring Clinical Meeting of the National-Kidney-Foundation; 04/2012
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    ABSTRACT: Patients with a history of myocardial infarction (MI) are often at risk for complications, including subsequent MI and death. Use of prognostic markers may aid in preventing these poor outcomes. Hyperuricemia is associated with increased risk for coronary heart disease (CHD) and/or mortality; however, it is unknown if serum urate (sUA) levels predict outcomes in patients with previous MI. The purpose of this study was to assess hyperuricemia as a biomarker of CHD outcomes in such patients. These were post hoc analyses of datasets from the Aspirin Myocardial Infarction Study, a 1:1 randomized, double-blind clinical trial, conducted from 1975 to 1979, that examined mortality rates following daily aspirin administration over three years in individuals with documented MI. The primary outcome measures were all-cause death, CHD mortality, coronary incidence, and stroke by quartile of baseline sUA. A sub-analysis of all outcome measures in the presence or absence of gouty arthritis was also performed. Of 4,524 enrolled participants, data on 4,352 were analyzed here. All outcomes were greatest for patients in the fourth sUA quartile. In multivariate regression models, the hazard ratios (HR) for patients in the highest quartile were 1.88 for all-cause mortality (95% confidence interval (CI), 1.45 to 2.46), 1.99 for CHD mortality (95% CI, 1.49 to 2.66), and 1.36 for coronary incidence (95% CI, 1.08 to 1.70). Participants with untreated gout had an adjusted hazard ratio ranging from 1.5 to 2.0 (all P < 0.01) for these outcomes. Participants with gout who were receiving treatment did not exhibit this additional risk. sUA and untreated gout may be independent prognostic markers for poor all-cause and CHD mortality in patients with recent acute MI.
    Arthritis research & therapy 01/2012; 14(1):R10. DOI:10.1186/ar3684 · 3.75 Impact Factor
  • American Journal of Kidney Diseases 04/2011; 57(4). DOI:10.1053/j.ajkd.2011.02.370 · 5.76 Impact Factor
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    ABSTRACT: Allopurinol is used to lower serum uric acid (sUA) levels in gout patients. The objective of this study was to investigate the influence of physician specialty on allopurinol treatment patterns and sUA control. This was a retrospective study using claims from a managed care database of US health plan enrollees. Gout patients at least 18 years of age who received allopurinol were identified from the database between January 1, 2002 and April 30, 2007. The index date was defined as the date of the earliest allopurinol claim, and patients were required to have health plan enrollment for at least 365 days prior to and following the index date for inclusion. Physician specialty was determined using the index allopurinol claim. Dosage of allopurinol prescription(s) and number of gout flares were determined from claims data. sUA measurements were used to assess goal attainment over a period of at least one year following the index allopurinol prescription. There were 3363 patients with gout of whom 69.9% received an index allopurinol prescription from a generalist/internist, 5.7% from a rheumatologist, 2.6% from a nephrologist, and 21.8% from a physician with other specialty. Of patients receiving their index prescription from a nephrologist, 38.7% reached the sUA goal of <6 mg/dL (357 μmol/L), as compared to patients prescribed by a rheumatologist, generalist/internist, or other physician (35.4%, 31.4%, and 39.4%, respectively; P = 0.015). When controlling for patient characteristics, multivariate analysis did not reveal statistically significant different odds of sUA goal attainment based on prescribing physician specialty, though separate analyses indicated that patients prescribed by a nephrologist had fewer gout flares. Change in allopurinol dosage from initial to final dose was more frequent among patients prescribed by rheumatologists and nephrologists. There is significant heterogeneity in the specialists' management of sUA levels in patients with gout, possibly reflecting differences in case mix and treatment approaches. Limitations related to the use of claims data, such as inability to observe medications filled over-the-counter, should be considered when interpreting study results.
    Current Medical Research and Opinion 04/2011; 27(4):737-44. DOI:10.1185/03007995.2011.552570 · 2.37 Impact Factor