Cutaneous uric acid and metabolite monitoring to improve individual response to pharmaceutical and dietary treatment in patients with gout - Project Summary Gout affects 8.3 million of US adults. Gout and hyperuricemia are associated with hypertension, progression of renal disease, cardiovascular disease, and dyslipidemia. Dietary modifications can lower SU by 1 mg/dL. Urate lowering therapy (ULT) has demonstrated improvement in clinical outcomes. Yet despite these findings and national guideline recommendations for the management of gout, knowledge about dietary purine content is poor and adherence with gout medications is the lowest among 7 chronic diseases. Our group has developed a cutaneous sensor patch that can detect uric acid (UA) in sweat. Sweat UA has strong correlation with serum urate (SU) levels making it an ideal non-invasive method to frequently sample subject’s uric acid levels. We postulate that providing patients with gout their pre- and post-prandial UA results will result in better dietary and medication adherence decisions. To better understand the impact of urate control on gout and other metabolic conditions, we seek to expand the breadth of metabolites and nutrients monitored by this system. We seek to extend the duration of use for the skin patch to include morning and evening meals. We seek to develop a friendly, easy to use interface for data collection and patient reports. We will evaluate the impact of the URic AcId + metabolite Monitoring System (UR+AIMS) enhancements on gout and other metabolic clinical outcomes though a 10-week randomized trial for subjects with gout either on or off urate lowering treatments (4 arms). Specifically, we will test whether the use of UR+AIMS with patient pre- and post-prandial uric acid reports results in improved serum urate control as measured by proportion of patients with SU < 6 mg/dL. Since urate is intertwined with other metabolic pathways, we will also evaluate whether UR+AIMS intervention results in improved blood pressure, blood sugar and lipid control. With the detailed (almost continuous) prospective data on urate and other metabolites, we will evaluate the changes in metabolites prior to a gout flare. These observations may lead to new understanding about the triggering factors preceding a gout flare. In addition to purine metabolites, we will be measuring the allopurinol (most common urate lowering medication) metabolite, oxypurinol. Effective dosing of allopurinol has not been achieved at population level. Confusion arises from conflicting dosing recommendations over the years and current dosing recommendations (start low and titrate up slowly to target dose that lowers SU < 6 mg/dL). Furthermore, impact of renal disease, body size and diuretics that all impact effective dose needed to achieve SU goal. With continuous oxypurinol measures, we will evaluate if the initial steady oxypurinol along with change in UA can predict the ultimate dose at the end of titration required to achieve SU < 6 mg/dL. This prediction rule would simplify future allopurinol dosing schedules, reducing the number of lab visits and provider interactions.
