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.
