Baseline Serum Urate Linked to Gout Flare, Hospitalization

Natalie McCormick, PhD

Credit: American College of Rheumatology

Higher levels of serum urate at baseline were linked to gout flares and rates of hospitalization for recurrent gout, according to a study published in JAMA Network Open.¹

Acute gout, caused by accumulation of monosodium urate crystallization in the joints, is characterized by severe pain, a temporary increase in major cardiovascular and venous thrombotic events, and reduced quality of life. It is typically due to chronic hyperuricemia, defined as serum urate levels >6.8 mg/dL.²

“Among people without a history of gout, population-based studies reported graded associations between baseline serum urate levels above the saturation point and the risk of gout even after 10 or more years following the initial serum urate measurement,” wrote lead investigator Natalie McCormick, PhD, associated with the Rheumatology & Allergy Clinical Epidemiology Research Center at Massachusetts General Hospital in Boston, and colleagues. “However, associations between serum urate levels and the risk of recurrent gout among patients with a history of gout are unclear.”

The retrospective study analyzed patients with gout in the UK Biobank between 2006 and 2010 who were followed up through either the Primary Care Linked Data medical record until 2017 or the Hospital Episode Statistics database until 2020. To evaluate the link between a single serum urate measurement and subsequent risk of flare and hospitalization, investigators collected information on recurrent acute gout using outpatient, hospitalization, and prescription/procedure records. Negative binomial regressions were used to adjust rate ratios.

A total of 3613 patients with gout were included in the study. The mean age was 60 years and most (86%, n = 3104) were male. During the follow-up period (mean 8.3 years), 1773 gout flares occurred. Most (95%, n = 1679) occurred in patients who had a baseline serum urate level of ≥6 mg/dL and 1731 (98%) occurred in patients with a baseline serum urate ≥5 mg/dL.

Rates of acute gout flares per 1000 person-years were 10.6 for patients with baseline urate levels <6 mg/dL, 40.1 for urate levels of 6.0 to 6.9 mg/dL, 82.0 for urate levels of 7.0 to 7.9 mg/dL, 101.3 for levels of 8.0 to 8.9 mg/dL, 125.3 for urate levels of 9.0 to 9.9 mg/dL, and 132.8 for urate levels ≥10mg/dL. Over a 10-year period, the rate ratio of flares were 1.0, 3.37, 6.93, 8.67, 10.81, and 11.42, respectively.

Similarly, hospitalization rates per 1000 person-years during the follow-up period were 0.18 for those with baseline serum urate <6mg/dL, 0.97 for 6.0 to 6.9mg/dL, 1.8 for urate levels of 7.0 to 7.9mg/dL, 2.2 for urate of 8.0 to 8.9mg/dL, 6.7 for 9.0 to 9.9mg/dL, and 9.7 for serum urate ≥10mg/dL. After adjusting for age, sex, and ethnicity, the rate ratios of hospitalization related to gout were 1.0, 4.70, 8.94, 10.37, 33.92, and 45.29, respectively (1.87 [1.57-2.23] per mg/dL).

Investigators noted patients in the UK Biobank generally have a better socioeconomic status and are healthier when compared with the rest of the UK population, which may be considered a limitation in terms of generalizability. Additionally, any acute gout flares not treated by a physician could not be accounted for which may have led to an underestimation of acute flares. Other limitations included the small number of patients in certain subgroups, such as racial groups, and the observational nature of the dataset, which may have residual and unmeasured confounders. Lastly, approximately half (55%) of patients in the UK Biobank did not have primary care record data available and were not included in the study.

“These findings support using a baseline serum urate to assess risk of recurrent gout over nearly 10 years of follow-up,” investigators concluded.

References

^{McCormick N, Yokose C, Challener GJ, Joshi AD, Tanikella S, Choi HK. Serum Urate and Recurrent Gout. JAMA. 2024;331(5):417-424. doi:10.1001/jama.2023.26640}

^{Choi HK, Mount DB, Reginato AM; American College of Physicians; American Physiological Society. Pathogenesis of gout. Ann Intern Med. 2005;143(7):499-516. doi:10.7326/0003-4819-143-7-200510040-00009}