Brief Report: Monosodium Urate Monohydrate Crystal Deposits Are Common in Asymptomatic Sons of Patients With Gout: The Sons of Gout Study

Abstract

ObjectiveTo estimate the prevalence and distribution of asymptomatic monosodium urate monohydrate (MSU) crystal deposition in sons of patients with gout.MethodsPatients with gout were mailed an explanatory letter with an enclosed postage‐paid study packet to mail to their son(s) age ≥20 years old. Sons interested in participating returned a reply form and underwent telephone screening. Subsequently, they attended a study visit at which blood and urine samples were obtained and musculoskeletal ultrasonography was performed, with the sonographer blinded with regard to the subject's serum urate level. Images were assessed for double contour sign, intraarticular or intratendinous aggregates/tophi, effusion, and power Doppler signal. Logistic regression was used to examine associations. Adjusted odds ratios (OR adj) and 95% confidence intervals (95% CIs) were calculated.ResultsOne hundred thirty‐one sons (mean age 43.8 years, mean body mass index 27.1 kg/m2) completed assessments. The serum urate level was ≥6 mg/dl in 64.1%, and 29.8% had either a double contour sign or intraarticular aggregates/tophi in ≥1 joint. All participants with MSU deposition had involvement of 1 or both first metatarsophalangeal joints. Intratendinous aggregates were present in 21.4% and were associated with intraarticular MSU crystal deposits (OR adj 2.96 [95% CI 1.17–7.49]). No participant with a serum urate level of ≤5 mg/dl had MSU crystal deposition seen on ultrasonography, and 24.2% of those with serum urate levels between 5 and 6 mg/dl had ultrasonographic MSU deposition. MSU crystal deposition was associated with increasing serum urate levels (OR adj 1.61 [95% CI 1.10–2.36] for each increase of 1 mg/dl).ConclusionAsymptomatic sons of patients with gout frequently have hyperuricemia and MSU crystal deposits. In this study MSU crystal deposits were present in participants with serum urate levels of ≥5 mg/dl. Evaluation of subjects without a family history of gout is needed to determine whether the threshold for MSU crystal deposition is also lower in the general population.

The impact of dysfunctional variants of ABCG2 on hyperuricemia and gout in pediatric-onset patients

“…In summary, our findings confirmed a heritability component for hyperuricemia and gout. This relationship was recently demonstrated in a cohort of asymptomatic male offspring of parents with gout, in which the male offspring had a significantly higher frequency of hyperuricemia, urate under-excretion, and prevalence of monosodium urate crystal deposits [24]. A positive family history is an important diagnostic clue; however, it may be absent in de novo mutations and where hyperuricemia/gout was either not diagnosed or not communicated to the rest of the family.…”

Upregulated expression of FFAR2 and SOC3 genes is associated with gout

“…Balancing sustained efficacy [7][8][9][10][11] with acceptable tolerability 1,12 A 2nd generation, JAK1 preferential inhibitor for moderate to severe RA [1][2][3][4][5][6] Refer to Summary of Product Characteristics (SmPC) before prescribing, and for full prescribing information.…”

Contentious Issues in Gout Management: The Story so Far

“…On the opposite side of the spectrum, some physicians believe that for a patient to develop tophi and severe symptomatic gout, it would usually be preceded by years of recurrent flares, since it has been well demonstrated that patients with asymptomatic hyperuricemia have MSU crystal deposits. [16][17][18][19] The 2020 American College of Rheumatology (ACR) recommendations support starting ULT if there are two or more flares in the previous year, evidence of tophi, or evidence of radiographic damage attributed to gout and conditionally recommend starting ULT for CKD stage 3, SU > 9mg/dL, or urolithiasis. 12 Will other societies support this?…”