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Hyperuricemic persons use more analgesics than normouricemic-is asymptomatic hyperuricemia really asymptomatic? #MMPMID41382159
BACKGROUND: Gout is a crystal deposition disorder that leads to painful joint inflammation. Its mandatory precursor-hyperuricemia-may be associated with musculoskeletal pain even in the absence of gout attacks. The utilization of different analgesics in hyperuricemia patients has, however, not been previously studied. The objective of this study was to assess the use of analgesics in normouricemic and hyperuricemic individuals and to examine the modifying effect of renal function on analgesic use. METHODS: We utilized data from the GOAL (GOod Ageing in Lahti region) study, a prospective investigation of predominantly non-gouty individuals aged 52-76 years in Finland. Information on serum uric acid (SUA) levels, various other laboratory parameters, comorbidities, medication usage, lifestyle choices, and socioeconomic factors, was gathered. The glomerular filtration rate was estimated using the CKD-EPI creatinine-cystatin C equation (ml/min/1.73 m(2)). Individuals with SUA values exceeding 360 mumol/L (approximately 6 mg/dL) were identified as hyperuricemic, while those with an estimated glomerular filtration rate of 67 or lower (25th percentile) were classified as having diminished kidney function. Data on participants who had purchased prescription analgesics was gathered. Persons with neoplasms were excluded from the study. The results for analgesic purchases over an 11-year follow-up period were adjusted for age, sex, education, smoking status, alcohol consumption, body mass index, and physical activity. RESULTS: Purchases of non-steroidal anti-inflammatory drugs (NSAIDs) increased with rising SUA levels in individuals with normal kidney function (from ~ 400 to ~ 960 purchases per 1000 person-years between SUA 360 and 800 mumol/L), but no increase was observed in those with reduced kidney function. Purchases of other analgesics increased with higher SUA levels in both kidney function groups: from ~ 250 to ~ 800 purchases per 1000 person-years in individuals with normal kidney function and from ~ 400 to ~ 970 purchases per 1000 person-years in those with reduced kidney function. The inflection point was at SUA of 360 mumol/L in all groups where the association was observed. CONCLUSIONS: Elevated SUA levels in our study associated with increase in the purchases of analgesics even among individuals without evidence of urate-lowering therapy use. For non-NSAID analgesics the association was detected in both persons with normal and reduced kidney function. This suggests that even in the absence of gout attacks, heightened SUA levels are associated with more frequent or intense pain, thereby increasing the demand for pain relief. Non-gouty hyperuricemia may not be asymptomatic.
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