Background In gouty arthritis, we most often start with a non-steroid anti-inflammatory drug (NSAID). Many patients with gout have comorbidities that make NSAIDs use problematic. In clinical practice, we observe more and more patients with gout attacks unresponsive to NSAIDs.
Objectives To determine factors associated with refractoriness to NSAIDs in gouty arthritis.
Methods We performed a prospective single-center clinical trial. 200 patients with gouty arthritis (GA) aged 28-78 years and meeting ACR criteria for acute GA were recruited during 2009-2011. There were 176 men and 24 women with mean age of 56,8 years. 123 (61,5%) patients had gout confirmed by the presence of monosodium urate crystals in synovial fluid or in tophus. NSAIDs were prescribed as an initiatial treatment for all patients. Patients with contraindications and intolerance to NSAIDs were excluded. We divided patients into 2 groups. Group 1 (n=117) received NSAIDs in adequate doses, average NSAIDs treatment duration being 22 days. Because of minimal clinical effect CSs were added to NSAIDs or replaced them. Group 2 (n=83) had clinical improvement and complete resolution of arthritis within the observation period.Both groups were similar in age, sex, duration of last attack (p>0,05 for all comparisons). We compared characteristics of patients of the 2 groups, which included demographic features, lifestyle, medical history, gout features, clinical status, laboratory, medication, comorbidity.
Results Patients with CSs treatment had greater evidence for polyarthritis (OR-22,8; 95% CI, 12,01 to 43,26; p<0,001) and radiologic damage (OR-6,66; 95% CI, 4,19 to 10,57; p<0,001). Among patients unresponsive to NSAIDs, arthritis of hand joints was more often observed (OR-3,27; 95% CI,2,05-5,01; p<0,05). Compared with patients-responders to NSAIDs, non-responders to NSAIDs had higher rates of nephrolithiasis (OR-2,41; 95%CI, 1,61 to 3,63; p<0,05) and subcutaneous tophus (OR-2,41; 95%CI,1,74 to 3,50; p<0,05). In CSs group, we also found statistically higher levels of hs-C-reactive protein (OR-4,03; 95%CI, 3,55-4,59; p<0,01) and ESR (OR-12,85; 95%CI, 11,28 to 14,64; p<0,0001). In patients unresponsive to NSAIDs, we observed a negative correlation with glomerular filtration rate and clear prevalence of chronic kidney disease (OR-4,04; 95%CI, 2,86-5,70; p<0,05). No differences between the groups were noted in the levels of the serum uric acid (546 vs 552 μmol/l, p>0,05). Cardiovascular diseases (hypertension, ischemic disease) were significantly more frequent in gout unresponsive to NSAIDs (OR-5,87; 95% CI, 5,04-6,83; p<0,001). The incidence of regular alcohol intake did not differ between the groups (37,2% vs 51,7%). Delayed initiation of anti-inflammatory treatment at the onset of gout attacks (92% vs 86%; p>0,05) was similar between the groups that can explain a prolongation of gout flares in the majority of our patients.
Conclusions In our population, the refractoriness to NSAIDs in gouty arthritis is associated with: severity of gout (polyarthritis involving hand joints, radiologic joints lesions, presence of subcutaneous tophus and nephrolithiasis, high levels of hs-C-reactive protein and ESR), concomitant chronic kidney and cardiovascular diseases. The role of uric acid was not confirmed. In such patients, we could consider corticosteroids to be a first-line therapy to treat gouty arthritis that allowed achieving fewer adverse effects of NSAIDs and shorter term of treatment.
Disclosure of Interest None Declared
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