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 in...

Background Cardiovascular diseases are common in gout, with the hypertension (HTN) being the most frequent. Taking NSAIDs in patients with gout can result in destabilization of pre-existing HTN or the development of new episodes of HTN. Objectives to determine the influence of NSAIDs on destabilization of HTN among patients with gouty arthritis and to study a level of compliance to anti-hypertensive treatment (AHT) in such patients. Methods 436 patients with GA and meeting ACR classification criteria for GA (1977) were recruited during 2009-2012. 88,9% of patients were males with the mean age of 55,4±10,3 years and average disease duration of 7,9±6,8 years. The initial treatment was a NSAID at an adequate dose. We performed the monitoring of blood pressure (BP) during the treatment period in patients with and without HTN. Elevated BP was defined as sitting BP >140/90mmHg. Destabilized HTN was considered as elevated BP with AHT correction. We registered new episodes of HTN and destabilized HTN in patients with GA and pre-existing HTN. Before this observation, 24,8% (n=108) of patients did not suffer from HTN and did not receive any anti- hypertensive drug. 75,2% (n=328) of patients had HTN of various duration and severity. Results Among 108 patients without HTN before the study, in 9,9% (n=43) of patients, HTN was diagnosed for the first time, and the treatment was prescribed. 328 patients with gout and concomitant HTN were divided into 2 groups: 47,2% (n=206) of patients regularly taking their anti-hypertensive treatment (AHT) and 28% (n=122) of patients taking AHT non-regularly or not taking it at all. Elevated BP during the NSAIDs treatment despite the effective AHT was evidenced in 59,7% (n=123) from 206 patients. On the other hand, in patients without regular AHT, unstable HTN in 74,6% (n=91) from 122 patients was registered. We found a significant difference in the number of patients with destabilized HTN (χ2=6,90; p=0,0086) between the groups. Conclusions Destabilized HTN during gout flares treated with NSAIDs was observed in 65,2% of patients with pre-existing HTN. In 9,9% of patients HTN was diagnosed for the first time. Among gouty and hypertensive patients, there is a low level of compliance to AHT: 37,2% of them did not regularly receive their AHT. Destabilized HTN in patients with GA induced by NSAIDs was only partly due to non-regular and ineffective AHT. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.1463

Background Renal dysfunction is common in gout and occurs due to various combinations of hyperuricemia, comorbidities (hypertension, atherosclerosis, diabetes), and medication (NSAIDs, allopurinol). In these conditions, the medication should be safe for kidneys. However, primary care general practitioners (GP) tend to prescribe high doses of NSAIDs in gouty arthritis that could lead to renal insufficiency, especially in case of a relatively long term treatment. Objectives To assess treatment of gouty arthritis administrated by GP and to determine changes in the renal function. Methods 100 patients enrolled with acute gouty arthritis fulfilled ACR 1977 classification criteria for acute gouty arthritis. 83% of patients were males with the mean age of 57,5 years and average disease duration of 8,8 years. Comorbidities included hypertension (77%), ischemic disease (7%), chronic cardiac failure (15%), diabetes (21%), and renal calculi (33%). 33 patients received Allopurinol 100-300 mg/day and 3 patients received 600 mg/day. Patients were given a short half-life NSAIDs prescribed by GP. Preferred NSAID was Diclophenac taken by 61% of patients at a daily dose of 175 mg or 200 mg. An average duration of treatment in primary care was 17 days. The treatment goal was not achieved, and the patients were admitted to the Rheumatology Unit. Changes in GFRs and also the factors decreasing renal function were studied during the follow-up. Results Maximal doses of NSAIDs were prescribed to 97 patients including 15 patients with GFRs <60 ml/min. 47 patients continued the same dosing within the treatment period. After NSAIDs treatment, 47% of patients had increased GFRs (86,8 vs 102,6, ml/min, p>0,05), the number of patients with GFRs <90 ml/min diminished from 28 to 19 (p=0,063). 53% of patients had decreased GFRs (95,8 vs 78,1 ml/min, p<0,05), the number of patients with GFRs less than 90 ml/min raised from 27 patients at the beginning of treatment to 39 patients after NSAIDs treatment (p=0,016). The number of patients taking high doses of NSAIDs during the treatment period was higher in the group with negative changes in GFRs (OR-2,73; 95%CI, 1,73 to 4,32; p=0,015). Comparing various features of these groups, we found that cases of infection making 20,8% (pneumonia 1, bronchitis 2, pyelonephritis 3, suppurrated tophis 5) (OR-9,75, 95%CI, 1,3-72,96; p=0,012) and symptoms of nhronic heart failure (OR-4,88; 95%CI 1,13 to 21; p=0,038) probably due to NSAIDs were more frequent in group with reduced GFRs. Conclusions In primary care, NSAIDs are preferred drugs for treating acute gouty arthritis. They are even prescribed in pre-existing renal insufficiency. The results of the study suggest that renal function during acute gout attack can improve or worsen. High doses of NSAIDs can produce a negative effect on renal function during the treatment period because of concomitant infections and chronic heart failure. Disclosure of Interest None Declared

Background Dexamethasone (D) is a potent corticosteroid without a mineralcorticoid action that makes it convenient for patients with gouty arthritis refractory to NSAIDs and associated with co-morbidities and polypragmasia. Using short term i. v. D seems to be effective and relatively safe. We did not find studies where i.v. D was administrated in patients with gouty arthritis and hypertension (HTN). Objectives To assess the hypertensive effect of i.v. D in patients with gouty arthritis refractory to NSAIDS and HTN and to compare it with i.v Prednisone (P) in equivalent doses. Methods We performed a randomized single-center clinical trial. 88 patients were enrolled during 2009-2012. All patients had gouty arthritis and met ACR 1977 criteria for acute gout. The initial treatment was a NSAID at an adequate dose taken for at least 14 days. We randomized patients in 2 groups: group 1 (n=53 patients) received D 0,15 mg/kg i.v.; group 2 (n= 35 patients) received P 1 mg/kg i.v., the both drugs in 100 ml 0,9% solution of NaCl, for 5 consecutive days. 41 (46,6%) patients had polyarthritis. All patients had HTN, 12 (13,6%) patients had ischemic heart disease. Blood pressure (BP) was monitored during the corticosteroid (CS) treatment. HTN was defined as sitting BP > 140/ 90 mmHg. We also studied the associations between HTN and characteristics of gout (history and sighs of gout, laboratory data, and drugs) by Spearman test. Results Elevated BP at the admission was observed in 32 patients (60,4%) receiving D and in 16 patients (45,7%) receiving P (p>0,05). 39 patients (73,6%) from group D and 29 (82,9%) from group P regularly took an anti-hypertensive treatment (AHT). The correction of AHT was conducted in 28 patients (52,8%) in group D and in 14 (40%) in group P. 27 (30,7%) patients taking AHT developed a destabilization of HTN during gout attacks due more probably to NSAIDs. During the CS treatment, BP rose more than the baseline level in 7 (13,2%) patients in group D and in 10 (28,6%) patients in group P (X2= 3,19, p= 0,074). At the same time during the CS treatment, BP rose >140/90 mmHg in 31 patients (58,5%) in group D and in 20 (51,7%) in group P (X2= 0,02 p>0,05). HTN was mild, asymptomatic in the majority of patients, palpitation and headache were observed in 3 cases. One case of aggravation of coronary disease on D treatment was noted. Direct statistically significant correlation was found between systolic BPs (r=0,70, p<0,05) and moderate correlation between diastolic BPs (r=0,52, p<0,05) at the admission and during the CS treatment (maximal BPs). No association between HTN and the parameters of gout severity has been found. Conclusions Short use of i.v. Dexamethasone in patients with gouty arthritis and hypertension was relatively safe. Elevated blood pressure during the corticosteroid treatment was observed in patients with unstable blood pressure before treatment. The instability of hypertension in gouty arthritis was induced by low compliance of gout patients for regular anti-hypertensive treatment (22...

Background The most of patients with gout have various associated diseases, from which hypertension (HTN) has an important prognostic value. The role of hyperuricemia (HUE) in the development of HTN remains a subject of the discussions. Objectives To study the factors, which participate in the formation of HTN in gout; to determine the associations between the risk factors, parameters of severity of HTN and uricemia. Methods 358 patients with the gouty arthritis (GA), admitted to the Rheumatology Unit during 2009-2012, filled classification criteria of the acute GA (1977, ACR). 285 (79,6%) patients had HTN. The co-morbidities: ischemic heart disease -120 (33,5 %) patients, diabetes-56 (15,6 %) patients, chronic kidney disease - 182 (50,8 %) patients, vascular coronary and cerebral accidents – 41 (11,5 %) patients. We chose 73 patients from the group with primary gout and concomitant HTN (group HTN+) and 73 patients (20,4 %) without HTN ( group HTN-), comparable in sex, age and duration of gout. Characteristics of gout and HTN were compared between the groups HTN+ and HTN-. We studied the correlation links between the serum levels of acid uric and the risk factors, parameters of severity of HTN. Results Among patients with HTN+ diabetes was more often observed, than in group without HTN (OR-2,6; 95%CI, 0,98-6,92; p< 0,05). Compared with patients from group HTN-, patients from group HTN+ had higher rates of ischemic heart disease (OR-3,29; 95 %Cl, 1,5-7,2; p< 0,001). In the patients of group HTN+ we also found statistically higher number of the cases of excess weight and obesity (OR-5,54; 95%CI, 4,90-6,25; p<0,05). No differences between the groups were noted in the serum levels of uric acid (HTN- 576±180 mmol/l vs HTN+ 537±123 mmol/l, p> 0,05). Glomerular filtration rate and the level of the serum creatinine were similar in both groups. We defined the direct statistically significant correlation links between the serum levels of acid uric and triglycerides in the general group (r=0,66) and in the group HTN- (r=0,52). No parameters of characteristics of HTN were correlated with the serum level of acid uric. Conclusions In clinical setting the majority of patients with gouty arthritis have hypertension- 79,6%. The serum level of uric acid in patients with gout is closely linked with the serum level of triglycerides. The development of hypertension in patients with gout is associated with diabetes, excess weight and obesity as well as ischemic heart disease. The direct role of hyperuricemia was not confirmed in it. Disclosure of Interest None Declared