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SAT0364 Dexamethasone and Hypertension in Patients with Gouty Arthritis Refractory to Nsaids
  1. E. Mikhnevich1
  1. 1University Of Medicine, Minsk, Belarus


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 (22,7%) and NSAIDs (30,7%). Hypertension in gout patients due directly to the corticosteroids was evidenced in 13,2% patients on Dexamethasone as compared with those on Prednisone - 28,6% patients.

Disclosure of Interest None Declared

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