Background Hypertension (HTN) is a prevalent comorbidity in gout and occurs due to various combinations of factors (hyperuricemia, pain, renal function, severity of HTN). During gout attack, the development of unstable HTN can occur, with NSAIDs playing an important role in its development.
Objectives to determine factors contributing to destabilized HTN in patients with gout arthritis (GA) regularly taking their antihypertensive treatment (AHT).
Methods 405 patients enrolled with acute GA fulfilled ACR 1977 classification criteria for acute GA (1977, ACR). 87,9% of patients were males with the mean age of 56,6±9,5 years and average disease duration of 8,4±6,8 years. All patients were given a short-life NSAIDs. Destabilized HTN was defined as sitting blood pressure (BP) >140/90mmHg, demanding correction of AHT. 74,1% (n=300) of patients had HTN and only 61,7% (n=185) of them regularly took their AHT. The latter were divided into 2 groups: group 1 (n=73) without elevated BP during the treatment period (group HTN-) and group 2 (n=112) with destabilized HTN (group HTN+). The groups were comparable in sex, age and duration of gout. Characteristics of gout, parameters of severity of HTN, doses of NSAIDs and duration of treatment, 60 parameters in total, were compared between the groups HTN+ and HTN-. We defined the factors of destabilized HTN in patients with acute GA and effective treatment of HTN.
Results Comparing various features of the groups HTN+ and HTN- we found that the patients from group HTN+ had more frequent episodes of proteinuria including MAU (OR-2,67; 95%Cl, 1,72-2,69; p=0,027). In the same group, we observed statistically more patients with elevated levels of C-reactive protein (OR-2,12, 95%Cl, 1,68 – 2,66; p=0,016). Before the first registration of raised BP, the duration of acute GA treatment with NSAIDs was statistically different between the groups: the patients receiving NSAIDs for 20 days and more (AUC =0,63, p=0,016, S=90,4%, Sp-33,9%, OR-3,23, 95%Cl - 2,61-4,00) had higher risk of HTN destabilization. We found no differences between the groups in pain characteristics (VAS, number of affected and tender joints).
Conclusions Destabilized HTN during gout flares treated with NSAIDs was observed in 60,5% of patients regularly receiving their AHT. Destabilized HTN in patients with GA despite regular and effective AHT before GA was associated with the presence of proteinuria and elevated level of C-reactive protein, as well as with the duration of NSAID treatment. In these cases, the AHT should be intensified during gout attacks treated with NSAIDs, more appropriate anti-inflammatory approach being required.
Disclosure of Interest None declared