Treatment strategies for osteoarthritis patients with pain and hypertension

Abstract

Out of 100 patients with osteoarthritis (OA), almost 40 have a concomitant diagnosis of hypertension. Nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors may trigger a rise in blood pressure (BP), which is more marked in patients with established hypertension. NSAIDs and COX-2 inhibitors attenuate the antihypertensive effect of several antihypertensive agents. Frequent BP controls are needed in treated hypertensive patients who are concomitantly receiving NSAIDs or COX-2 inhibitors because even a small increase in BP may be associated with an important rise in the risk of major cardiovascular complications. In meta-analyses, an increase in systolic BP of 5 mmHg was associated with a 25% higher risk of cardiovascular events. These data have been confirmed in randomized studies with rofecoxib and celecoxib, where a modest increase in BP was associated with a significantly higher risk of cardiovascular disease. There is emerging evidence that the COX-inhibiting nitric oxide donator (CINOD) class is promising in the treatment of patients with OA. Naproxcinod, the first CINOD investigated in clinical trials, is composed of the traditional NSAID naproxen covalently bound to the nitric oxide (NO)-donating moiety butanediol mononitrate (BDMN). The molecule has the potential to provide a sustained release of NO. In clinical studies, naproxcinod prevented the BP rise in normotensive and hypertensive patients observed with naproxen. The BP benefit of naproxcinod over naproxen was greater in patients concomitantly receiving angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers. These investigational data suggest that naproxcinod is a valuable alternative to NSAIDs and COX-2 inhibitors for treatment of OA patients.

Is the prevalence of arterial hypertension in rheumatoid arthritis and osteoarthritis associated with disease?

“…Antirheumatic therapy may provoke HT or interfere with its control, particularly in the case of NSAIDs used for the treatment of OA [10] and RA and for various DMARDs and GCs used to treat RA [3]. Our results, which showed no association of HT with NSAID use in RA and OA and an association of HT with leflunomide use (see supplementary data available at Rheumatology online, table 1-S) and with the duration of GC use in RA were similar to the findings of others for RA [17,32].…”

“…The CV disease risk and the presence of CV disease risk factors in OA were found to be lower [8] or similar [9] to those in RA. The CV disease risk in OA has been attributed to a high prevalence of classic CV disease risk [9], and in the case of HT, to medication, especially the use of non-steroidal antiinflammatory drugs (NSAIDs) and cyclooxygenase-2 inhibitors [10].…”

Sedentary behavior and blood pressure control among osteoarthritis initiative participants

“…We then excluded participants who used non-steroidal anti-inflammatory drugs (NSAIDs) (n = 439), which are known to increase BP. 12–15 Finally, to mitigate against the common bias in pharmacoepidemiology that sicker patients are generally treated with more potent therapy (e.g., increased dosage or number of drugs), 16 we excluded all participants who used antihypertensive medications during 30 days before the 48 month visit (n = 679). After these exclusions, 707 adults contributed to the analytic sample.…”

Potential pharmacodynamic drug-drug interaction between concomitantly administered lisinopril and diclofenac sodium: a call for appropriate management in hypertensive osteoarthritic patients

“…Female patients required were non-pregnant, non-lactating or not susceptible to pregnancy (i.e., Table 1 Pharmacological effects of PGs on renal function (12,20,21). Female patients required were non-pregnant, non-lactating or not susceptible to pregnancy (i.e., Table 1 Pharmacological effects of PGs on renal function (12,20,21).…”

“…Another important mechanism involved is the increased peripheral vascular resistance by inhibiting vasodilatory PGs and by potentiating vasoconstricting endothelin-1 (ET 1 ) (7) . The pharmacological effects of PGs (12,20,21) and ACEIs (14,22,23) on renal function are shown in Tables 1 and 2 , respectively. Such pharmacodynamic drug-drug interactions have been reported several studies involving NSAIDs such as rofecoxib, aspirin, indomethacin, ibuprofen, diclofenac, celecoxib or piroxicam and ACEIs (13 -19) .…”