Gout Drug May Help Prevent Repeat Heart Attacks

Content

• Statistical Analysis Clinic
• The Impact Of Gout On Heart Disease
• What Are The Symptoms Of Gout?
• What Happens If You Do Not Receive Treatment?
• Uncontrolled Blood Pressure And Additional Cardiovascular Disease Risk Factors
• How Gout Can Affect Your Lung Health

Physicians easily recognize the diagnostic features, in particular when the metatarso-phalangeal joint of the first toe is affected . A sudden red, swollen and very painful joint indicating monoarticular arthritis is highly characteristic, as is complete recovery, mostly within 1 or 2 weeks. Our aim was to examine the relationship between gout on the one hand and cardiovascular diseases and cardiovascular risk indicators on the other. Calcium pyrophospate disease—CPPD—has been noted in patients who have multiple injuries to a joint, though many patients will not have any injury prior to an attack.

Statistical Analysis Clinic

Regardless of mechanism, it is clear that hypertension and hyperuricemia are positively related, with about a quarter of all individuals with a blood pressure in the hypertensive range (i.e. uncontrolled blood pressure) also meeting criteria for hyperuricemia . Our study found that febuxostat does not increase the overall risk of major adverse cardiovascular events among patients with gout and hyperuricemia. However, our analysis also showed an increased the risk of cardiovascular death with febuxostat.

The Impact Of Gout On Heart Disease

The buildup of uric acid crystals in the kidneys can cause problems that can range from reduced function to kidney failure. Damage is progressive, but the right treatment can often slow it down. A 2018 study published in Arthritis Research & Therapy reported that people with gout have a 78% higher risk of moderate kidney disease, which typically has no symptoms. The same study noted about 1 in 4 people with gout have this level of renal damage. Anakinra (brand name Kineret®) is a biologic medication that blocks the inflammatory protein IL1.

A more recent meta-analysis addressing the association between SUA and incidents HF and/or the prognosis of HF patients, was performed by Huang et al. Five studies reporting on incident HF and 28 studies reporting on HF outcomes were included. The results showed that hyperuricaemia was associated with an increased risk of incident HF (HR 1.65; 95 % CI [1.41–1.94]). In addition, for every 1 mg/dl increase in SUA the risk of all-cause mortality and the composite endpoint in HF increased by 4 % and 28 %, respectively. Subgroup analyses supported the positive association between SUA and HF. Gout is caused by increased uric acid in the blood, which deposits crystals in the joints, sparking an inflammatory response—the same process that often leads to dangerous blood clots, triggering heart attacks and strokes.

Upregulation of xanthine oxidase activity rather than decreased renal excretion of uric acid is an important factor underlying the increased serum uric acid levels in heart failure patients. Endothelial dysfunction might be caused by accelerated inactivation of nitric oxide by reactive oxygen species, and xanthine oxidase is a source of reactive oxygen species production. There are several potential explanations for our findings and those of the CARES trial.

How serious is gout?

If left untreated, gout can cause erosion and destruction of a joint. Advanced gout. Untreated gout may cause deposits of urate crystals to form under the skin in nodules called tophi (TOE-fie).

Gout flare-ups occur when the kidneys fail to excrete enough uric acid in urine and it forms needle-like, white crystals inside joints, leading to intense inflammation and sudden, severe pain, soreness, swelling, and redness. These physiological abnormalities were at least partially reversible by the administration of the nonreversible xanthine oxidase inhibitor febuxostat . The European Society of Cardiology brings together health care professionals from more than 150 countries, working to advance cardiovascular medicine and help people lead longer, healthier lives.

What Happens If You Do Not Receive Treatment?

The loss of blood flow can damage the tissues in the heart and cause a cardiac arrest – where the heart stops working, completely. In addition to recommending medicines for you to take, your health care professional may also recommend diet and lifestyle changes to manage your gout, such as losing weight and eating fewer foods that are high in purines. For more information about gout, visit the National Institute of Arthritis and Musculoskeletal and Skin Diseases webpage. Uloric is approved to treat a type of arthritis called gout in adults. Health care professionals should reserve Uloric for use only in patients who have failed or do not tolerate allopurinol.

Do heart medications cause gout?

Yes. Diuretics can increase your risk of developing gout, a type of arthritis caused by the buildup of uric acid crystals in a joint. This may happen because diuretics increase urination, which reduces the amount of fluid in your body.

Some have called for the FDA to reconsider its recommendations, but no changes made to date. The FAST trial gives considerable comfort to those patients presently on febuxostat. It is generally agreed that we have no evidence that febuxostat is a negative for the heart, just the question of the CARES trial as to whether it is not as protective as allopurinol. The FAST trial challenges this, and it may well be that they are equally protective. Although exercise is great for helping lose weight and is generally fine for gout patients, when you have a gout flare in your toe, foot, ankle or knee it is advised to stay off the foot as much as possible until the flare resolves.

Uncontrolled Blood Pressure And Additional Cardiovascular Disease Risk Factors

According to another pathogenetic hypothesis, SUA functionally up-regulates XO, which is a key enzyme in purine metabolism. XO-derived ROS may account for a range of detrimental processes in the pathophysiology of HF, such as cardiac hypertrophy, myocardial fibrosis, LV remodelling and contractility impairment. In addition, UA per se may represent a ‘proinflammatory’ substance, frequently associated with other inflammatory markers such as CRP, interleukin-6 and neutrophil leukocytes.

Uric acid levels and atrial fibrillation in hypertensive patients. Challenges of conducting a trial of uric-acid-lowering therapy in CKD. Oxidative stress with an activation of the renin-angiotensin system in human vascular endothelial cells as a novel mechanism of uric acid induced endothelial dysfunction. Uric acid levels, left ventricular mass and geometry in newly diagnosed, never treated hypertension.

Recent Research Confirms Links Between Gout, Heart Disease, And Strokes

Other studies have analysed the association between SUA and CV risk in hypertensive and/or patients with diabetes. The effect of elevated SUA levels on the incidence of CADs seems to be stronger in women than in men, as shown by an epidemiological study conducted in the US, which originally enrolled 3,102 subjects between 1960 and 1962, with a follow-up of 7 to 9 years. Uric acid represents the final product of purine metabolism, in humans mainly regulated by the xanthine-oxidoreductase enzyme, which converts hyoxantine to xanthine and xanthine to UA. Dietary factors may influence serum UA , increasing its levels or decreasing them .