I am seeing more gout cases than I ever used to. I am also learning more and more about the linkages between gout, uric acid and the cardiometabolic diseases – stroke, heart failure, angina, hypertension, dyslipidemia and diabetes.
I have reflected before on the lack of knowledge, even among physicians, about gout treatment. That doesn’t at all mean I am professing to be an expert on the subject, only that I have developed an interest in it.
A while back, while trying all the usual angina medications for my patient with Cardiac Syndrome X, I read about using the gout medication, allopurinol, for angina. Every time I return to this topic I find more interesting facts and theories about allopurinol, gout, and heart disease.
It turns out that this old, generic, gout medication can decrease angina symptoms and heart attacks, improve pump function in heart failure patients, and lower blood pressure. These effects can be seen even in heart disease patients with normal levels of uric acid. We know allopurinol can reduce so called “oxidative stress”, believed to be at the core of many disease processes from heart disease to dementia.
In people without heart disease, but with high levels of the gout chemical, uric acid, allopurinol can improve both cholesterol and blood sugar levels.
Less known, but perhaps even more interesting, is that diets that reduce blood levels of uric acid have effects similar to allopurinol. Traditionally, such diets were severely protein-restricted, since uric acid is a by-product of protein metabolism. Newer research has shown that a high-protein diet low in sugar, fructose and saturated fat is more effective in reducing gout attacks and has better effect on cardiovascular risk than traditional, low-protein, gout diets. Both the high-protein, low-fructose diet and allopurinol reduce insulin resistance, which helps improve blood pressure, blood sugars and lipid levels. They also both increase elimination of uric acid through the kidneys.
I have been aware of the increased heart attack risk among patients with inflammatory conditions, which received attention when Ridker published his papers on C-reactive protein (CRP). Many clinicians, and many laboratories, hold the belief that very high CRP levels are a marker only of autoimmune disease but not of cardiac risk. Somehow, only mildly elevated levels are thought to be dangerous. Unfortunately, very high CRP levels, except perhaps (?) in acute illnesses, regardless of cause, are associated with very high cardiac risk.
Gout may be the oldest disease we know. First described by the Egyptians more than 4,000 years ago, gout was called the Disease of Kings, although it is now seen in all socioeconomic groups, but varies in incidence among age, sex and ethnic groups. In most areas of the world, gout incidence is on the rise
Hippocrates, writing 2,500 years ago, pointed out that eunuchs, prepubescent boys and premenopausal women don’t tend to get gout. These are also the groups of people who are least likely to develop heart disease. The new findings about uric acid, allopurinol and heart disease illustrate that, in medicine, very few ideas are entirely new.
IF THE CRP IS POSTIVE +++ WHAT WOULD THE URIC ACID BE
RE NORMAL JUST RAISED OR MARKEDLY RAISED