Uric acid is a metabolite of purine metabolism.Purine is dynamically present in every active multiplying cell .Uric acid is formed when Xanthine oxidase acts on Xanthine and hypoxanthine which are products of purine . The estimation of serum uric acid level can give us a rough estimate of cell metabolism and turn over. We need to understand there is a dietary source for purines as well.
UA is mainly excreted in urine . Normal levels of UA is 3-6mg in women and can be 1 mg higher in men
Biological actions of uric acid
UA is a physiological molecule . It is more of an byproduct and devoid of any unique action. Hence , most physicians still believe it to be an unwanted dangerous toxic molecule. What we fail to realise is , uric acid is a strong natural reducing agent .Hence it acts as an antioxidant .(Comparable to Ascorbic acid Vit C !)
Some believe excess uric acid is a natural metabolic weapon against cellular degeneration . In fact , hypo- urecemia has a well known association with multiple sclerosis and augmenting UA is known to improve multiple sclerosis.
However, the problem with this physiological molecule is , we do not know yet, when the levels become pathological .We know uric acid in excess can lead to urate stones in kidney and Gout in joint . Does these crystals have any effect on coronary and cerebral circulation ?
Is uric acid a marker of inflammation and cell turn over ?
Yes it is. What ESR means to inflammation , uric acid means for cell turnover . Since Inflammation induces white cell turnover uric acid level becomes a marker of inflammation as well .
Uric acid in excess is a marker of vascular damage as atherosclerosis is an inflammatory process , especially with pulmonary endothelial damage. So , in patients with primary pulmonary vascular diseases like PPH , uric acid levels may indicate the progression or regression of PAH.
Some studies have correlated right atrial pressure with uric acid levels.
Uric acid and hypoxic states
Uric acid formation is more in hypoxic states as hypoxia depletes ATP and adenine metabolism is promoted and more inosine and Xanthines are produced . Uric acid can be a simple marker of increased oxidation stress of human biological system.
No surprise to note pulmonary hypertension an important hypoxic state increase uric acid levels .
Why uric acid is rarely considered as a useful diagnostic marker in cardiology ?
- The major reason is it is an old molecule and has lost its flavor .
- The name is not exotic (Like BNP, Di dimer etc)
- Finally it is a cheap investigation and hence lacks the required glamor.
- Uric acid levels are non specific (Like any other modern molecules Tropinin , CRP etc! ) No one would like to compare uric acid vs hs CRP one to one as a marker of inflammation in vascular disease.
- UA levels depend on kidney function .
- Dietary influence can be significant (Especially meat, Liver Beans, Cauliflower etc)
Knowing the basal level of uric acid in a given patient , help us monitor the net cell turnover during medical management of chronic illness.
UA’s Clinical utility in cardiology practice
Importance of UA in PAH is well recognised now . Most studies on PAH use it as a marker or even to define a therapeutic endpoint But , please remember elevated uric acid is a simple index of elevated cell turnover and oxidative stress and it mainly represent the effect of pathology rather than a pathology itself.
So , attempting to reduce uric acid levels with drugs like Allopurinol may not improve the vascular function as one would wish ! The only indication for reducing uric acid level is when the levels become too much and it starts depositing in body.
Uric acid is a useful bio marker for vascular function. It can indicate the quantum of inflammatory , metabolic and cell turnover of any progressive vascular disease. With serial measurements it definitely helps us in monitoring cardiovascular disease especially pulmonary hypertension as lung tissue is major source of this molecule . Now , uric acid is used for prognosticating cardiac failure also.