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SERUM URIC ACID ONE OF THE MOST USELESS TESTS IN PRIVATE PRACTICE

OP Kapoor

Ex. Hon. Physician, Jaslok Hospital and Bombay Hospital, Mumbai, Ex. Hon. Prof. of Medicine, Grant Medical College and JJ Hospital, Mumbai 400 008.

By now I have seen hundreds of reports of blood uric acid and I am fed up of the wrong treatment and the wrong interpretation starting from the pathologists, to the GPs, specialists, physicians and orthopaedic surgeons. Till lately, I used to find even senior pathologists reporting the normal readings of serum uric acid as 2-4 mg. It took them few years to change that normal reading. Even till today very few pathologists write the correct reading which is upto 7 mg in males and upto 6 mg in females. (Like the reading of blood cholesterol, in the last few years, the Americans had accepted the reading of 7-8 mg in the males as the higher reading). The fact is that this test does not help in the management or in the diagnosis in private practice.

Yes, a slightly raised Uric Acid is “associated” with obesity, hypertension, use of diuretics, hyperlipidaemia, diabetes mellitus, congestive cardiac failure etc. but does not “cause” any of these diseases. There is very little evidence to show that Uric Acid causes heart attacks.

The haematologists see a number of patients of hyperuricaemia. To patients of leukaemia they prescribe a lot of Alopurinol. But these are cases of “secondary hyperuricaemia” which are extremely common in practice and rightly deserve the treatment to prevent any kidney damage.

Many practitioners including Orthopaedic Surgeons diagnose bone or joint disorders with slightly elevated reading of uric acid as gout. This is wrong. The gout arthritis occurs typically as an attack of pyogenic arthritis with all the symptoms of infection like pain, redness, swelling over the joints and even leucocytosis and the aspiration of the “pus like” fluid. Only if the doctors ask for examination of fluid for uric acid crystals will they not miss the diagnosis of gout. I have seen many such patients who would of course respond to the treatment given by his clinician because basically all gout attacks subside with passage of time and with administration of any NSAID group of drugs. Thus many patients are underdiagnosed specially because serum uric acid in many of the patients remains normal during the attack. This diagnosis should be thought of mainly in very healthy fat, alcoholic patients who may be having associated BP and diabetes and have a positive family history and otherwise look very healthy and from upper class society.

Although, administration of colchicine in proper doses and/or NSAID group of drugs in large doses (like Indomethacin 25 mg 1 or 2 hourly) will reduce the duration of the attack, the management of the blood uric acid is a separate issue altogether and should not be confused with the attack of gout.

Even in patients whose uric acid is more than 7, the usual advise of losing weight, omitting alcohol, omitting diuretics and repeating the levels every year should be enough.

Only if the patient gets the 3rd attack of gout within one year, should the treatment of serum uric acid be started and then of course it is useful to rule out urate kidney stones and do a blood creatinine level before starting the drugs. Really speaking in patients who have no kidney stones and had no history of renal colic, alopurinol or probenecid, any of these drugs could be given provided the dose is correct and provided the patient follows other instructions of losing weight, omitting or reducing alcohol markedly and possibly become a vegetarian and take fish or white meat 2-3 times a week. The minimal dose of alopurinol is a single tablet of 300 mg which is now available in India.

The compliance of the patient is less when the drug is prescribed as 100 mg three times a day. The 100 mg tablets are useful in patients whose creatinine levels are high and who are in renal failure. These tablets should not be stopped and “restarted” if the patient gets an acute attack and should be continued in the same dose.

Probenecid is equally effective and could be certainly given if there is no history of kidney stones or renal colic or raised blood creatinine. The minimal dose of 1 tablet of 500 mg twice a day be given but this may have to be increased to double the dose.

Vice versa, if the patient is not taking these drugs, and there is a definite indication to start the drug then they should be started 2-3 weeks after the gouty attack and the NSAID group of drugs and/or colchicine should be continued for a few weeks to cover a fresh attack of gout which may be precipitated by these drugs.

The above two drugs certainly reduce the incidence of kidney stones, chronic renal failure, appearance of tophi, attacks of olecrenon bursitis etc. Once started, patients of gout will have to be given these drugs life time, unlike in haematological conditions where often larger doses are prescribed only for short periods.

Finally, if this is the position of gout, what about hundreds of asymptomatic hyperuricaemic patients detected in health check ups? Majority of them are wrongly treated and are prescribed alopurinol.

It is worth noting that if you are shown a high reading of blood uric acid, get two more readings from two other laboratories before sentencing the patient to life time drug therapy of alopurinol or probenecid. There is absolutely no hurry to start these drugs unless uric acid levels are more than 10 mg which is more commonly seen in haematological practice. Usually I will give the above non pharmacological advise regarding, diet, weight, alcoholic intake and tell the patient to see me every year with a report of blood uric acid. As long as it is not increasing to near 10 mg or the patient, does not get an attack of gouty arthritis, there is no need to put him on drugs.

ACKNOWLEDGEMENT

I am thankful to Dr. Sanjeev Amin for his useful suggestions.


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