Gout/Uric Acid: MYTHs/Facts & Role of our Clinicians

Schazad

New Member
Besides cursing them who still write down Typhidot/Widal in our endemic areas where enteric is highly prevalant, let's do the same for the ones who offer pharmacologic "antihyperuricemic therapy" to all people with increase uric acid levels without knowing that asymptomatic hyperuricemia except where co-existant hyperuricosuria(uric acid excretion Greater than 1100mg/24hrs) is present, warrant no treatment in absence of established Gout/Recurrent acute gouty arthritis attacks/uric acid nephrolithiasis/urate nephropathy.

All those who present with any kind of pain elsewhere in body whether it's Fibromyalgia/osteoporosis/osteomalacia/Somatic Symptom disorder or any other reason identified or unidentified, if having increase uric acid levels is offered pharmacologic treatment as if all these aches pains are secondary to increase uric acid levels. This is lack of knowledge as well as stupidity on part of clinicians to do the same.

Most common reasons also include conditions like "Plantar fascitis(present with intense heel pain in particularly after prolonged rest or as patient wake-up in morning and place his foot on ground after awakening) and "Heel spurs" which have no remote link with increase uric acid levels but again as more than 90% clinicians including specialists in our country do not recognise these disorders, consider them secondary to increase uric acid levels and offer pharmacologic antihyperuricemic therapies.

This issue need to be addressed at mass level that asymptomatic hyperuricemia is not a disease just a predisposing condition for few disorder/risk factor for conditions as mentioned above and thus warrant no treatment except in those situations mentioned above or associated secondary causes like myeloproliferative disorders/tumor lysis syndrome/genetic disorders etc

Treatment should only be started if a patient develop gout/uric acid nephrolithiasis/uric acid nephropathy as when these conditions develop and one offer therapy, these are all readily treatable and on the other hand if we offer long-life antihyperuricemic treatment, this may rather be very harmful in particularly current literature review suggest those being offered Febuxostat are at much higher risk to suffer from serious Cardiovascular events. (In a way by doing that our clinicians are helping population control department).

Also remember all major guidelines uptill now don't suggest pharmacologic treatment if uric acid levels are increased in setting of established CV disease/Early CKD(not secondary to uric acid nephropathy)/metabolic syndrome.

The paragraph ahead is an excerpt from Up-to-date (best available resource of medical information for physicians all over the world) suggesting the same.

(With the exception of acute uric acid nephropathy [34], the initial clinical manifestations of urate or uric acid crystal deposition are not life-threatening and are readily treatable. This observation, plus the lack of an established causal role of hyperuricemia in chronic kidney disease (CKD) [4,53,83] and the other associated disorders like cardiovascular disease and metabolic syndrome, has restrained enthusiasm in the United States for prophylactic antihyperuricemic drug therapy in the vast majority of individuals with asymptomatic hyperuricemia).

And this excerpt too (In all persons with persistent asymptomatic hyperuricemia in whom treatable secondary causes have been excluded, we provide counseling regarding the use of nonpharmacologic (lifestyle) interventions to reduce the degree of hyperuricemia. We also provide such counseling to patients with evidence of monosodium urate (MSU) crystal deposition only on imaging. These lifestyle interventions are very similar to those used for the prevention of recurrent gout, including reduction to ideal body weight by means of adjustment of dietary volume and composition, avoidance of alcohol and sugar-sweetened beverages, and regular exercise).
 
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