12/23/2015    Barry Mullen, DPM

Gouty Tophus with Normal Uric Acid (Todd G. Lewis, DPM)

Respectfully, Dr. Lewis' reply not only contains
some inaccuracies, it harbors a certain
sarcasm/elitist attitude not condoned by your
peers, at least not this one anyway.

First, 24 hour urine urine acid clearance studies
cannot diagnose gout. When ordered, they merely
determine whether hyperurecemia is linked to over
production or under excretion of uric acid. This
may influence long term uricosuric management if
needed. Only joint aspirates viewed under
polarized microscopes definitively diagnose gout.
Furthermore, obtaining serum uric acid levels 10-
14 days after an acute attack subsides is not a
waste of time as you infer, rather an essential
test to help determine whether a patient is even
a suitable candidate for long term uricosuric
therapy.

Recall that obtaining levels during an acute
attack typically yields false low levels since
the uric acid has already precipitated out of the
blood stream to its target tissue. Be patient and
wait to allow their systems to return to their
homeostatic levels. I've seen patients with acute
gout attacks with normal serum uric acid levels,
but most harbor some elevation. Sometimes, an
acute gout attack occurs on a one time basis from
binge eating and drinking, especially this time
of the year (holidays), so their levels often
return to normal very quickly.

The therapeutic serum uric acid goal is 6. Its
maintenance often becomes a quality of life issue
to prevent additional future gout attacks which
may not only affect joints, but internal organs
as well again. That's the critical component in a
patient's education process that may influence a
patient to adhere to your therapy
recommendation(s). You cannot know whether a
patient is hyperurecemic unless you test for it.
Additionally, when tophi form, it implies a
longstanding history of elevated serum uric acid
levels. Just because a patient hasn't provided a
prior gout history doesn't mean they never
incurred an acute attack.

Perhaps other mitigating medical factors exist
that hinder pain perception, or an individual's
inflammatory response; so, while obtaining a
good medical history is important, not all
patients are good historians and cannot always be
relied upon. As just one example, perhaps this
patient has a concurrent underlying peripheral
neuropathy that hinders their pain perception
and/or a concurrent auto-immune disorder that
suppresses their inflammatory response.

All that said, I believe our role is to treat the
acute gout attack, educate the patient about its
link to uric acid, its potential detrimental
effect to body, and to offer some suggestions how
to self manage themselves. Most importantly,
refer them back to their internists for long term
uric acid management if needed. In that education
process, stress that dietary reductions in uric
acid cannot be expected to lower serum
concentrations by more than 2 points.

Bottom line, its genetic, often linked to
hyperurecemia and often needs long term
management. Also, it is critical to stress the
importance of adequate hydration. Many gout
patients are hypertensive and take diuretics as a
component of their blood pressure management.
They often consciously reduce their water intake
because of pre-existent polyuria tendencies, a
wicked combination that increases serum uric acid
concentrations. Lastly, on occasion however, if I
come across a patient whose internist, for
whatever reason, won't aggressively manage the
hyperurecemia when present, then I will follow
through and prescribe a uricosuric agent.

Please keep in mind if you choose to do so, you
should also maintain your patients on Colcrys for
approximately 2 months during this new uricosuric
transition since rapid drops in serum uric acid
concentrations post initial uricosuric therapy
can precipitate new gout attacks.

Barry Mullen, DPM, Hackettstown, NJ

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