7 Fast Facts about Gout
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7 Fast Facts about Gout

Plus Gout Q&A

  1. The term “gout” is originally derived from the Latin “gutta” which literally translates to “drop.”  Back in the 13th century, gout was thought to originate from a “drop” of bad humor in an inflamed joint.
  2. Gout in the first metatarsalphalageal joint, where it occurs in up to 50% of cases, is sometimes referred to as Podagra, named for an ill-tempered mythological virgin and torturer of feet.
  3. In 2018, we have a sound understanding of pathophysiology behind gout attacks and have very effective treatment options when appropriately implemented.  Despite this, up to 70% of patients with gout will have recurrent flares and many will go on to develop chronic joint changes and advanced arthritis. A “treat to target” approach can prevent reoccurrences and long-term effects.
  4. The goal uric acid level for patients with non-tophaceous gout is less than 6.0mg/dL and less than 5.0mg/dL for those with tophaceous deposits.  When prescribing urate-lowering therapy, many primary care physicians undertreat.  The maximum dose of allopurinol is 800mg daily and, while most patients will not require a dosage that high, many will require doses higher than 400mg daily to reach their target uric acid level.
  5. Many primary care physicians are hesitant to start urate-lowering therapy for patients with chronic kidney disease.  Contrary to preconceptions, allopurinol can be used in renal insufficiency.  Start at 50mg orally per day and uptitrated by 50mg intervals to reach target uric acid level in the serum with creatinine clearance greater than 20.  It is quite common for patients with renal insufficiency to require doses higher than 300 or 400mg daily.  Those with creatinine clearances less than 20 may have a lower maximum dosage. In patients intolerant to allopurinol therapy, think febuxostat.
  6. Some medications, including diuretics, low-dose aspirin and immunosuppressants (cyclosporine and tacrolimus) can complicate this disease and are an important consideration in the evaluation of patients with gout. 
  7. Gout can coexist with septic arthritis. 

To make a referral to Dr. Stanishewski at SVMC Rheumatology, call 802-447-4555.

 

Gout Q&A
with Matthew Stanishewski, DO, SVMC Rheumatology

As most of us who practice medicine are aware, gout is an inflammatory arthritis which results in sudden episodes of severe pain and swelling which can be particularly disabling unless properly identified and treated. 

  • Episodes are heralded by warmth, swelling and redness with skin hypersensitivity. 
  • The first metatarsalphalageal joint is most commonly affected (up to 50% of cases) however flares can occur in just about any joint. 
  • In 2018, we have a sound understanding of pathophysiology behind gout attacks and have very effective treatment options when appropriately implemented.  Despite this, up to 70% of patients with gout will have recurrent flares and many will go on to develop chronic joint changes and advanced arthritis.  Hopefully this discussion will help to dispel common myths regarding gout treatment and urge providers to adopt a “treat to target” approach to therapy. 
     

What is gout and how is it diagnosed?

Gout occurs when excess uric acid, a byproduct of purine breakdown, collects in the body.  Precipitation of needlelike monosodium urate crystals deposit in the joints.  Intermittent “flares” are triggered by sudden fluctuations in serum uric acid levels, trauma, dehydration and other factors including diet.  Foods high in purine content, such as shellfish and red meats, organ meats, sardines and anchovies, alcohols (particularly beer and wine), sugary drinks and foods that are high in fructose are potential triggers.  Some medications, including diuretics, low dose aspirin and immunosuppressants (cyclosporine and tacrolimus) can complicate this disease and are an important consideration in the evaluation of patients with gout. 

Although humans carry the uricase gene, it is inactive and therefore we as a species lack the ability to oxidize uric acid to the more soluble compound allantoin.   Serum uric acid levels are both age and sex-dependent.   It is rare in males under age 30 and in premenopausal females.  Onset in men under age 25 is usually related to a defect in purine degradation, renal insufficiency and/or alcoholism.   Alcohol intake and body mass index are two of the most important predictors of hyperuricemia and gout in the general population.

The precipitation of uric acid crystals within the joint stimulates an intense inflammatory response mediated by multiple cytokines (IL-1β, IL-6, IL-8 and TNF), chemotactic factors and the induction of the NLRP3 inflammasome.

Gout usually occurs in 3 phases.  The first is characterized by sudden pain and swelling which usually resolves in 7-10 days.  This is followed by a short or long period of quiescence, then recurrent sudden attacks of gout.  After a number of years, if left untreated, chronic changes can occur, characterized by persistent swelling, mild to moderate joint pain and stiffness, and presence of tophaceous deposits.  Erosive and destructive arthritis can be directly correlated to recurrent flares and delayed treatment.

 

You think your patient has an acute gout flare.  What do you do?

Think arthrocentesis.  Proper diagnosis of an acute inflammatory mono or oligo-articular arthritis is made with formal arthrocentesis of the involved joint with synovial fluid analysis for culture, cell count and crystal analysis.  Always remember that gout can coexist with septic arthritis. 

Think anti-inflammatory.  Indomethacin is the classic non-steroidal anti-inflammatory (NSAID) considered for mild to moderate gout flares, however any NSAID can be efficacious if instituted early enough.  An alternative for acute treatment is colchicine 1.2mg orally at the first sign of flare and 0.6mg one hour later.   This can be continued at the 0.6mg dose on an every-12 hour basis until the flare resolves, holding or decreasing the dose for the development of diarrhea (which is the major adverse effect of colchicine).  Avoid using colchicine or adjust dose accordingly in patients with renal failure or baseline neutropenia.   If the patient has chronic renal or hepatic disease, intra-articular corticosteroid injection (monoarthritis) or a short course of corticosteroids (oligo or polyarthritis) could be considered over 10-12 days.

Think frequency.  How many flares has the patient had over the past 12 months?  If the answer is more than 2, consider urate lowering therapy in patients with elevated uric acid levels.

 

You think your patient has gout, but the uric acid level is normal.  What should you do?

The level was drawn too early in relationship to the acute flare.  Up to a third of patients with an acute gout flare can have a falsely low serum uric acid during the acute flare. 

Redraw one to two weeks after the initial flare has completely resolved to obtain an accurate uric acid level.

Make sure an arthrocentesis was performed, as this could represent an alternate form of crystal arthropathy (such as pseudogout) or septic joint

 

Your patient has been diagnosed with gout and has had 3 flares in the past year.  The uric acid level is 9.8.  You want to start urate lowering therapy.  What dose should you start with and how do you titrate appropriately?

Think allopurinol.  This xanthene oxidase inhibitor is cost-effective and tolerable for most patients.  In otherwise healthy adults, a starting dose of 100mg orally per day should be considered.  The uric acid level should be redrawn at 4-6 week intervals and the dose uptitrated by 100mg at a time.

Treat to target.  The goal uric acid level for patients with non-tophaceous gout is less than 6.0mg/dL and less than 5.0mg/dL for those with tophaceous deposits. 

Do not undertreat.  Plenty of primary care physicians fail their patients by undertreating gout.  The maximum dose of allopurinol is 800mg daily and while most patients will not require a dosage that high, many will require doses higher than 400mg daily to reach their target uric acid level.

For those who fail or are otherwise intolerant of allopurinol, think of febuxostat as an alternative option.

For those with recurrent flares while starting urate lowering medication, consider colchicine prophylaxis.  0.6mg of colchicine orally per day can help prevent flares related to serum changes in uric acid over the first 6 months of therapy. 

 

I want to start urate lowering therapy, but my patient has chronic kidney disease.  What do I do?

Think allopurinol.  Many physicians have a preconception that allopurinol is contraindicated in renal insufficiency, which is untrue.  Allopurinol can safely be started at 50mg orally per day and uptitrated by 50mg intervals to reach target uric acid level in the serum with creatinine clearance greater than 20.  It is quite common for patients with renal insufficiency to require doses higher than 300 or 400mg daily.  Those with creatinine clearances less than 20 may have a lower maximum dosage.

Think febuxostat in patients intolerant to allopurinol therapy.

 

Can hyperuricemia in gout be managed by diet alone?

Unfortunately, the purine content of a typical daily diet contributes to only about 1.0 mg/dL of total serum uric acid concentration.  Therefore, avoiding specific foods to control uric acid levels is not particularly helpful over the long term.

Purine rich foods that have the potential to “shift” serum uric acid levels should be avoided.  Organ meats, shellfish, sardines, anchovies and high fructose drinks are notorious for triggering attacks of gout, but avoiding these foods may not change the uric acid level much.

 

When is the optimum time to start allopurinol therapy?

Classically, urate lowering therapy should be started after the acute flare resolves. 

 

What if my urate lowering therapies have been maximized without reaching the target uric acid level in my patient?

  • Consider a rheumatology consult.
  • In the appropriate patient, consider lesinurad in conjunction with either allopurinol or febuxostat.  This agent belongs to a new class of urate lowering pharmaceuticals called selective uric acid reabsorption inhibitors. 

 

My patient has erosive, debilitating gout with multiple large tophaceous deposits.  How do I treat this patient?

  • Consider a rheumatology consult.
  • Treat with urate lowering medications as above, with target uric acid level <5.0mg/dL.
  • The patient can be considered for debulking therapy with pegloticase, a pegylated uricase which is very effective at lowering total serum uric acid but with a higher incidence of adverse effects.
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