Back to the Basics: Gout

Gout, characterized by recurrent attacks of acute inflammatory arthritis and an appearance of red, swollen, tender joints, was the topic for discussion as Benroe Blount, MD, MPH, MAAFP, addressed the full session. Gout and pseudogout can present as monoarticular or polyarticular and asymmetric or symmetric. Although any joint pain is a possibility, approximately 50% of all cases affect the big toe or the first metatarsal joint—this condition is called podagra.

There are four stages of gout: asymptomatic hyperuricemia, acute flares of crystallization, intervals between flares, and advanced gout.

• Asymptomatic hyperuricemia. Most people with hyperuricemia never develop clinical gout. For those who do, hyperuricemia can last 20 years before the first attack. Onset before 35 often is related to an inherited defect.
• Acute flares of crystallization. Acute flares of gout occur after abrupt onset of severe, often nocturnal, joint inflammation. Symptoms include warmth, swelling, erythema and pain, as well as a possible fever. If untreated, gout can last for 3-10 days. However, Dr Blount said his personal experience is that untreated gout can last much longer—in many cases, as long as a year. Crystallization can also occur in other joints, bursa, and tendons.
• Intervals between flares. Although asymptomatic, if left untreated, gout may advance. Intervals will shorten, crystals will enter asymptomatic joints, and the body urate stores will increase. “During flare intervals, the patient is getting silent tissue deposition and hidden damage,” said Dr Blount.
• Advanced gout. Characterized by chronic arthritis and joint damage visible on an x-ray, this condition involves polyarticular acute flares on upper extremities. The average time from initial attack to chronic gout is 11.6 years. 

Tophi are solid urate deposits in tissues; when more than one tophi is visible, the patient is in stage 4. “You can get rid of tophi, but you cannot get rid of joint damage unless you replace the joints,” said Dr Blount. Risk factors of tophi include a long duration of hyperuricemia, high serum urate, and long periods of active, untreated gout.

Note: Calcified, overhanging edges on an x-ray are indicative of gout.

Diagnosis

First, collect the patient’s history and complete a physical exam. The next step is a synovial fluid analysis, also considered the gold standard in diagnosis. Note: Serum urate levels have no influence on gout diagnosis. However, it is useful to draw blood to measure the levels to know the target baseline for treatment.

Risk Factors

Gout risk factors include: gender (male or postmenopausal female), age (older), hypertension, DM, HLD, use of pharmaceuticals (diuretics, ASA, cyclosporine), history of transplant, alcohol intake (highest with beer, lowest with whiskey and does not increase with wine), high BMI/obesity, and a diet high in meat, seafood, and sugar-sweetened (not diet) drinks.

Treatment

Treatment goals include rapidly ending acute flares, protecting against future flares, and reducing the chance of crystal inflammation. Next, focus on preventing disease progression and lowering urate serum levels.

Medical considerations include the use of NSAIDs. Pay attention to the interaction with warfarin and remember it is contraindicated for renal disease, peptic ulcer disease, GI bleeders, ASA-induced reactive airway disease, ASA-treated coronary artery disease, and congestive heart failure. 

Although not as effective “late” in the flare, colchicine is the only agent on the US market that is FDA-approved to prevent flares. The recommended dosage is 0.6 mg q per day or bid for six months. If patients are not prescribed NSAIDs or colchicine, the odds of a repeat flare are at 40% versus 3% with the treatment. 

Finally, corticosteroids can be used for glycemic control, and may be used for patients who have contraindications to NSAIDs and colchicine. New guidelines say 10 mg/day, but Dr Blount recommended ≤ 20 mg/day. 

Future Prevention

Finally, for protection against future flares, Dr Bount reviewed at least 6 months of colchicine at 0.6 to 1.2 mg/day and/or low doses of NSAIDs. Both decrease frequency and severity of flares, and prevent flares with the start of urate-lowering medication.  

Also, of note, cherry intake lowers the risk of gout flares by 35% and cherry extract intake lowers risk by 45%. Allopurinol alone reduces the risk by 53%, and combined with cherries, reduces the risk by 75%. 

Dr Blount also touched on urate-lowering therapy, which is only to be started 1-2 weeks after an acute attack subsides. The goal is to lower urate to < 6.0 mg/dl.