What is Gout?
Gout is a very painful joint condition caused by the accumulation of uric acid crystals in and around the joint. The crystals can also deposit in kidneys, causing kidney stones and even kidney failure.
Uric acid results from the breakdown of purines (component of proteins). A diet rich in proteins (especially red meat & crustacean seafood) and fruit sugars, coupled with dehydration (excessive sweating during exercise, or consumption of diuretics like alcohol) can therefore trigger Gout. That said, Gout is largely genetic, due to mutations which impair the excretion of uric acid through the gut and kidneys. This is why the disease tends to run in families. Males are more commonly affected due to their larger muscle mass, and higher physical activity or social habits risking dehydration. Genetically predisposed females tend to manifest only after menopause when estrogen production stops, as the female hormone helps in renal excretion of uric acid.
This genetic predisposition also explains Gout’s association with other metabolic conditions like diabetes, hypertension and high cholesterol. They are all risk factors for cardiovascular diseases like heart attack, stroke, vascular dementia and erectile dysfunction.
What are the Symptoms of Gout?
For years before the first Gout attack occurs, at-risk individuals doing routine medical screening may have noticed elevated blood uric acid levels, defined as above saturation point (7 mg/dL or 400 µmol/L) at core body temperature. This is the asymptomatic stage.
The acute Gout attack commonly starts suddenly as a sharp throbbing pain in the ankle or big toe, typically peaking as an excruciatingly tender red hot swelling within 6-8 hours, but usually resolves in 5-7 days.
As the crystal burden worsens, attacks become more frequent, and last longer, to the point of constant inflammation and pain. More joints can become affected, and sizable deposits of urate crystals may be visible as lumps (tophi) at the toes, heels, fingers and elbows. Gout has reached the chronic stage, mimicking other chronic inflammatory arthritis like Rheumatoid Arthritis. Without proper treatment, permanent joint damage and disability will accrue.
How is Gout Diagnosed?
The diagnosis is usually obvious based on the symptoms and signs enumerated above. The blood uric acid level is usually quite high between acute Gout attacks, but may be falsely normal or even low during the attack due to stress production of cortisol hormone increasing the excretion of uric acid. When in doubt, imaging studies like ultrasound and dual-energy CT scan of the affected joint may show characteristic features highly supportive of Gout. Ultimately, the diagnosis can be confirmed if needle-shaped crystals engulfed by white blood cells are seen from fluid extracted from the inflamed joint and examined under a polarising microscope.
The main mimics of episodic acute Gout attacks are Pseudogout (due to calcium crystals deposition) and Psoriatic Arthritis. Gout may even co-exist with these conditions, making diagnosis challenging.
Blood and urine tests will also be performed to check for diabetes, high cholesterol, and kidney disease.
How is Gout managed?
Being a mainly genetic disease triggered and aggravated by unhealthy lifestyle choices, holistic management to prevent disability and reno-cardiovascular complications calls for long-term medication to keep blood uric acid level below 5-6 mg/dL (300-360 µmol/L), as well as the cultivation of healthy lifestyle habits.
Adequate hydration is important, especially when exercising. A good gauge is to drink enough water to maintain clear urine throughout the day. When taking diuretic beverages like alcohol, tea or coffee, one has to consciously pair such drinks with more water intake.
A mediterranean-type (pescetarian) diet rich in leafy greens and fish has anti-oxidative properties and is low in purines. When coupled with regular aerobic exercise, the loss of excess body fat and weight will pay rich dividends, not just for Gout, but the other metabolic diseases as well.
During an acute attack, resting the affected joint and cold compress, together with aggressive hydration and taking an anti-inflammatory analgesic (NSAIDs/coxibs) will help. With intense pain and swelling, a 3-5 days’ course of high-dose corticosteroid may be needed. The steroid may also be injected into the joint under ultrasound guidance for faster and more focused relief. In refractory inflammation, Interleukin-1 (IL1) inhibition is used. Very rarely, recombinant Uricase enzyme may be needed to break down urate crystals rapidly, like in an impending acute kidney failure.
For the longer-term maintenance, Xanthine Oxidase inhibitors (which reduce uric acid production) and Uricosuric agents (which increase the excretion of uric acid) are the mainstay of Urate Lowering Therapies. When this is initiated, NSAIDs or low-dose corticosteroid may be prescribed as daily prophylaxis in the first 3-6 months to minimise the risk of crystal dissolution flares.
