About Uric Acid
Gout is a disease of urate burden, resulting from years of hyperuricemia, in which a patient’s uric acid level is greater than 6.8 mg/dL. Over time, hyperuricemia can lead to tissue deposition of monosodium urate crystals (MSU).
Aggregates of urate crystals are known as tophi. They are microscopic at first, and can exist silently for years in the setting of sustained asymptomatic hyperuricemia. Over time, they can become macroscopic and can be seen during physical exams as lumps or nodules. Uric acid can also crystallize in the renal collecting system and form calculi.
A flare of gout is a rapid onset of an acute inflammatory response to urate crystals, typically first occurring in the joints of the lower extremities. MSU crystals can deposit in joints, bursa, bone and other soft tissue such as ligaments, tendons and skin. At first, gout flares are intermittent with asymptomatic periods between flares. Untreated, hyperuricemia can lead to chronic inflammatory arthritis, which is often deforming.
Monitoring Uric Acid Levels in Those with Gout
Most experts agree that lowering and keeping uric acid levels to less than 6.0 mg/dL is necessary to prevent the consequences of hyperuricemia and gouty arthritis. It is recommended to monitor the serum uric acid levels of patients with hyperuricemia and gout every six months. Uric acid measurement is not part of most routine metabolic profiles and must be ordered separately.
The typical presentation of gouty arthritis is recurrent flares of articular and peri-articular rapid onset inflammatory responses, affecting one or several joints. If left untreated, polyarticular inflammatory arthritis can develop as the disease progresses.
At first, urate crystals often exist silently in tissue for long periods of time. For reasons not completely understood, the urate crystals can trigger an intense bout of acute arthritis known as a flare. Identified triggers of gout flares include trauma; binges of alcohol or high protein foods; dehydration; and prolonged bed rest, often postoperatively.
Uric acid is the normal end product of purine metabolism. A marked increase in total body uric acid stores is fundamental to the development of gout. Hyperuricemia is a serum urate greater than 6.8 mg/dL in either adult men or women that does not change with laboratory norms. These norms vary by regions. They are population based ranges, not biochemical limits of urate solubility.
This is the accumulation of MSU crystals in joints, bones or soft tissue, including cartilage. Tophi are microscopic at first, but become macroscopic and are visible as firm nodules over time.
Uric acid stones can develop promoted by acidic urine. Interstitial nephropathy may also develop.
Did you know?
- Not everyone with hyperuricemia will develop gout. Only an estimated 1 in 5 people with a uric acid level above 7 mg/dL will ever experience symptoms of gouty arthritis.
- Those with a uric acid level above 9 mg/dL have a 50% chance of developing gouty arthritis.
- When uric acid levels reach 12 mg/dL, the chances of developing gout increases to 75%.
- One in three gout patients has not had their uric acid levels checked within the past five years.