Gouty Arthritis Diagnosis and Management
Dr. Abdulmaguid El-Ashmawy
Professor. of Rheumatology . Al Azhar University
Is a heterogeneous group of diseases found exclusively in man, manifested by:
1- Increase in the serum urate concentration.
2- Recurrent attacks of characteristic type of arthritis: acute or relapsing–self limiting-severe inflammatory- presence of monosodium urate monohydrate (MSU )crystals.
3- Tophi: ( urate deposits)
5-Uric acid uroliathiasis. urate stone.
Gout is caused by MSU crystals deposition. Gout is one of the oldest diseases in the medical literature, known since the time of the ancient Greeks.
Acute urate nephropathy is a form of acute renal failure that may occur when serum sric acid rapidly rises such as in patient with blood malignancies following chemotherapy . SUA increases up to >14mg exceeds it`s solubility leading to uric ascid crystal formation.
In patients who have had gout for many years renal disease is common. (25 % developed protinuria, 50% developed renal insufficiency , 25% developed end-stage renal diseases).
Sex distribution: M:F 2-7:1
Annual Incidence/1000: M (1 – 3) F( 0.2) .
Accounts for approximately 5 percent of all cases of arthritis.
Genetics : up to 18 % with gout have a family history of the disease. (polygenic disorders).
Men, particularly those between the ages of 40 and 50y.
Children and young adults: rare
Women, rarely develop the disorder before menopause. (>60y.) People who have had an organ transplant are more susceptible to gout.
1-Diet, rich in purines can cause or aggravate gout in some people. higher consumption of meat, seafood, beer, and fractuse containing food products.
2-Drug , low dose aspirin, thiazide diuretics.
The serum urate level is raised, but gout as manifested by arthritis , tophi, or uric acid stones has not yet appeared . Is clearly a risk factor for gout, It is necessary but not sufficient cause of gout.
In male subjects at risk for the primary gout this stage appears at puberty. In female is usually delayed until menopause.In patients with hyperuricemia secondary to enzyme deficiency this trait is present from birth.
After 20 t0 30 years may ended with gouty attack.
Women: 6 mg/dl.Men :
7mg/dl. Child (M&F) 3
: 4 mg per dl. Male at
puberty have elevation of12-
Gout may be either
primary or secondary (see Etiology). Primary gout is related to underexcretion or overproduction of uric acid, often associated with a mix of dietary excesses or alcohol overuse and metabolic syndrome. Secondary gout is related to medications or conditions that cause hyperuricemia, such as the following.
• Myeloproliferative diseases or their treatment
• Therapeutic regimens that produce hyperuricemia
• Renal tubular disorders
• Lead poisoning
• Hyperproliferative skin
• Enzymatic defects (eg, deficient hypoxanthineguanine phosphoribosyl transferase, glycogen storage diseases) Signs and symptoms
Symptoms of gout include the following:
• Sudden onset of a painful, hot, red, swollen joint, particularly in the foot at the big toe.
• Arthritis in other sites –the instep, ankle, wrist, finger joints, and knee.
• Monoarticular involvement most commonly, though polyarticular acute flares are not rare, and many different joints may be involved simultaneously or in rapid succession
• In gout, attacks that begin abruptly and typically reach maximum intensity within 812- hours.
• In some cases, polyarticular arthritis that can resemble rheumatoid arthritis Physical findings may include the following:
• Involvement of a single (most common) or multiple joints
• Signs of inflammation – Swelling, warmth, erythema (sometimes resembling
cellulitis), and tenderness
• Fever (also consider infectious arthritis)
• Migratory polyarthritis (rare)
• Posterior interosseous nerve syndrome (rare)
• Tophi in soft tissues (helix of the ear, fingers, toes, prepatellar bursa,
• Eye involvement – Tophi, crystal-containing conjunctival nodules, band
keratopathy, blurred vision, anterior uveitis (rare), scleritis
Complications of gout include the following
• Severe degenerative arthritis
• Secondary infections
• Urate or uric acid nephropathy
• Increased susceptibility to infection
• Urate nephropathy
• Renal stones
• Nerve or spinal cord impingement
• Fractures in joints with tophaceous gout
Joint aspiration and synovial fluid analysis.
• Serum uric acid measurement (though hyperuricemia is not diagnostic of gout)
• 24-hour urinary uric acid evaluation
• Blood studies (including white blood cells [WBCs, triglyceride, high-density lipoprotein, glucose, and renal and liver function tests) Plain radiographs may show, Erosions with overhanging edges are generally considered pathognomonic for gout (though also found in other diseases). Ultrasonographic findings in established gout include the following:
• A “double-contour” sign, consisting of a hyperechoic, and hypoechoic heterogeneous material with an anechoic rim
• Bony erosions adjacent to tophaceous deposits
• Computed tomography (CT) – Complementary to plain radiography for recognizing erosions in gout
• Magnetic resonance imaging (MRI) – MRI with gadolinium is Recommended Management
Gout is managed in the following 3 stages:
• Treating the acute attack.
• Providing prophylaxis to prevent acute flares.
• Lowering excess stores of urate to prevent flares of gouty arthritis and to prevent tissue deposition of urate crystals.
Agents used in this setting include the following:
• Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin most of the other NSAIDs can be
used as well, Cyclooxygenase-2 (COX-2) inhibitors have been used with success. Do not use aspirin, because it can alter uric acid levels and potentially prolong and intensify an acute attack. To control the acute attack, NSAIDs are prescribed at full dosage for 25- days.
• Corticosteroids Prednisone can be given at a dose of approximately 40 mg for 13- days, which is then tapered over approximately 2 weeks (tapering more rapidly can result in a rebound flare).
• Colchicine (now less commonly used for acute gout than it once was) The regimen currently favored consists of 1.2 mg of colchicine, followed by 0.6 mg 1 hour later to initiate treatment of the early gout flare, Colchicine should generally be avoided if the glomerular filtration rate (GFR) is lower than 10 mL/min, and the dose should be decreased by at least half if the GFR is lower than 50 mL/min. Colchicine should also be avoided in patients with hepatic dysfunction, biliary obstruction, or an inability to tolerate diarrhea.
• Adrenocorticotropic hormone (ACTH) (40 IU subcutaneously.
• Combinations of drugs (colchicine plus NSAIDs, oral corticosteroids plus colchicine, intra-articular steroids plus colchicine or NSAIDs) Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled (unless kidneys are at risk because of an unusually heavy uric acid load). Long-term management of gout is focused on lowering uric acid levels. Agents used include the following:
Because these agents change serum and tissue uric acid levels, they may precipitate acute attacks of gout. This undesired effect may be reduced by prophylaxis with the following:
• Colchicine or low-dose NSAIDs
• Low-dose prednisone (if patients cannot take colchicine or NSAIDs) Nonpharmacologic measures that may be warranted are as follows:
• Avoidance or restricted consumption of high-purine foods
• Avoidance of excess ingestion of alcoholic drinks, particularly beer
• Avoidance of sodas and other beverages or foods sweetened with high-fructose corn syrup
• Limited use of naturally sweet fruit juices, table sugar, and sweetened beverages and desserts, as well as table salt.
• Maintenance of a high level of
hydration with water (≥8 glasses of liquids daily).
• A low-cholesterol, low-fat diet, if such a diet is otherwise appropriate for the
• Weight reduction in patients who are obese.
Agents used in this setting include the following:
Other therapeutic agents that may be considered include the following:
• Uricase and pegloticase
• Vitamin C