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GOUT AND PSEUDOGOUT ANDRES QUICENO, MD Rheumatology Division Presbyterian Hospital of Dallas
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Definition Gout is a syndrome caused by the inflammatory response to tissue deposition of monosodium urate crystals (MSU).
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Classification Acute gout. Tophaceus Gout. Asymptomatic Hyperuricemia. Primary Gout. Secondary Gout.
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Etiology Hyperuricemia is the common denominator in gout. Two-thirds of uric acid are excreted by the kidney and the rest in the GI tract. 90% of cases of gout are secondary to under-excretion. Overproduction is secondary to defects in the HGPRT or PRPP.
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Etiology The inflammatory response is secondary to the response of the leukocytes to the MSU crystals. Acute gout is most likely secondary to the formation of new crystals. Factors that precipitate gout includes: surgery, trauma, alcohol, starvation and medications.
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Pathology The most frequent sites of deposition of MSU crystals are: cartilage, epiphyseal bone, periarticular structures and the kidney. A tophus is a foreign body reaction that includes the MSU crystals surrounded by fibrous tissue. In the kidney the deposition of MSU crystals causes interstitial fibrosis and arteriosclerosis.
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Epidemiology The prevalence of asymptomatic hyperuricemia is 5 to 8%. The prevalence of gout is 13 cases per 1000 men and 6.4 cases per 1000 women. The higher the uric acid, the higher the risk to develop gout. 90% of patients with primary gout are men.
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Epidemiology Women rarely develop gout before the menopause, because estrogens are thought to be uricosuric. Peak incidence in men is in the fifth decade. Primary gout is associated with: obesity, hyperlipidemia, diabetes mellitus, hypertension and atherosclerosis.
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Epidemiolgy Causes of secondary gout include: Excessive dietary purine intake, increase nucleotide turnover (e.g., lymphoproliferative disorders, hemolytic anemia, psoriasis), Glycogen storage diseases, diminished renal function, ketoacidosis, lactic acidosis, hyperparathyroidsm and medications.
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Clinical Manifestations Acute gout: acute arthritis is the most common manifestation. The most common is the podagra. 50% of patients experience their first attack in this joint. 80% of the attacks are monoarticular and typically involve the lower extremities. (MTP’s, ankle and knee).
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Clinical Manifestations Less common sites of involvement include wrist, fingers and elbow. Differential diagnosis includes septic arthritis, cellulitis or thromboflebitis. Attacks subside in 3 to 10 days. Recurrent attacks can involve more joints and usually persist longer.
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Clinical manifestations Repeated attacks could cause joint erosions. Polyarticular attacks are common in patients with established poor controlled disease. These attacks could also involve periarticular structures.
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Clinical Manifestations Intercritical gout: It is the asymptomatic period between crises, but MSU crystals can still be recovered if necessary. The duration of this period varies, but untreated patients may have a second episode within two years. Some patients evolve to chronic polyarticular gout without pain free intercritical episodes.
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Clinical Manifestations Chronic tophaceus Gout: The clinical characteristic is the deposition of solid urate in the connective tissue. It is associated with early age of onset, long duration of untreated disease, frequent attacks, upper extremity involvement, polyarticular disease and elevated serum uric acid.
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Clinical Manifestations Transplant patients treated with cyclosporine and/or diuretics have an increased risk for tophaceus gout. The most common sites for tophi are: the olecranon, prepatellar bursa, ulnar surface and Achilles tendon.
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Clinical Manifestations Tophi in the hands can cause joint destruction. Tophi can ulcerate the skin and excrete a chalky material composed of MSU crystals. Tophi progress insidiously with increased stiffness and pain.
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Clinical Manifestations Renal disease: this includes urolithiasis, urate nephropathy (deposition of MSU crystals in the interstitium), and uric nephropathy ( deposition of MSU crystals in the collecting tubes). The prevalence of urolithiasis is 22% in primary gout and 42% in secondary gout.
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Clinical Manifestations Uric acid nephropathy may present acutely in patients being treated for malignancy. Urate nephropathy is slowly progressive and associated with hypertension and proteinuria.
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Diagnostic Tests Uric Acid: normal values range from 4.0 to 8.6 mg/dl in men to 3.0 to 5.9 mg/dl in women. Urinary levels are normal below 750 mg/ 24h. Urinary levels above 750 mg/dl in 24h in gout or > 1100 mg/dl in asymptomatic hyperuricemia indicates urate overproduction.
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Diagnostic tests Joint Fluid: in acute gout it is inflammatory (>2000 cells/ml); MSU crystals are identified with the polarized light microscope. In acute gout the crystals are usually intracellular. The MSU crystals do not exclude the possibility of septic arthritis, for this reason it is also recommended to request a Gram smear.
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Diagnostic Tests 24 urine collection for uric acid determination is useful in assessing the risk of renal stones and planning for therapy. Radiological examination is helpful to exclude other kinds of arthritis. Long term gout shows erosive arthritis with the characteristic “punched-out” erosions.
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Differential Diagnosis Acute Gout: septic arthritis, pseudogout, Reactive arthritis, acute rheumatic fever and other crystalline arthropathies. Chronic tophaceus gout: Rheumatoid Arthritis, Pseudogout, seronegative spondyloarthropathies and erosive osteoarthritis.
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Therapy Usually there is no justification for treatment of asymptomatic hyperuricemia. But some physicians treat if serum uric acid is > 12 mg/dl and there is risk of nephrolithiasis. In the setting of malignancy, when tumor lysis can cause hyperuricemia, allopurinol is recommended.
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Therapy Acute Gout: NSAID’s, corticosteroids or oral colchicine can be used. NSAID’s are the preferred modality. When NSAID’s are contraindicated, corticosteroids are effective.
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Therapy Intra-articular corticosteroids are an alternative when systemic therapy is contraindicated. Colchicine has been the medication traditionally used for acute gout, but it has significant GI toxicity and delayed onset of action.
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Therapy Intercritical Gout: the focus in this stage is prevention and prophylaxis. Patients with only one or few attacks it is acceptable to wait and treat the acute attacks. Patient with frequent attacks should be offered medical therapy.
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Therapy Diet is usually impractical, ineffective and rarely adhered to in clinical practice. Indications for pharmacological therapy includes: inability to reverse secondary causes, tophaceus gout, recurrent acute gout and nephrolithiasis.
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Therapy The pharmacological agents indicated for gout include: uricosuric (probenecid, sulfinpyrazone) or inhibitors of uric acid production (allopurinol). Uricosuric agents are indicated in patients with normal renal function, under-excretion and no evidence of tophi.
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Therapy Patients taking uricosuric agents are at risk for urolithiasis. This can be decreased by ensuring high urinary output and by adding sodium bicarbonate 1 gram TID. The available agents include: probenecid (1-2 g/day) and sulfinpyrazone (50-400 mg BID). Dose should be increased to decrease uric acid < 6.0 mg/ml
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Therapy Allopurinol decreases uric acid in overproducers and underexcreters; it is also indicated in patients with a history of urolithiasis, tophaceus gout, renal insufficiency and in prophylaxis of tumor lysis syndrome.
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Therapy Allopurinol: usual dose is 300 mg/day. Maximal recommended dose is 800 mg/day. In renal insufficiency dose should be decreased to 200 mg/day for creatinine clearance < 60ml/min and to 100 mg/day if clearance < 30 ml/min).
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Therapy Start with small doses of allopurinol to reduce the risk of precipitating an acute gout attack. Most common side effects are rash (2% of patients) but rarely patients can develop exfoliative dermatitis that can be lethal. Chronic use of colchicine (0.6-1.2 mg/day) is used as prophylaxis for acute attacks.
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PSEUDOGOUT Calcium pyrophosphate Crystal Deposition Disease (CPPD) is the syndrome secondary to the calcium pyrophosphate in articular tissues. This includes: Chondrocalcinosis, Chronic CPPD and Pseudogout.
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Pseudogout Etiology: It is unknown, but can be secondary to changes in the cartilage matrix or secondary to elevated levels of calcium or inorganic pyrophosphate. Pathology: CPPD crystals are found in the joint capsule and fibrocartilaginous structures. There is neutrophil infiltration and erosions.
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Pseudogout Demographics: It is predominantly a disease of the elderly, peak age 65 to 75 years old. It has female predominance (F:M, 2-7:1). Prevalence of chondrocalcinosis is 5 to 8% in the general population.
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Pseudogout Disease Associations: hyperthyroidsm, hypocalciuria, hypercalcemia, hemochromatosis, hemosiderosis, hypophosphatasia, hypomagnesemia, hypothyroidsm, gout, neuropathic joints, amyloidosis, trauma and OA.
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Pseudogout Clinical Manifestations Pseudogout: Usually presents with acute self-limited attacks resembling acute gout. The knee is involved in 50% of the cases, followed by the wrist, shoulder, ankle, and elbow.
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Pseudogout In 5% of patients gout can coexist with pseudogout. The diagnosis is confirmed with the synovial fluid analysis and/or the presence of chondrocalcinosis in the radiographs. Acute Pseudogout primarily affects men.
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Psedogout Chronic CPPD: predominately affects women; it is a progressive, often symmetric, polyarthritis. Usually affects the knees, wrists, 2nd and 3rd MCP’s, hips, spine, shoulders, elbows and ankles. Chronic CPPD differs from pseudogout in its chronicity, involvement of the spine and MCP’s.
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Pseudogout Chondrocalcinosis: Generally is an incidental finding in XRays. Diagnostic Tests: Inflammatory cell count in the synovial fluid. Rhomboidal or rodlike intracellular crystals. Imaging studies reveal chondrocalcinosis usually in the knee, but can be seen in the radial joint, symphisis pubis and intervertebral discs.
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Pseudogout Differential Diagnosis: Includes septic arthritis, gout, inflammatory OA, Rheumatoid Arthritis, neuropathic arthritis and Hypertrofic Osteoarthropathy.
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Pseudogout Therapy: It is similar to gout and includes intrarticular corticosteroids. Colchicine can be used in acute attacks and also in prophylaxis. There is no specific treatment for chronic CPPD. It is important to treat secondary causes and colchicine could be helpful.
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