gout - med.unr.edu · pdf filegout shows erosive arthritis with the characteristic...

GOUT

Ewa Olech, MD

Rheumatology Division

Case

• A 78 year old man is seen in the clinic for a painful swelling of the left elbow. Over the past year, he has had a few episodes of pain and swelling in his right knee and left foot, for which he received ibuprofen and once was treated with an antibiotic.

• He also has hypercholesterolemia and hypertension and is on simvastatin, hydrochlorothiazide and metoprolol.

• He drinks several beers a day but does not smoke. His exam is remarkable only for the appearance of his hands

Labs

• His labs reveal (normal ranges):

• WBC 11.4/cu mm (4-10/cu mm).

• Hb 13.5 g/dL (11-14g/dL).

• Platelets 96/cu mm (150-450/cu mm),

• AST 65 U/L (20-45 U/L), ALT 64 U/L (20-45 U/L).

• Creatinine 1.7 mg/dL (0.6-1.2 mg/dL)

• ESR 86mm/hr (0-20mm/hr)

What is the most appropriate next step, respectively?• Aspiration of the olecranon bursa was performed

• Findings under polarized microscopy showed the presence of intracellular negatively birefringent crystals

• Treatment consists of injection of steroids (in the absence of an obvious infection) into the olecranon bursa.

• In addition to intra-articular injections, other treatments for acute gout include NSAIDs, colchicine, and oral glucocorticoids.

• Urate-lowering therapy should not be initiated during an acute attack.

• If a patient is already on urate-lowering therapy or it was briefly interrupted, it should be continued or restarted.

Definition• Gout is a syndrome caused by the inflammatory response to tissue

deposition of monosodium urate crystals (MSU).

Classification• Acute gout

• Tophaceus Gout

• Asymptomatic Hyperuricemia

• Primary Gout

• Secondary Gout

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

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.

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

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.

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.

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).

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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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