DEFINITION

Gout is a term used to refer to a group of disease states caused by tissue deposition of monosodium urate due to prolonged hyperuricemia. Clinical manifestations of gout include acute arthritis, soft tissue inflammation, chronic tophus formation, gouty nephropathy, and nephrolithiasis. Untreated hyperuricemia in patients with gout may lead to chronic destructive deforming arthritis.

ETIOLOGY

• Hyperuricemia and gout develop from excessive,uric acid production, a decrease in the renal excretion of uric acid, or both.
• Primary hyperuricemia results from an inborn error of metabolism and may be attributed to several biochemical defects.
• Secondary hyperuricemia may develop as a complication of acquired disorders (e.g., leukemia) or as a result of the use of certain drugs (e.g., diuretics). Consumption of alcohol, especially beer, increases the risk of gout, and fructose-rich beverage intake is associated with hyperuricemia. Lead toxicity can lead to gouty arthritis. Blood lead levels in the range currently considered acceptable are associated with increased prevalence of gout and hyperuricemia.
• Individuals with hyperuricemia who are predisposed with genetic factors develop clinical gout.

PHYSICAL FINDINGS & CLINICAL

PRESENTATION

1. ACUTE GOUT:

• Rapid onset of pain and swelling and erythema of a distal joint and/or periarticular soft tissue.
• May present as monoarthritis of any joint. Acute gout of the first metatarsophalangeal (MTP) joint is known as podagra
• 10% to 15% of attacks are polyarticular
• Spontaneous resolution occurs over days to weeks

1. CHRONIC TOPHACEOUS GOUT:

• Insidious onset of painless arthritis and soft tissue swelling
• Distal small joints characteristic
• May be confused with nodal osteoarthritis

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS OF

1. A. ACUTE GOUT

• Infectious arthritis
• Cellulitis
• Pseudogout

DIFFERENTIAL DIAGNOSIS OF

1. CHRONIC GOUT

• Osteoarthritis (especially nodal OA in women)
• Rheumatoid arthritis
• Psoriatic arthritis

Section II describes the differential diagnosis of acute monoarticular and oligoarticular arthritis.

WORKUP

Arthrocentesis and examination of synovial fluid.

• Uric acid: All patients with gout are hyperuricemic at some time, but during an acute attack the serum uric acid may be normal or low.
• Synovial aspirate: usually cloudy and markedly inflammatory in nature. Urate crystals in fluid are needle-shaped and strongly negatively birefringent under polarized microscopy.
• CBC: mild leukocytosis often present
• Inflammatory markers: ESR and CRP often elevated

IMAGING STUDIES

• Plain radiography for diagnosis and evaluation.
• No typical findings in early gouty arthritis but late disease is associated with characteristic punched-out marginal erosions and overhanging edges

TREATMENT OPTIONS

FOR ACUTE GOUT

• Nonsteroidal anti-inflammatory medication

+ Indomethacin 75 mg bid

+ Ibuprofen 800 mg tid

+ Naproxen 500 mg bid

• Low-dose colchicine (less toxic and as effective as traditional high-dose colchicine): 1.2 mg colchicine PO, followed by 0.6 mg PO 1 hr later.
• Intra-articular corticosteroid injection (treatment of choice for monoarticular large joint attack): Triamcinolone hexacetomide 40 mg or equivalent for knee
• Systemic corticosteroid therapy: Prednisone 40 mg PO for 3 days, then taper over 10 days (effective and safe, but evidence is lacking)

NONPHARMACOLOGIC THERAPY

Lifestyle and dietary modification may be effective in highly motivated patients. Should be attempted  only in patients with modestly elevated uric acid, as dietary modification can only lower uric acid 1 mg%. Discontinuation of diuretic therapy may help.

PHARMACOLOGIC TREATMENT OF SYMPTOMATIC HYPERURICEMIA

ALLOPURINOL:

• The initial dose should be low (100 mg/day depending on creatinine clearance) in patients with renal insufficiency and those with very high uric acid levels.
• The most common therapeutic dosage of allopurinol is 300 mg/day, but dose may be increased by 50-100 mg every two to three weeks until the target serum uric acid level is achieved.

FEBUXOSTAT:

• Novel xanthine oxidase inhibitor that has been shown to be more potent than allopurinol 300 mg daily for reducing serum uric acid.
• The metabolism of febuxostat is primarily hepatic, which obviates the need for dose adjustments due to renal insufficiency.

BENEMID and SULFINPYRAZONE:

• These uricosuric agents may only be used in patients with good renal function and urinary uric acid less than 600 mg in a 24-hr collection.

PEGLOTICASE:

• Intravenous pegylated uricase was approved by the FDA in 2010 for treatment of severe refractory tophaceous gout. It is a pegylated recombinant mammalian uricase that rapidly degrades urate when given intravenously.

Source: learningmedical
“Gout (Gouty Arthritis): Symptoms, Treatment, Causes, & More (With Treatment Protocol)”