Gout

Epidemiology: middle aged men > women. Most premenopausal women with gout have a family history of the disease.

Etiology:

    • Hyperuricemia

      • overproducers

      • underexcreters - 90% of cases of primary gouty arthritis.

    • Inborn errors of metabolism (Lesch-Nyhan)

    • High protein diet

    • Alcohol

    • Diuretics (decrease urate excretion)

    • Secondary gout: renal dz, ASA, nicotinic acid, cyclosporine, ethanol, starvation, lactic acidosis, DKA, dehydration, pre-eclampsia, myeloproliferative and lymphoproliferative d/o, hemolytic anemia, polycythemia, cyanotic CHD.

Clinical features:

    • Clinical phase is divided into:

      • Asymptomatic hyperuricemia

      • Acute gouty arthritis

      • Intercritical gout

      • Chronic tophaceous gout

    • Acute gouty arthritis is characterized by onset of extreme pain in small Jts, accompanied by redness and swelling. 50% of first gout attacks involve first MTP Jt, ankles. Occasionally polyarticular.

    • Precipitating factors: surgery, dehydration, fasting, binge eating of food high in protein, organ meats (high purine); heavy ingestions of alcohol.

    • If not treated attack can persists for day. Tx aborts sx within hours.

    • Tophi - aggregates of urate crystals and giant cells. These can erode away at tissue

    • Podagara - inflammation of first MTP, Jt.

Dx:

    • Aspirated Jt. fluid reveals needle-shaped monosodium urate crystals with negative birefringence.

    • CPPD crystals seen in pseudogout are pleomorphic and weakly positively birefringent

    • Elevated uric acid - but not always. Many do have elevated uric acid levels, but do not develop gout.

    • In order to demonstrate the characteristic birefringence, it is necessary to use a microscope with a first-order red compensator and a rotating stage. Urate crystals are bright (strongly birefringent), needle shaped and yellow (negatively birefringent) when lying parallel to the axis of the compensator (an axis reference is usually etched into the housing of the compensator).

    • In order to demonstrate the characteristic birefringence, it is necessary to use a microscope with a first-order red compensator and a rotating stage. Urate crystals are bright (strongly birefringent), needle shaped and yellow (negatively birefringent) when lying parallel to the axis of the compensator (an axis reference is usually etched into the housing of the compensator).

DDx: pseudogout, apatite disease, septic arthritis, RA, trauma, cellulitis,

Lab:

    • Hyperuricemia - elevated in only 30% of cases.

    • Elevated WBC

    • Elevated ESR

    • Isothenuria

Tx:

    • Prophylaxis:

      • Allopurinol - xanthine oxidase inhibitor

      • Probenecid - increased renal urate excretion

      • Dietary discretion - reduce intakes of high protein and high fat foods, discontinue alcohol

    • Acute attacks:

      • Indomethacin - NSAID

      • Colchicine - inhibit chemotaxis

      • Intra-articular corticosteroids - in monoarticular gout

ASA is c/i as it decreases urate excretion.

Gout and hyperuricemia

Definition: A d/o purine metabolism, resulting in urate depostion in Jt. spaces, resulting in inflammation and exquisite pain.

PSOS for Acute Gout:

Consult: Rheumatology

Diet: Avoid EtOH, foods high in purines (organ meats, sardines, anchovies). Avoid ASA

Labs/Dxtics: CCP, CBC with diff, Sr. uric acid, X-ray painful joint, Synovial fluid analysis, ESR, ANA, VDRL, RA, Lyme serology, BC x 2, UA (complete), Glu check AC/HS.

Tx:

  • IVF

  • Indomethacin 50 mg PO q6h x 2 days, then

    • 50 mg PO q8h x 3 days, and then

    • 25 mg PO q8h x 2 – 3 days. Give with meals

  • Nabumetone 500 mg PO bid (max 2 gm/day)

  • Glucocorticoids - useful when NSAIDs are contraindicated.

    • Triamcinolone hexacetonide, 20 – 40 mg for knee joints, and lower doses for smaller joints.

    • Prednisone 40 – 60 mg PO day x 1-2 day, until a response is seen, then tapered x 7 – 10 days.

  • Colchicine (useful when NSAIDs and glucocorticoids are C/I are not tolerated). Watch for N/V/D. Avoid in CKD. Effective if given in the first 12 - 24 hours of an acute attack.

    • Colchicine, 0.6 mg PO q1-2 h till sx control (max: 6 mg/day or N/V/D), then 0.6 mg PO bid

    • Colchicine IV (rarely used—used only in polyarticular gout, hosp. IP. Absolute C/I: Cr Cl <10mL/min. Can cause myelosuppression, hepatic necrosis, renal failure, DIC, Sz, death, tissue necrosis if extravasation occurs. Should not be diluted in D5W or Dextrose containing sol as it precipitates.

      • Colchicine, 1 - 2 mg in 10 – 20 ml NS given slowly over 3 – 5 minutes, F/up with 1 mg 6h later (max 4 mg/day). Reduce dose in elderly and renal and hepatic dz. No further doses given, if IV administer. Avoid further Colchicine PO or IV x 7 days.

      • Colchicine, 0.6 mg PO bid as a maintenance dose should be given a few days prior to manipulation of the uric acid level to avoid precipitation of an acute attack.

  • Allopurinol (xanthine oxidase inhibitor): no value in acute gouty arthritis. Prevents recurrence. But Pts who have been on anti-hyperuricemic Tx can contd. taking these meds during an acute attack.

    • Allopurinol 300 mg PO qd. Increase by 100 mg q2-4 wks to achieve maintenance dose that will keep uric acid level within normal range. Adjust for Cr. Cl: <20 mL/min: 100 mg q3rd day (MWF). Dose is also decreased in Pts with hepatic impairment.

    • If an acute attack occurs while Pt. is on Tx with allopurinol, c/w same dosage, while treating the attack.

    • SE: skin rash, exfoliative dermatitis, fever, eosinophilia, renal and hepatic injury - 5% Pts. Pts. with renal insufficiency and on diuretics are at highest risk of AKI.

    • Potentiates anticoagulants; blocks azathioprine and 6-MP metabolism, hence reduce the dosage of these drugs by ~60 - 75%.

  • Uricosuric drugs: block renal tubular reabsorption of uric acid.

    • Prior to starting Pt on these drugs, 24-h measurement of CrCl and Urine uric acid is obtained, because these drugs are ineffective if GFR is <50. Also not recommended if Urine uric acid levels are high, 800 mg/24 hr - risk of urate stone formation.

    • Risks minimized by IVF, alkalinizing urine.

    • If Pt. gets an acute gouty attack while on these drugs; c/w same dosage and treat acute attack.

    • Probenecid, 500 mg PO daily, raise dosage in increments of 500 mg qwk, until Sr. uric acid levels normalize or Urine uric acid >800 mg/24 hr. Max dose, 3000 mg/day

      • Salicylates and probenecid are antagonistic and must not be used together.

      • Probenecid reduces renal excretion of PCN, indomethacin, sulfonylureas. SE are minimal.

    • Sufinpyrazone has uricosuric acid same as probenecid, but inhibits platelet function. Dose, 50 mg PO bid, increase in increments of 100 mg qwk, till serum uric acid level normalize. Max dose, 800 mg/day.

  • Thiamine, 100 mg PO/IM/IV qday x 3 days

  • MVT, 1 PO qday

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