Gout by mohammad nour alsaeed

1. GOUT
 presented by : MOHAMMAD NOUR AL SAEED
 GROUP : 3
 Course : 6th
 Faculty : General Medicine

2. Gout is an inflammatory crystalline arthritis. Elevated uric acid
leads to deposition of monosodium urate (MSU) crystals in the
joints resulting in a red, hot, swollen joint. Gout typically begins
as a monoarthritis, but can become polyarthritic. Treatment of
acute episodes include NSAIDs, colchicine, or intraarticular
steroids. Chronic therapy includes lowering the uric acid level
using dietary modifications and urate-lowering drugs.

3. • Gout affects 1% to 2% of the U.S. population and
approximately 6% of men older than 80 years of age.
• Gout is more prevalent in men than women.
• Gout usually begins after age 30 years in men and after
menopause in women; it is familial in approximately 40% of
patients.

4. • Defective uric acid metabolism with inefficient renal urate
excretion leads to underexcretion of uric acid and an elevated
serum uric acid level.
• Overproduction of uric acid, instead of underexcretion, occurs
in approximately 10% of patients with gout, and also leads to
elevated serum uric acid levels.
• Elevated serum uric acid leads to deposition of MSU crystals in
the joints and the kidneys.
• Crystals trigger proinflammatory cytokines, which cause local
inflammation, tissue necrosis, fibrosis, and subchondral bone
destruction.

6. • Medications that cause hyperuricemia—Thiazide diuretics,
cyclosporine, aspirin (<1 g/day).
• Conditions associated with gout—Insulin resistance, obesity,
hypertension, hypertriglyceridemia, hypercholesterolemia,
congestive heart failure, renal insufficiency, early menopause,
organ transplant.
• Dietary—Increased intake of meat and seafood, alcohol, soft
drinks, and fructose.

7. Diagnostic characteristics useful in predicting gout, based on the 1977
criteria developed by the American College of Rheumatology, are:
• Monoarthritis.
• Redness over the joints.
• First metatarsophalangeal (MTP) joint involved .
• Unilateral first MTP joint attack.
• Unilateral tarsal joint attack.
• Tophi identified .
• Hyperuricemia.
• Asymmetric swelling in joint on radiograph.
• Subcortical cysts on radiograph.
• MSU crystals in joint fluid .
• Joint fluid culture negative.
The presence of 6 of these 11 criteria helps confirm gout (positive likelihood
ratio [LR+] 20, negative likelihood ratio [LR–] 0.02).

8. • Gout usually begins at night as an acute attack over several
hours.
• Fever, chills, and arthralgias sometimes precede gout.
• The affected joint is swollen, red, hot, and painful to touch and
movement . Symptoms subside in 3 to 10 days.
• Dietary or alcohol excess, trauma, surgery, and serious medical
illness can precipitate gout attacks.

9. Initially, only one joint may be affected, but other joints
commonly involved are fingers and toes (75%) and knees and
ankles (50%).
• The most common site is the first MTP joint and the name for
gout at this site is podagra .
• Joint involvement is often asymmetric.
• Tophi may be seen at the MTP joint, elbow, hands, and ears .

10. • Serum uric acid is often elevated, but is variable from week to
week and normal in 25% of patients with gout.
• Measure 24-hour urine for excretion of uric acid.
• On microscopy, the presence of MSU crystals from synovial
fluid or a tophus that are negatively birefringent in polarized
light (yellow against a red background) helps to confirm the
diagnosis, but there are limited data on the accuracy of crystal
identification.
• Even with light microscopy refractile needle-shaped crystals of
uric acid can be visualized in the joint fluid .

11. ACUTE GOUT
• Prescribe an NSAID, such as indomethacin 50 to 75 mg every 6
to 8 hours, in patients without renal impairment (serum
creatinine should be <2) or peptic ulcer disease. SOR
• Colchicine can be used in patients who cannot take NSAIDs.
Colchicine 1.2 mg followed by 0.6 mg after 1 hour has equivalent
efficacy and lower side effects compared to a high dose of 4.8
mg given over 6 hours. One third of patients will respond. SOR
• In monoarticular gout, consider an intraarticular injection
with long-acting steroid (e.g., triamcinolone acetonide, 10 to 40
mg, depending on the size of the joint). SOR

12. CHRONIC GOUT
The treatment of chronic gout includes modifications in diet
and existing medications (if possible) and lowering urate levels.
Treatment measures include:
• Nonpharmacologic:
Reduce the intake of protein-rich foods (e.g., organ meats, red
meats, and seafood).
Increase fluid intake to 2000 mL/day.
Lower alcohol intake.
Consume dairy products as these may be protective against
gout.

13. • Medications:
Change medications—Discontinue aspirin (low dose up to 2 g/day causes uric acid
retention) and consider stopping a thiazide diuretic.
Lower urate levels with xanthine oxidase inhibitors (e.g., allopurinol), uricosuric agents
(e.g., probenecid) or uricase agents (e.g., pegloticase).
The level of urinary uric acid helps to determine which medication should be used with
levels >600 mg/24 hours indicating a need to halt production with xanthine oxidase
inhibitors and levels less than 600 mg/24 hours indicating a need for uricosuric drugs.
Allopurinol (100 to 300 mg/day for mild gout; for patients with moderate to severe
tophaceous gout give 400 to 600 mg/day with a maximum daily dose of 800 mg/day). Titrate
allopurinol to a serum uric acid level less than 6. SOR
Give colchicine (0.6 mg twice daily for the first 6 months of therapy) concomitantly during
initiation of allopurinol to reduce the frequency and severity of acute flares. SOR

14. Consider uricosuric agents (probenecid, 250 mg twice daily increasing to 2 to 3 g/day or
sulfinpyrazone, 50 to 100 mg twice daily increasing to 200 to 400 twice daily) in patients
with uric acid excretion of less than 600 mg/24 hours, with normal renal function, younger
than age 60 years, and no history of renal calculi. SOR
Consider oral potassium citrate (10 to 20 mEq 3 to 4 times a day) to prevent crystal
precipitation in the urine as uricosuric agents increase urinary uric acid excretion.
Pegloticase, a mammalian recombinant uricase, is a medication that degrades urate when
administered by intravenous infusion. Early randomized controlled trials show
improvements in pain and quality of life; however, adverse events are high. This may be an
option for patients with severe gout, allopurinol intolerance or refractoriness, and serum uric
acid greater than 8 mg/dL despite conventional therapy.
• Complementary and alternative therapy:
A number of Chinese and Vietnamese medicinal plants and herbs have xanthine oxidase
inhibitory activity, but few have been tested for clinical effectiveness.

15. Thank you for your attention