Gout

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Gout

  • often familial
  • characterizedearly by a recurring acute arthritis, usually monarticular, and later by chronic deforming arthritis.
  • The associated hyperuricemia is due to overproduction or underexcretion of uric acid—sometimes both.
  • Secondary gout- acquired causes of hyperuricemia
    • diuretics, low-dose aspirin, cyclosporine, and niacin
    • myeloproliferative disorders
    • multiple myeloma
    • hemoglobinopathies
    • chronic kidney disease
    • hypothyroidism
    • psoriasis
    • sarcoidosis
    • lead poisoning
  • Alcohol ingestion promotes hyperuricemia
  • Hospitalized patients frequently suffer attacks of gout because of changes in diet, fluid intake, or medications
  • 90% of patients with primary gout are men
  • usually over 30 years of age.
  • In women, the onset is typically postmenopausal.
  • The characteristic lesion is the tophus
    • a nodular deposit of monosodium urate monohydrate crystals, with an associated foreign body reaction.
    • Tophi are found in cartilage, subcutaneous and periarticular tissues, tendon, bone, the kidneys
  • Urates have been demonstrated in the synovial tissues (and fluid) during acute arthritis
  • the acute inflammation of gout is believed to be activated by the phagocytosis by polymorphonuclear cells of urate crystals
  • release from the neutrophils of chemotactic and other substances capable of mediating inflammation.
  • chronichyperuricemia can be  found in people who never develop gout or uric acid stones.
  • Rapid fluctuations in serum urate levels, either increasing or decreasing, are important factors in precipitating acute gout.
  • late, chronic stage of gouty arthritis
    • tophaceous invasion of the articular and periarticular tissues
    • with structural derangement and secondary degeneration (osteoarthritis).
  • Uric acid kidney stones
    • are present in 5–10% of patients with gouty arthritis.
    • therisk of stone formation reaching 50% in patients with a serum urate level above 13 mg/dL.
  • Chronic urate nephropathy
  • caused by the deposition of monosodium urate crystals in the renal medulla and pyramids.

 

  • Symptoms and signs
    • Acute gouty arthritis
      • sudden in onset
      • frequentlynocturnal
      • The MTP joint of the great toe is the most susceptible joint ("podagra") (MCQ)
      • Gouty attacks may develop in periarticular soft tissues such as the arch of the foot.
      • Hips and shoulders are rarely affected.
      • occasionallypresents with asymmetric polyarthritis
      • As the attack progresses, the pain becomes intense.
      • The involved joints are swollen and exquisitely tender
      • the overlying skin tense, warm, and dusky red.
      • Fever is common and may reach 39 °C.
      • Local desquamation and pruritus during recovery from the acute arthritis are characteristic of gout
    • Tophi
      • may be found in the external ears, hands, feet, and olecranon and prepatellarbursae (MCQ)
      • They usually develop years after the initial attack of gout.
    • Asymptomatic periods of months or years commonly follow the initial acute attack.
    • After years of recurrent severe monarthritis attacks of the lower extremities and untreated hyperuricemia, gout can evolve into a chronic, deforming polyarthritis of upper and lower extremities that mimics rheumatoid arthritis.

 

  • Laboratory findings
    • The serum uric acid is elevated (> 7.5 mg/dL) in 95% of patients who have serial measurements during the course of an attack (MCQ)
    • However, a single uric acid determination is normal in up to 25% of cases, so it does not exclude gout, especially in patients taking urate-lowering drugs.
    •  During an acute attack, the ESR and white cell count are frequently elevated.
    • Identification of sodium urate crystals in joint fluid or material aspirated from a tophusestablishes the diagnosis.
    • The crystals, which may be extracellular or found within neutrophils, are needle-like and negatively birefringent when examined by polarized light microscopy (MCQ)
  • Imaging
    • Later, punched-out erosions with an overhanging rim of cortical bone("rat bite") develop.
    • When these are adjacent to a soft tissue tophus, they are diagnostic of gout.
  • Differential Diagnosis
    • A radiographic appearance similar to that of gout may be found in rheumatoid arthritis, sarcoidosis, multiple myeloma, hyperparathyroidism, or Hand-Schüller-Christian disease.
    • Chronic lead intoxication
      • result in attacks of gouty arthritis (saturnine gout) (MCQ)
      • causesabdominal pain, peripheral neuropathy, chronic kidney disease
      • basophilic stippling of red cells–  clue to the diagnosis.
    • Treatment
        • Asymptomatic hyperuricemia
          • Asymptomatic hyperuricemia should not be treated
          • uric acid–lowering drugsneed not be instituted until arthritis, renal calculi, or tophi become apparent.
        • Acute attack
          • Arthritis is treated first and hyperuricemia weeks or months later, if at all.
          • Sudden reduction of serum uric acid often precipitates further episodes of gouty arthritis.
        • NSAIDs
          • NSAIDs are the treatment of choice for acute gout (MCQ)
        • Colchicine
          • Neither oral nor intravenous colchicine should be used for the treatment of acute gout flares.
          • useoral colchicine during the intercritical period toprevent gout
        • Corticosteroids
          • Corticosteroids often give dramatic symptomatic relief in acute episodes of gout and will control most attacks.
          • They are most useful in patients with contraindications to the use of NSAIDs.
          • If the patient’s gout is monarticular, intra-articular administration (eg, triamcinolone) is most effective.
          • For polyarticular gout, corticosteroids may be given intravenously (eg, methylprednisolone) or orally (eg, prednisone).
          • Gouty and septic arthritis can coexist, albeit rarely. Therefore, joint aspiration and Gram stain with culture of synovial fluid should be performed before corticosteroids are given.
      • Management between attacks
        • Diet
          • Potentially reversible causes of hyperuricemia are a high-purine diet, obesity, alcohol consumption, and use of certain medications
          • Beer consumption appears to confer a higher risk of gout than does whiskey or wine.
          • Higher levels of meat and seafood consumption are associated with increased risks of gout
          • a higher level of dairy products consumption is associated with a decreased risk.
          • Although dietary purines usually contribute only 1 mg/dL to the serum uric acid level, moderation in eating foods with high purine content is advisable
          • A high liquid intake and, more importantly, a daily urinary output of 2 L or more will aid urate excretion and minimize urate precipitation in the urinary tract.
        • Drugs to be avoided
          • Thiazide and loop diureticsinhibit renal excretion of uric acid and should be avoided in patients with gout.
          • low doses of aspirinaggravatehyperuricemia, as does niacin.
        • Colchicine
          • Patients unlikely to benefit from chronic medical therapy.
            • Patients with a single episode of gout who are willing to lose weight and stop drinking alcohol
          • Patients  most likely to benefit from chronic medical therapy.
            • older individuals with mild chronic kidney disease who require diuretic usepatients with history of multiple attacks of gout
            • In general, the higher the uric acid level and the more frequent the attacks, the more likely that chronic medical therapy will be beneficial
          • Indications for daily colchicine therapy
            • colchicine can be used to prevent future attacks.
            • Patients who have coexisting moderate chronic kidney disease or heart failure
              • shouldtake colchicine only once a day
              • avoid the peripheral neuromyopathy that can complicate the use of higher doses.
            • colchicine can also be used when uricosuric drugs or allopurinol are started
              • tosuppress attacks precipitated by abrupt changes in the serum uric acid level.
        • Reduction of serum uric acid
          • Indications for a urate lowering intervention include
            • frequent acute arthritis not controlled by colchicine prophylaxis
            • tophaceous deposits
            • kidney damage.
          • Hyperuricemiawith infrequent attacks of arthritis may not require treatment.
          • If instituted, the goal of medical treatment is to maintain the serum uric acid at or below 5 mg/dL, which should prevent crystallization of urate.
          • Two classes of agents may be used to lower the serum uric acid—the uricosuric drugs and allopurinol
            • uricosuric drugs and allopurinol are of no value in the treatment of acute gout
            • The choice of uricosuric drugs vs allopurinoldepends on the result of a 24-hour urine uric acid determination.
              • A value under 800 mg/d indicatesundersecretion of uric acid
                • is amenable to uricosuric agentsif kidney function is preserved
                • is amenable toallopurinol if kidney function is limited.
              • Patients with more than 800 mg of uric acid in a 24-hour urine collection are overproducers
                • is amenable to only allopurinol.
          • URICOSURIC DRUGS
            • The following uricosuric drugs may be used:
              • Probenecid,
              • sulfinpyrazone,
            • block the tubular reabsorption of filtered urate
            • reduce the metabolic urate pool,
            • prevent the formation of new tophi and reduce the size of those already present.
            • When administered concomitantly with colchicine, they may lessen the frequency of recurrences of acute gout.
            • The indication for uricosuric treatment is the increasing frequency or severity of acute attacks.
            • Uricosuric agents are ineffective in patients with chronic kidney disease, with a serum creatinine of more than 2 mg/dL.
            • Adverse effects
              • Hypersensitivity to either with fever and rash
              • gastrointestinal complaints
            • Probenecid also inhibits the excretion of penicillin, indomethacin, dapsone, and acetazolamide.
            • Precautions with uricosuric drugs include maintaining a daily urinary outputof 2000 mL or more in order to minimize the precipitation of uric acid in the urinary tract.
              • This can be further prevented by giving alkalinizing agents (eg, potassium citrate) to maintain a urine pH of above 6.0.
            • Uricosuric drugs should not be used in patients with a history of uric acid nephrolithiasis.
            • Aspirin in moderate dosesantagonizes the action of uricosuric agents, but low doses (325 mg or less per day) do not
              • Doses of aspirin greater than 3 g daily are themselves uricosuric.
          • Allopurinol
            • The xanthine oxidase inhibitor allopurinol
            • promptlylowers plasma urate and urinary uric acid concentrations
            • facilitates tophus mobilization.
            • The drug is of special value in
              • uric acid overproducers
              • tophaceous gout
              • patients unresponsive to the uricosuric regimen
              • gouty patients with uric acid renal calculi.
            • It should be used in low doses in patients with chronic kidney disease
            • it is not indicated in asymptomatic hyperuricemia.
            • The most frequent adverse effect is the precipitation of an acute gouty attack.
            • Hypersensitivity to allopurinol
              • occurs in 2% of cases
              • can be life-threatening.
              • The most common sign of hypersensitivity is a pruritic rash that may progress to toxic epidermal necrolysis, particularly if allopurinol is continued
              • vasculitis and hepatitis are other manifestations.
            • Drug interactions
              • The combined use of allopurinol and ampicillin causes a drug rash in 20% of patients.
              • Allopurinol and Probenicid
                • Allopurinol can increase the half-life of probenecid
                • probenecidincreases the excretion of allopurinol.
                • Thus, a patient taking both drugs may need to use slightly higher than usual doses of allopurinol and lower doses of probenecid.
    • Gout in the transplant patient
          • Hyperuricemia and gout commonly develop in many transplant patients because
            • they have decreased kidney function
            • theyrequire drugs that inhibit uric acid excretion (especially cyclosporine and diuretics).
          • Treating these patients is challenging
            • NSAIDs are usually contraindicated because of underlying chronic kidney disease
            • intravenous colchicine should not be used because of its narrow therapeutic index (particularly in kidney dysfunction)
            • corticosteroids are already being used.
          • Often the best approach for monarticular gout—after excluding infection—is injecting corticosteroids into the joint
          • For polyarticular gout, increasing the dose of systemic corticosteroid may be the only alternative.
          • Allopurinol
            • should be started at a low dose in patients with kidney dysfunction
            • Allopurinol potentiates the effect of azathioprine.
              • dose of azathioprine should be reduced by 75% before allopurinol is started.

 

        • Prognosis
          • The younger the patient at the onset of disease, the greater the tendency to a progressive course.

 

Chondrocalcinosis&Pseudogout

    • Chondrocalcinosis is the presence of calcium-containing salts in articular cartilage.
    • commonly associated with (MCQ)
      • hemochromatosis
      • hyperparathyroidism
      • ochronosis
      • diabetes mellitus
      • hypothyroidism,
      • Wilson disease
      • gout.
    • Pseudogout
      • also called calcium pyrophosphate dihydrate (CPPD) deposition disease
      • is most often seen in persons age 60 or older
      • is characterized by acute, recurrent and rarely chronic arthritis involving large joints
      • involvesmost commonly the knees and the wrists
      • almost always accompanied by chondrocalcinosis of the affected joints. Other joints frequently affected are the MCPs, hips, shoulders, elbows, and ankles.
      • Pseudogout, like gout, frequently develops 24–48 hours after major surgery.
      • Identification of calcium pyrophosphate crystals in joint aspirates is diagnostic of pseudogout.
          • therhomboid-shaped crystals differ from the needle-shaped gout crystals.
          • A red compensator is used for positive identification, since pseudogout crystals are blue when parallel and yellow when perpendicular to the axis of the compensator.
          • Urate crystals give the opposite pattern
      • X-ray examination shows
          • calcification (usually symmetric) of cartilaginous structures
          • signs of degenerative joint disease (osteoarthritis).
      • Unlike gout, pseudogout is usually associated with normal serum urate levels.



    What is the Best Way to Diagnose Gout in the Foot?.m4v
    Hi… I’m Dr Christopher Segler, a podiatrist in San Francisco and this video will explain the best way to diagnose gout in the foot. Gout is one of the most painful conditions that can affect your foot. Gout hurts because you actually get thousands of needle-shaped uric acid crystals inside the joint. And if you’re watching this, your foot has probably become red, hot, and swollen as all of those sharp crystals have accumulated in the foot… most likely at the big toe joint. Wearing shoes is almost impossible when you have gout. In fact people who have gout will say it is so painful they can’t even stand to have the bed sheets on top of their foot. They have to sleep with the feet sticking out of the covers. Because the big toe joint is so painful you really should know the best way to diagnose gout in the foot, so that you can get the best treatment.
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