Gout In Kiswahili “maumivu ya jongo”

Notes
  • A metabolic disorder of purine metabolism. It occurs when uric acid plasma levels are elevated causing it to crystallize in the form of monosodium urate. These crystals then form tophi (deposits) in joints, on tendons and in the surrounding tissues.
  • When urate crystals break from the protein mesh-walled tophi, immune-mediated inflammatory reaction, with the main proteins in the inflammatory cascade being interleukin-1β, occurs.
  • The known triggers of precipitation of uric acid include:

_Cold (hence more likelihood of the toe being affected)

_Increased uric acid levels

_Acidosis

_Reduced articular hydration

_Extracellular matrix proteins e.g. proteoglycans, collagens and chondroitin sulfate

_Thiazide diuretics

_Aspirin (even low dose)

_Ethambutol

_Pyrazinamide

_Tumour lysis syndrome (following cytotoxic therapy)

_Hemolytic anemia

_Polycythemia

_Myeloproliferative /lymphoproliferative disorders

  • Statistics: Global prevalence of gout - 0.08%.
Symptoms
  • For acute gout;

_Excruciating pain of single joints, mainly big toe

_Erythema and warmth over the effected joints

_Tophi (mainly in pinna and areas underlying olecranon bursa)

  • Intercritical gout (interval between attacks)

_Signs of renal disorder may appear

_Uric acid nephrolithiasis

_Bone disorders

Diagnosis
  • Clinical evaluation
  • Acute arthritis of the great toe (podagra)
  • X-ray (but not useful in acute gout)
  • Synovial fluid where monosodium urate spiked rod crystals or tophi are identified (expertise required)
  • Blood test for hyperuricemia (above 420 μmol/l in male 360 μmol/l in female). This test is of limited use because some individuals are hyperuricemic without gout (about 50%) while others have no hyperuricemia and yet they have gout)
  • WBC and ESR may be elevated due to gout in the absence of infection.
Differential
  • Septic arthritis
  • Pseudogout
  • Rheumatoid arthritis
  • Basal cell carcinoma or other neoplasms (especially gouty trophi outside the joints)
Prevention
  • Reduce meat (especially roasted) and seafood
  • Avoiding obesity
  • Reduce alcohol uptake
  • Taking coffee (not tea)
  • Reduce sleep apnea
Management
  • Acute gout is treated with;

NSAIDS or COX-2;

Either;

_Tabs Ibuprofen 400 - 800mg TID

Or;

_IM  Diclofenac 75mg  STAT the  PRN

Or;

_Tabs Naproxen 250mg BD

Or;

_Other NSAIDS or COX-2s

_Tabs Colchicine, initially one mg then 500mcg every two to three hours until the pain is relieved or vomiting or diarrhoea occur or a total dose of 10mg has been administered.  The treatment should not be repeated within 3 days.  Prevention of attacks during initial treatment with allopurinol or uricosuric drugs: 500mcg BD or TID.

  • Intercritical and tophaceous gout;

_Colchicine to prevent acute gout flares during initiation of allopurinol therapy:

*Tabs Colchicine 0.5-0.6mg BD for around 2 weeks THEN

*Tabs Allopurinol;

Tabs Allopurinol 100mg OD.

Increase by 100mg monthly (to max. of 400mg/day; average 300mg/day)  until the plasma level or uric acid is below 0.3 m m/L

upto  life  long

Or;

*Tabs Probenecid 250mg BD

_Increase Vitamin C uptake (Tabs  Vitamin C 1500mg daily is useful)

  • Systemic corticosteroids (oral or parenteral or intra-articular by an expert) should be given to patients who cannot tolerate NSAIDS or COX-2.

    Either;

_Tabs Prednisone or Prednisolone 0.5mg /kg/day x 7-10 days.

Or;

_Tabs Prednisone or Prednisolone 0.5mg /kg/day x 2-5 days then taper for 7-10 days.

Or;

_IM Triamcinolone 60mg STAT the repeat the prednisone or Prednisolone regime  with the above  options.

  • Asymptomatic hyperuricemia needs not be treated pharmacologically; observe the preventive measures below;
Drug Index 2.0 is here
Our new update features a more powerful search feature and easier login. Having any issues? Contact us today. Contact Us