Gout

See: Therapeutic Principles & Anti-Gout Meds


Discussion:

  • gout refers to articular dz of MSU deposits (tophi) in soft tissues.
  • it is caused by deposition of monosodium urate crystals in poorly perfused tissues, as well as bursae, ligaments, articular cartilage, and synovial membranes;
  • on avgerage, a family history of gout can be obtained in less than half patients'
  • male / female ratio ranging from 7:1 to 9:1
    • females with gout tend to be postmenopausal;
  • pathophysiology
  • predisposing conditions:
    • common chronic diseases assoc w/ gout include alcoholism, obesity, hypertension, CAD, and hypertriglyceridemia;
    • one beer a day may increase the uric acid level by 0.4 mg/dL and cause 50% increase in incident gout;
    • increased dietary purine intake;
    • decreased puring biosynthesis (lack of serum enzyme uricase);
    • medications: thiazide diuretics and antimetabolites
    • conditions which increase purine biosynthesis:
      • myeloroliferative disorders (polycythemia, AGL, CGL)
      • multiple myeloma;
      • sickle cell;
      • prolonged use of diuretics (thiazide diuretics may precipitate gout);
    • references:
  • diff dx:
  • prognosis:
    • arthritis remits completely and then recurs with increasing frequency;
    • in a pt w/ h/o acute gout, there is an 86% occurance of recurrent acute attack 3-5 days postoperatively if no prophylaxis is used;
    • after 1st attack, 2/3 of these pts will develop 2nd attack w/in 1 year;
    • w/in 2 years, three fourths will suffer a second attack;
    • 1/10 of these pts will not have 2nd attack for following 10 years;
    • w/ chronic gout, tophi develop in cartilage, tendons, and bursae in some patients

Clinical Presentation:

  • age: attacks of gout usually begin in males between ages of 30 and 50;
    • when women are affected they are usually post-menopausal (and are not on supplemental estrogen);
    • gout in women should prompt a more detailed work up of enzyme deficiency;
  • patients may complain of very mild attacks developing w/o provocation that abate w/o specific treatment;
  • podagara:
    • classic presentation of acute attack of first MTP joint;
  • hand:
    • may be confused with a hand infection;
    • may present with synovial swelling, joint swelling, tenosynovitis;
    • in the hand look for oval periarticular erosions;
    • multiple erosions will be distributed throughout the carpi and phalanges bilaterally;
    • erosions have sclerotic borders and will often have overhanging edges;
    • unlike classic RA, in early gout, hand and wrist joints will have preserved joint spaces and normal mineralization;

  • nephrolithiasis is major extraarticular manifestation;
    • in the urinary tract, the pH is less than 5.7, which causes urate to form of uric acid, which has poor solubility can cause precipitation of uric acid crystals;
    • only small % of pts w/ gout get tophi, but many get renal stones;
    • pure uric acid stones are found in 80%, & uric acid is probably nidus for Ca-Phos & oxalate calculi in remainder;
    • in 1/2, sx from renal stones actually precede arthritis.

Laboratory Studies for Gout


- Radiographs:

  • in the hand look for oval periarticular erosions;
  • multiple erosions will be distributed throughout the carpi and phalanges bilaterally;
  • erosions have sclerotic borders and will often have overhanging edges;
  • unlike classic RA, in early gout, hand and wrist joints will have preserved joint spaces and normal mineralization;
  • example:
    • case of histologically proven gout involving the proximal 5th metatarsal:


Therapeutic Principles & Anti-Gout Meds





Original Text by Clifford R. Wheeless, III, MD.

Last updated by Data Trace Staff on Monday, October 30, 2017 2:52 pm