Gout

= characterized by derangement of purine metabolism manifested by:

• hyperuricemia
• deposition of positively birefringent monosodium urate monohydrate
crystals in synovial fluid leukocytes
• gross deposits of sodium urate in periarticular soft tissues (synovial
membranes, articular cartilage, ligaments, bursae)
• recurrent episodes of arthritis

P.97

Age >40 years; males (in women gout may occur after menopause)
:
Cause:

• Primary Gout (90%)

Incidence 0.3%; M:F = 20:1; 5% in postmenopausal women
:
• Disturbance:
o overproduction of uric acid due to inborn error of metabolism
o inherited defect in renal urate excretion
o Idiopathic (99%)
 normal urinary excretion (80–90%)
 increased urinary excretion (10–20%)
o Specific enzyme / metabolic defect (1%)
 increased activity of PP-ribose-P synthetase
 partial deficiency of hypoxanthine-guanine
phosphoribosyltransferase
• Secondary Gout (10%)
o Rarely cause for radiographically apparent disease
o increased turnover of nucleic acids:
 Myeloproliferative disorders + sequelae of their
treatment: polycythemia vera, leukemia, lymphoma, multiple
myeloma
 Blood dyscrasias: chronic hemolysis
o increase in purine synthesis de novo due to enzyme defects:
 Glycogen storage disease Type I (von Gierke = glucose-
6-phosphatase deficiency)
 Lesch-Nyhan syndrome (choreoathetosis, spasticity,
mental retardation, self-mutilation of lips + fingertips) due to
absence of hypo-xanthine-guanine phosphoribosyltransferase
o acquired defect in renal excretion of urates (due to reduction in
renal function):
 Chronic renal failure
 Drugs, toxins: lead poisoning
 Endocrinologic: myxedema, hypo- /
hyperparathyroidism
 Vascular: myocardial infarction, hypertension
Histo tophus (PATHOGNOMONIC LESION) composed of crystalline / amorphous
: urates surrounded by highly vascularized inflammatory tissue rich in
histiocytes, lymphocytes, fibroblasts, foreign-body giant cells (similar to a
foreign-body granuloma)
Clinical stages in chronologic order:

• Asymptomatic hyperuricemia
• Acute gouty arthritis
o Gout accounts for 5% of all cases of arthritis
Precipitated trauma, surgery, alcohol, dietary indiscretion, systemic
by: infection
o • monoarticular (90%)
o • polyarticular (10%): any joint may be affected
Prognosis usually self-limited (pain resolving within a few hours /
: days) without treatment
• Chronic tophaceous gout
o = multiple large urate deposits in intraarticular, extraarticular,
intraosseous location
Prevalence: <50% of patients experiencing acute attacks; M:F = 20:1
Histo: cartilage degeneration + destruction, synovial
proliferation + pannus, destruction of sub-articular bone +
proliferation of marginal bone
Distribution symmetric polyarticular disease (resembling rheumatoid
: arthritis), asymmetric polyarticular disease, monoarticular
disease
o • more severe prolonged attacks
o • may ulcerate expressing whitish chalky material
Cx tendon rupture, nerve compression / paralysis
:
• Gouty nephropathy / nephrolithiasis
o Acute urate nephropathy
o Uric acid urolithiasis
 May precede arthritis in up to 20% of cases!
 • renal hypertension
 • isosthenuria (inability to concentrate urine)
 • proteinuria
 • pyelonephritis

Cx increased incidence of calcium oxalate stones (urate crystals

: serve as a nidus)
Location:

• joints: hands + feet (1st MTP joint most commonly affected = podagra)
> ankles > heels > wrists (carpometacarpal compartment especially common
and severe) > fingers > elbows; knees; shoulder; sacroiliac joint (15%,
unilateral);
o involvement of hip + spine is rare
• bones, tendon, bursa, bones
• external ear; pressure points over elbow, forearms, knees, feet
• Radiologic features usually not seen until 6–12 years after initial
attack
• Radiologic features present in 45% of inflicted patients
• @ Soft tissues
o eccentric juxtaarticular lobulated soft-tissue masses (hand, foot,
ankle, elbow, knee)
Site tendency for extensor tendons, eg, quadriceps, triceps, Achilles
: tendon
o calcific deposits in periphery of gouty tophi in 50% (sodium
urate crystals are not radiopaque, tophi radiographically visible only
after calcium deposition of an underlying abnormality of calcium
metabolism)
o bilateral effusion of bursae olecrani (PATHOGNOMONIC),
prepatellar bursa
o aural calcification
• @ Joints
o joint effusion (earliest sign)
o periarticular swelling (in acute monoarticular gout)
o preservation of joint space until late in disease (IMPORTANT
CLUE):
 cartilage destruction (late in course of disease)
o absence of periarticular demineralization (due to short duration
of attacks; important DDx for rheumatoid arthritis)
o eccentric erosions with thin sclerotic margins:
 scalloped erosion of bases of ulnar metacarpals
o chondrocalcinosis (5%):
Location menisci (fibrocartilage only)
:
 Patients with gout have a predisposition for calcium
pyrophosphate dihydrate deposition disease (CPPD)

P.98

Cx secondary osteoarthritis
:

o round / oval well-marginated subarticular cysts (pseudotumor)

up to 3 cm (containing tophus / urate crystal-rich fluid)
DDx rheumatoid arthritis (marginal erosions without sclerotic rim,
: periarticular demineralization)
• @ Bone
o “punched-outâ€‌ lytic bone lesion ‫آ‬± sclerosis of margin =
“mouse / rat biteâ€‌ from erosion of long-standing soft-tissue tophus
o “overhanging marginâ€‌ (40%) = elevated osseous spicule
separating tophaceous nodule from adjacent erosion (in intra- and
extraarticular locations) (HALLMARK)
o proliferative bone changes:
  club-shaped metatarsals, metacarpals, phalanges
 enlargement of ulnar styloid process
 diaphyseal thickening
o ischemic necrosis of femoral / humeral heads
o intraosseous calcification:
 punctate / circular calcifications of subchondral /
subligamentous regions (DDx: enchondroma)
 bone infarction due to deposits at vascular basement
membrane (DDx: bone island)
• @ Kidney
o renal stones (in up to 20%):
 pure uric acid stones (84%): radiolucent on radiographs,
hyperdense on CT
 uric acid + calcium oxalate (4%)
 pure calcium oxalate / calcium phosphate (12%)
• MR:
o tophus (most frequently) isointense to muscle on T1WI
o low or intermediate signal intensity on T2WI
o homogeneous intense enhancement

Rx colchicine, allopurinol (effective treatment usually does not improve

: roentgenograms)
DDx:

• CPPD (pseudogout symptomatology, polyarticular chondrocalcinosis

involving hyaline and fibrocartilage + degenerative arthropathy with joint
space narrowing)
• Psoriasis (progressive joint space destruction, paravertebral
ossification, sacroiliac joint involvement)
• Rheumatoid arthritis (nonproliferative marginal bone erosions,
fusiform soft-tissue swelling, symmetric distribution, early joint-space
narrowing, osteopenia)
• Joint infection (rapid destruction of joint space, loss of articular cortex
over a continuous segment)
• Amyloidosis (bilateral symmetric involvement, periarticular
osteopenia)
• Xanthomatosis (laboratory work-up)
• Osteoarthritis (symmetric distribution, elderly women)