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Crystal-induced arthropathies

-Crystalline deposition in articular and periarticular tissues that may have both acute and chronic progression
-Accompanied by inflammatory responses


Crystal species in associated d/o

-Monosodium urate: gout (yellow when parallel, negative birefringence)
-Calcium pyrophosphate: pseudogout (yellow when perpendicular, positive birefringence)
-Hydroxyapatitie: calcific periarthritis
-Uric acid does not occur in synovial fluid (only in urine/blood), monosodium urate occurs in synovial fluid


Crystal inflammation

-Stimulates release of inflammatory mediators: arachidonic acid (ACA) metabolites, ILs (IL1, IL6, IL8), TNF
-Promotes granulocyte influx


Clinical presentation of gout

-Intermittent attacks
-First MTP joint (big toe) frequently first
-Recurrent attacks, tophaceous deposits over time
-Tophaceous gout: usually after 10 yrs of gout, no longer pain free btwn attacks
-There is subQ deposits of monosodium urate (tophi), can be in unusual places but often unilateral
-W/o Rx 50% will get them


Conditions associated w/ urate overproduction

-HGPRT deficiency: salvage pathway for purines (HGPRT prevents catabolism of purines into uric acid)
-PRPP synthetase super activity: nz responsible for de novo purine synthesis
-Myeloproliferative disease
-Glycogen storage disease


Gout lab findings

-Most pts w/ hyperuricemia do not have gout, but most gout pts have elevated uric acid
-Visual confirmation of crystals in joint fluid, w/ inflammation in synovial fluid
-Radiographic features: X-rays negative in early gout, erosions apparent w/ atrophy/hypertrophy of certain areas
-Results in overhanging edge appearance


Excretion of uric acid in gout

-Normally uric acid is excreted mostly by kidneys (small amount from intestines)
-Most cases of gout are not over production of uric acid, but underexcretion of it
-These pts have normal purine metabolism but faulty renal excretion
-Some pts will have overproduction of purines, and will have large (normal) excretion of urinary uric acid
-Solubility of purine metabolites important for excretion


Rx of gout

-For acute attacks use Colchicine: inhibits release of chemotactic protein to prevent inflammation (effective early in attacks and to prevent future attacks)
-NSAIDs (indomethacin), GCCs, uricosurates
-For Rx of hyperuricemia: asymptomatic pts do not need Rx usually, otherwise use xanthine oxidase inhibitor allopurinol



-Xanthine oxidase inhibitor (XO is nz in common pathway for purine degradation)
-Indications: urate overproducer, tophus formation, nephrolithiasis, excessive cell turnover



-Calcium pyrophosphate dihydrate crystal deposition disease (CPPD)
-Crystals present in cartilage: chondrocalcinosis
-Acute onset of self-limited attacks that may last 2 weeks
-First in knee joints for 50% of pts, all joints can be affected
-Asymptomatic btwn attacks, can have fever w/ attacks
-Chronic Sx in some pts
-Associated w/ hyperparathyroidism and hemochromatosis


Pathogenesis of pseudogout (CPPD)

-Associated w/ hyperparathyroidism and hemochromatosis
-Normal plasma and urinary excretion of inorganic pyrophosphate, but synovial fluid pyrophosphate elevated
-Crystals form in joint fluid and elicit cytokine response


Rx of CPPD

-NSAIDs, colchicine, GCCs can pharmacologically help
-Aspiration of joint capsule and steroid injections


Calcium phosphate disease

-Generally more periarticular Sx, may also cause local inflammation
-High percentage of OA pts have CaPO in joint fluid
-Both acute and chronic forms
-Large joint (shoulder, hips, ect) destruction arthritis
-Calcinosis cutis: accumulation in soft tissues, mostly in pts w/ scleroderma
-Clinical Sx generally tendonitis, X-rays reveal soft tissue calcification
-Rx: NSADs, local GCCs, physical therapy to prevent contracture