Crystal Arthritis

    Table of contents




    • Crystals are deposited, and "flare" when there is immune activation.
      • Causes of flare can be acute diuresis, AKI, dehydration, etc..
    • Usually precipitates in "cooler" joints (MTP, ankle, hand - distal joints)
    • Eventually can settle down on their own (i.e. heat can dissolve them)
    • Causes:  Hyperuricemia
      • Overproduction
        • Dietary
        • ETOH
        • Nucleotide turnover
      • Underexcretion
        • Renal Disease
        • Lead Nephropathy
      • Drugs:
        • Cyclosporin, Alcohol, Nicotinic Acid, Thiazides, Lasix, Ethambutol, ASA (low dose), Pyrazinamide
    • NOTE: Uricosuric Effect (Anti-gout)
      • Losartan, Amlodipine, Fenofibrate
    • History:

      joints Gout.png

      • Gender
      • Age
      • Joint localization
        • 1st MTP, knee, ankle, mid-tarsal joints
      • History of the attack
      • Medications:
        • ASA, diuretics, CyA
      • Family history
      • Co-morbidities (i.e. Nephrolithiasis)
    • Diagnosis:
      • Joint Tap is GOLD STANDARD
      • Negatively birefringent crystals on microscopy
      • Imaging UNCHANGED!!!!
        • Unless there are tophi, then see punched out erosions
    • Stages of Gout
      • Asymptomatic Hyperuricemia
      • Acute Gouty Arthritis
      • Intercritical Gout (attacks with normal periods in between, no tophi)
      • Chronic tophaceous Gout
        • Tophi start to form with chronic
        • Nodules on joints, ear, elbow (Olecranon bursa) - where temperature is cooler.
    • Treatment
      • Non-Pharmacologic
        • Alcohol cessation (especially in acute attack)
        • Secondary causes/meds
          • Obesity, diet, EtOH, HTN, Lipids, Meds, CKD
        • Weight loss, exercise, hydration
          • Avoid organ meats, high fructose sodas, ETOH overuse, anti ETOH in gout attack
          • LIMIT: REd meat and seafood, ETOH
          • Encourage: low-fat diet and vegetables
        • D/C drugs that cause it (i.e. HCTZ, diuretics), but prefer the following instead (uricosuric effects)
          • Uricosuric Effect (Anti-gout) - Losartan, Amlodipine, Fenofibrate
      • Phamacologic
        • Acute Gout
          • First-Line
            • NSAIDs
              • full dose until attack resolved
            • Colchicine (don't use in liver/renal/heart failure)
              • 1.2mg then 0.6mg in 1 hour then 0.6mg po bid/od
            • Prednisone (oral or IA)
              • 30mg po x5mg then taper to zero
            • Monotherapy or combination therapy
            • If initial therapy doesn't work (i.e. if not 50% better in 24hrs), consider multiple.
        • Urate-Lowering Therapy
          • Indications for treatment with urate-lowering therapy:
            • 1.  ≥2 flares in 1 year
            • 2.  Tophaceous gout
            • 3.  Urolithiasis
            • 4.  Attack in context of CKD (Stage ≥ II)
          • See above for indications
          • NOTE: Always prophylax patients with anti-inflammatory agents when starting urate-lowering therapies. (colchicine usually)
          • Allopurinol (100mg daily, and 50mg in CKD)
            • Inhibits xanthine oxidase 
            • Titrate dose up to q4w 
            • Can go higher than 300mg/day, but monitor LFTs (approved for up to 800mg/day, but usually need 200-400mg/day)
            • q1-3mo LFTs
            • Caution Renal Failure:
              • Can build up and cause hypersensitivity rxn.
              • Can use in some CKD (one study from Australia ok'ed), as long as target uric acid level.
            • Caution Hypersensitivity rxn:
              • Warn to stop if fever/rash (hypersensitivity rxn):
              • Fever, Rash, Marrow/Renal/Hepatic Failure, SJS
              • Desensitization is possible in old days, but now can use febuxostat. 
            • Absolute Contraindication: 6-MP and Azathioprine (require xanthine oxidase to clear)
          • Febuxostat
            • Also Xanthine Oxidase inhibitor (cannot use with azathioprine and 6-MP)
            • 40-80mg/day, target uric acid level 
            • Not covered by ODB
            • Only indicated if not tolerating allopurinol
            • Can substitute allopurinol if not tolerated (do not use together)
            • Toxicity:
              • LFT abnormalities (transient)
              • Very well tolerated!!
          • Probenecid
            • Inhibit renal tubular transporter (blocks resorption of uric acid)
            • Increases risk of kidney stones
            • Doesn't work in renal insufficiency (urate won't be delivered to tubules)
            • Must aggressively hydrate
          • Pegloticase
            • Pegylated Uricase - Dissolves uric acid. 
            • Similar to rasburicase (used to treat TLS), but highly immunogenic, not used in gout.
            • Pegylated uricase is less immunogenic. (anti-pegloticase antibodies common)
            • Effective in gout, if allopurinol tx failure, but works in 40% of patients. 
            • Concern for cardiovascular disease (2 deaths), avoid in CV disease. 
            • Can be used to help resolve tophi
          • Urate Lowering Therapy Targets


            - Non-Tophaceous  Gout < 350

            - Tophaceous Gout < 300

    • New Therapies
      • Anakinra (IL-1beta)
      • Lesinurad
      • Arhalophenate
        • Urate-lowering with anti-inflammatory properties (no need to prophylax)

    Pseudogout - CPPD

    Source: Thompson (2010) Tarascon Book - Rhemautology


    • Calcium Pyrophosphate Dehydrate Deposition
      • It's a salt that is deposited in the cartilage and appears as chondrocalcinosis on radiographs
      • Sometimes the crystalline form can be released from cartilage into the joint causing inflammatory arthritis. 
    • Presentation
      • There are many types!!!
      • Acute Pseudogout (25%)
        • Acute pain swelling, erythema, and warmth. 
        • Often have systemic malaise and fever
        • Mimic acute gout, but less intense, take longer to peak, and lasts days to two weeks. 
        • Typically knees, but most joints have been reported.
        • Typically large joints:
          • Knee, acetabular labrum in the hip, symphysis pubis, distal radio-ulnar joint, annulus fibrosis of the intervertebral discs
      • Chronic:
        • Asymptomatic chondrocalcinosis (CPPD deposition into cartilage - can make seconday OA)
        • Pseudo Osteoarthritis
          • CPPD deposition into cartilage can cause secondary OA
          • Usually knees & shoulders (fine line paralleling humerus)
        • Pseudo Rheumatoid Arthritis
        • Pseudo Neuropathic Joint
    • Risk Factors:
      • Hemochromatosis
      • Hyperparathyroidism
      • Hypophosphatemia
      • Hypomagnesemia
      • Hypothyroidism
      • Amyloidosis, Post-trauma, Age, Family hx. 
    • Management
      • General: Rest, ice, elevate, immobilize briefly.   Physiotherapy for ROM
      • Intra-articular Corticosteroids:
      • analgesics & NSAIDs: for symtompatic relief
      • Systemic Steroids
        • For severe attacks unresponsive for NSAIDs and injection. 
        • Prednisone 30mg po daily tart tapering by 5mg every otehr day until finished (12days)
      • Colchicine 0.6mg po BID-TID (rarely used)
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