Table of contents
- 1. Gout
- 2. Pseudogout - CPPD
.
Gout
- 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
- Overproduction
- NOTE: Uricosuric Effect (Anti-gout)
- Losartan, Amlodipine, Fenofibrate
- History:
- 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.
- NSAIDs
- First-Line
- 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
-
- Acute Gout
- Non-Pharmacologic
- 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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