CRYSTAL ARTHRITIS

GOUT (monosodium urate)

PSEUDOGOUT (calcium pyrophosphate)
HYDROXYPATITE

GOUTY ARTHRITIS/ GOUT

Purines are not properly processed in our body

Excreted through kidneys and urine
Hyperuricemia: build-up of uric acid in body and joint fluid
- Preclinical Period:
6.8mg/dl based on urate supersaturation
5-8%- most asymptomatic- 20% get gout
Onset males age 30, females postmenopausal
Duration 10-15 years before gout
80% due to undersecretion, 20% due to overproduction (determined by
24 hr urine collection)
Can also occur as a result of overproduction of uric acid
Is an attack of uric acid desposits in joints
Usually found in joints of feet and legs
Inflammatory arthritis mediated by crystallization of uric acid within joints
Often associated with hyperuricemia
Prevance in US= 2.7% (6 million)
Incidence: 62.3/100,00 (2-fold increase)
Associations: DM, HTN, Metabolic syndromes, obesity, CVD, renal stones,
CPPD
Risk factors: genetics, age, CRF, serum uric acid, diet, alcohol, medications
Meds: decrease urate pool
- High dose salicylate
- Losartan
- Fenofibrate
- Amlodipine
- Vitamin C
- Probenecis, sulfinpyrazone, benzbromarone
- Allopurinol, uricase, febuxostat
Meds: increase the urate pool
- Diuretics
- Low dose salicylates
- B-blockers
- PZA, Ethambutol
- Cyclosporin, tacrolimus
- Insulin
Urate precipitation leads to acute gouty arthritis
- Local factors: temperature, pH, trauma, joint hydration
- Systemic factors: hydration state, fevers, meds, alcohol, co-morbid
conditions
Attack resolves spontaneously 10-15 days

FOUR STAGES OF GOUT:

ASYMPTOMATIC
ACUTE
Sever and sudden onset
Involved one or few joints
Frequently starts nocturnally
Joint is warm, red, and tender
First attack 4th-6th decade for men
Women almost always postmenopausal
Classically monoarticular LE- podagra (50%). (vs
pseudopodogra)>ankle>gonagra>UE
Proximal joint, central arthropathy uncommon
Diagnosis: EULAR
- Acute attack 6-12 peak intensity with S/W/E/T
- Aspiration always recommended if possible
- Prompt polarized microscopic analysis performed
- Definite dx: requires crystal confirmation
- Gout and sepsis can coexists: fluid should be sent Grams stain,
culture
- Radiographs not necessary
- Risk factor assessment
THERAPY (for all crystal diseases):
- Corticosteroids: intrarticular>systemic
- NSAIDs: fast acting full dose if no contraindicationd
- Colchicine (PO, IV route dangerous)
* narrow therapeutic window (bone marrow suppression,
myopathy, neuropathy)
* purgative effects- pt. often run before they walk
- ACTH
- NEVER ALLOPURINOL
INTERCRITICAL
70% prevalence of MSU crystals remain in the joint
Last month to years for 75-80%. 20% never have another attack
Medicines:
- Uricosurics:
Probenecid 1-3 grams/day
Sulfinpyrazone 200-400 mg/day
Benzbromarone 100-200 mg/day
- Uric Acid Lowering Therapy

Lifestyle, dietary modification

Diet high in vegetables, dairy, water beneficial
Initiate uric acid lowering therapy after 1 or 2 episodes of acute
gouty arthritis
Always prophylaxis for first 6 months with low dose steroids,
NSAIDs, or colchicine

Contraindications:
* Tophi
* CRI (GFR>35 ml/min)
* H/O urolithiasis
* intolerance
* Rapid cell turnover states
25% of failure rate- mild CRI
Interact with ASA, NSAIDs, PCN, eaptopril
Watch for rash, GI, HA, dyscrasias, nephrosis
URICOSTATICS
FEBUXOSTAT
*Not yet FDA approved
*Hepatic toxicity, HA, Diarrhea
*80-120 day safer, more effective
*No dose reduction for renal, hepatic insufficiency
Combination uricourics and uricostatics offer additional benefit
URICASE- converts uric acid to allantoin
- Recombinant uric acid oxidase: RASURICASE
*puremeteral route(not clear?)- can be given only once due
to antibody production
*Black box warning- anaphylaxin, benolysis(?),
methanoglobinemia (?)
- Pegytated preparation approved for urate nephropathy to
tumor lysis syndrome
*Experimitive (?)
*sq administrative (?)
Fenofibrate Lozartan
E3010- new class of anti-inflammatory compounds
Y-700, scopoletin

CHRONIC
Usually present after 10 years of acute intermittent gout
Tophi deposition
Chronic swollen joints
Joint destruction
Absolutely requires allopurinol
Continuous or persistent over a long period of time
Symptoms:
Joint pain
- Affects one or more joint: hip, knee, ankle, foot, shoulder,
elbow, wrist, hand, or other joints
- Great toe, ankle and knee are most common
Swelling of joint
- Stiffness
- Warm and red
- Possible fever
Skin lump which may drain chalky material
Diagnosis Gout:

X-rays
Arthrocentesis- extraction of joint fluid
Examination of joint
Patient medical history
Disease of Kings: rich foods have higher occupation of protein.
This could cause major problems for a person affected with gout
Organ meats
Wild game
Seafood
Lentils
Peas
Asparagus
Yeast

CALCIUM PYROPHOSPHATE DEPOSITION DISEASE

Acute Pseudogout
- Positive birefringent rod shaped crystals
- More likely in OA joint- knee>wrist>MCPs>hips,shoulders,ankles
- Pseudorheumatoid pattern
- Osteoarthritis with/out pseudogout
- Chondrocalcinosis
- Neuropathic joint
- Tumoral CPPD depositions
PSEUDOGOUT
- Hyperparathyroidism
- Hemochromatosis
- Hypothyroidism
- Hypomagnesaemia
- Hypercalcemia
- Hypophophatasia
Treatment
- Colchicine: reduces pain, swelling, and inflammation; pain subsides within
12 hrs and relief occurs after 48 hrs
- Allopurinol: decreases the production of uric acid
- Probenecid and sulfinpurazone: prevent absorption of uric acid in the
tubules of kidney
- Reduce alcohol intake
- Increase water intake
- Watch diet for food rich in purines
- Birth control pills long term treatment: role for bishoshonates and low
dose warfarin
Associations
- Chondrocalcinosis and hereditary (rarely)