Crystal arthritis

• Majority caused by crystals of sodium urate or calcium pyrophosphate
• Rarely acute synovitis is caused by calcium or cholesterol crystals
• Neutrophils ingest the crystals and release inflammatory enzymes and cytokines resulting in the activation of Complement and the attraction of more neutrophils into the joint
• Crystals may be found in asymptomatic joints – why they initiate an attack is unclear
• In pseudogout crystal shedding from the cartilage causes an attack

 

Gout and Hyperuricaemia

 

Epidemiology

• Prevalence of gout is 2 in 1000
• Prevalence of hyperuricaemia is 5%
• Prevalence increasing and mostly seen in developed world
• Males>females
• Hyperuricaemia is classed as being 2SD from the mean >420umol/L in men and >360umol/L in women. This is close to the limit of urate soluability
• Serum levels of urate increase with;
  • Age
  • Obesity
  • High protein diet
  • High alcohol consumption
  • Hyperlipidaemia
  • Diabetes
  • IHD
  • Hypertension
• There is often a family hx

 

Pathogenesis

• Often unknown ateology
• Uric acid levels depend upon the balance between;
  • Purine synthesis
  • Ingestion of dietary purines
  • Elimination of urate by the kidney and intestine
• 60% of urate is turned over daily
• Uric acid is the last step in the breakdown of purines. The two last steps, the conversion of hypoxanthine to xanthine and xanthine to uric acid are catalysed by the enzyme xanthine oxidase
• Uric acid excretion
  • It is completely filtered by the glomerulus
  • Almost all of it is reabsorbed by the proximal tubule
  • Around 50% is secreted by the distal tubule
  • There is also some post-secretory reabsorption which takes place
  • Low dose asprin blocks urate secretion
  • Insulin resistance enhances urate reabsorption
  • Most gout patients have impaired urate excretion
  • 1/3 of urate is excreted in the faeces
• Overall causes of hyperuricaemia
  • Impaired excretion of uric acid
    • Chronic renal disease
    • Drug therapy e.g. thiazide diuretics and low dose asprin
    • Hypertension
    • Lead toxicity
    • Primary hyperparathyroidism
    • Hypothyroidism
    • Increased lactic acid production from alcohol, exercise, starvation
    • Glucose-6-phosphatase deficiency
  • Increased production of uric acid
    • Increased purine synthesis
    • Increased purine turnover
      • Myeloproliferative disorders
      • Lymphoproliferative disorders
      • Carcinoma

 

Clinical features

• Hyperuricaemia causes four clinical syndromes;
  • Acute urate synovitis – gout
  • Chronic polyarticular gout
  • Chronic tophaceous gout
  • Urate renal stone
• Acute gout
  • Typical presentation – middle aged man, first onset of agonising joint pain in the MTP joint
  • Untreated attacks last around 7 days
  • Attack may be precipitated by food, alcohol, dehydration or starting a diuretic
• Chronic polyarticular gout
  • Unusual
  • Seen in old men on long standing diuretic treatment
  • Renal failure
  • When men have been started on allopurinol too quickly after an attack
• Chronic tophaceous gout
  • Formation of sodium urate crystals in the skin and around the joints
  • May occur on ear, Achilles tendon or fingers
  • Associated with chronic joint pain
  • Periarticular deposits lead to a halo of radio-opacity and clearly defined punched out bone cysts on X-ray

 

Investigations

• Clinical signs/symptoms are generally diagnostic as is rapid response to NSAIDs
• Joint fluid microscopy  - needle shaped crystals under polarised light
• Serum urate often raised but the level falls immediately after an attack
• Serum urea and creatine measured for signs of renal impairment

 

Treatment

• NSAIDs e.g. naproxen, diclofenac, indomethacin
• In patients with renal impairment or a history of peptic ulceration alternatives are;
  • Colchicine
  • Corticosteroids
• Patient should be given dietary advice – lower alcohol consumption (especially beer), reduce total calorie intact, avoid offal, some fish, shellfish and spinach
• Allopurinol (only used when patient has renal impairment or the previous treatments are ineffective
  • Should never be started within 1mth after an attack
  • Should always be given with the cover of corticosteroids or colchicines before and after starting
  • Blocks xanthine oxidase
  • Relatively non toxic but should be used in low does in renal impairment
  • Most common side effect is skin rashes, rarely bone marrow suppression

 

 

Pseudogout

 

• Calcium pyrophosphate deposits in hyaline and fibrocartilage
• Produces the radiological appearance of chondocalconosis
• Shedding of crystals produces an acute synovitis
• More common in elderly women
• Usually affects knee or wrist
• In younger people it may be associated with;
• Hyperparathyroidism
• Haemochromatosis
• Wilson’s disease
• Alkaptonuria

 

Diagnosis

• Joint fluid looks purulent
• Crystals differ from gout – rhomboidal in shape
• Attacks may be associated with raised WBC and fever

 

Treatment

• Aspiration of joint reduced pain
• NSAIDs/cochicine
• Intrarticular injection of corticosteroids