Gout and hyperuricaemia

What is Gout and hyperuricaemia?

Gout is a condition in which there are deposits of a chemical (sodium urate) in joints, causing arthritis, as well as in soft tissues and the urinary tract.Urate or uric acid is a chemical formed from the breakdown of purines - DNA building blocks derived from protein. Hyperuricaemia means that a person has too much uric acid in the blood - which is associated with gout. When uric acid precipitates in a joint (often the big toe) it causes an acute arthritis. Uric acid can also be deposited in:

soft tissue, causing tophi (white chalky deposits) and tenosynovitis - tendon inflammation.
urinary tract, causing stones and potentially renal failure (since 2/3 of uric acid is excreted by the kidney)

Statistics on Gout and hyperuricaemia?

Gout is a condition mainly seen in developed countries. It affects approximately 0.25% of Europeans. It is 10 times more common in men. It rarely occurs before puberty and more prevalent in the upper social classes.Hyperuricaemia affects approximately 5% of the population - hence not everybody with hyperuricaemia develops gout - other factors must be important.

Risk Factors for Gout and hyperuricaemia

One third of patients with gout have a positive family history.

Uric acid levels increase with obesity, a high protein diet, high alcohol consumption, diabetes mellitus, cholesterol, ischaemic heart disease, and hypertension.

Secondary causes of hyperuricaemia can be caused by

Impaired excretion of uric acid: chronic renal failure, thiazide diuretics, hypertension;

Increased production of uric acid: polycythaemia, leukaemia, cytotoxics, psoriasis;

An acute attack of gout may be precipitated by - surgical operation, dietary or alcoholic excess, starvation, infection or drugs (especially thiazide diuretics).

Progression of Gout and hyperuricaemia

There are four clinical syndromes:

Acute urate arthritis (gout): this is the classical presentation with an acutely painful, inflamed joint (often the big toe) which resolves within a week.

Chronic polyarticular gout: involving numerous joints and gradually causing joint damage and potentially loss of function.

Chronic tophaceous gout: smooth white deposits of urate in the soft tissues.

Urate renal stone formation: urinary stones may present with acute urinary colic, and chronically can lead to kidney failure.

How is Gout and hyperuricaemia Diagnosed?

Urea and Electrolytes - there may be signs of renal impairment.

Serum uric acid - often elevated but not necessarily.

X-ray: may not reveal much until late in the disease.

Prognosis of Gout and hyperuricaemia

Acute gout will resolve within 7 days even if untreated;

A chronic gout involving many joints (polyarticular) may rarely develop, which has a worse prognosis since it leads to gradual joint destruction and loss of function, though treatment will help prevent this.

Involvement of the urinary tract can lead to chronic kidney (renal) failure,though treatment can also potentially halt its progression.

How is Gout and hyperuricaemia Treated?

1. Acute attacks - treat with oral NSAIDs in high doses:

Naprosen 750mg immediately, then 500mg every 8-12 hours.

Indomethacin 75mg immediately, then 50mg 6-8hrly;

Diclofenac: 75-100mg immediately, then 50mg 6-8hrly.After 48hrs doses are reduced and continued for another week.

Oral colchicine may be used if NSAIDS are contra-indicated but may cause diarrhoea.

May use joint injection of corticosteroids - methylprednisolone depot.2. Long-term therapy - considered when the acute attack subsides to prevent further attacks:Obese patients should lose weight, alcohol consumption should be reduced, drugs such as thiazide diuretics and saliculates should be withdrawn. Should avoid purine rich foods (offal, oily fish, excess protein)

Drugs to reduce serum uric acid

allopurinol - drug of choice. Do not use in acute attacks (nor for following 3 weeks). Also when started may precipitate an acute attack so use in conjunction with a NSAID (non steroidal anti-inflammatory drug).

Gout and hyperuricaemia References

[1] Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford Universtiy Press. 2001.[2] Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002.