Crystal joint disorder- gout
Gout is an inflammatory arthritis that results from the deposition of urate crystals in or around the joints. Although urate crystal deposition is associated with hyperuricaemia, only one quarter of people with hyperuricaemia progress to develop symptomatic gout (the likelihood is directly related to the duration and degree of hyperuricaemia).
Gout is a disease principally of middle-aged men in developed countries. The prevalence of gout in the USA and UK is 300 per 100 000 and is increasing. Males are affected 10 times more frequently than women. The incidence in women increases after the menopause as oestrogen has a uricosuric effect.
The end product of purine nucleotide breakdown is uric acid. Seventy-five per cent of uric acid is excreted in the kidneys; the rest is lost in the faeces. Uric acid is effectively filtered at the glomerulus, however 90% is subsequently reabsorbed.
Hyperuricaemia is defined as a uric acid level greater than 0.42 mmol/L in men and 0.36 mmol/L in women, and develops as a consequence of under-excretion (80%) of uric acid by the kidney, overproduction (20%) of uric acid, or both. An elevated uric acid level is present in up to 5% of the general population at any one point during adult life and is related to age, sex, body habitus and genetic constitution. Under-excretion of uric acid accounts for by far the majority of patients with hyperuricaemia, however the reason for this is unclear.Up to 20% of affected individuals report a family history of the condition. Lesch-Nyhan syndrome is a rare X-linked genetic disorder resulting from the absence of an enzyme responsible for purine metabolism and is characterized by early-onset gout, spasticity, choreoathetosis, mental retardation and compulsive self mutilation.
Overproduction of uric acid occurs in acquired disorders leading to an excessive rate of cell, and therefore nucleic acid, turnover. These include myeloproliferative and lymphoproliferative disorders, haemolytic anaemias, Paget's disease of bone and psoriasis. Certain medications such as low-dose aspirin, diuretics and ciclosporin alter renal tubular handling of uric acid and can contribute to the development of gout. Diuretics are the main cause of hyperuricaemia but clinical gout is an uncommon association.
Acute attacks of gout occur when monosodium urate crystals are deposited in oversaturated joint tissues. Inflammation occurs as a consequence of ingestion of crystals by polymorphonuclear leukocytes with subsequent release of inflammatory mediators. In a minority of patients gouty tophi develop following multiple episodes of acute gout. Urate crystals in synovial fluid may precipitate de novo or result from rupture of preformed synovial deposits . The histopathology of the gouty tophus reveals a core of monosodium urate crystals surrounded by a chronic foreign body granuloma.
Scope of disease
An acute attack of gouty arthritis may cause significant morbidity as a result of severe pain and subsequent immobility. Tophi may cause joint destruction and neural impingement if the spine is involved.Renal impairment from unchecked hyperuricaemia may occur, however renal failure is a rare complication. Acute uric acid nephropathy is now exceedingly uncommon with hyperhydration and the prophylactic use of allopurinol prior to chemotherapy. Other renal complications include chronic urate nephropathy and uric acid stones.Uric acid calculi may develop in up to 10% of gout sufferers, especially in hotter climates. The stones may be radiolucent (uric acid alone) or radio-opaque (combined with calcium salts). Most commonly they are due to overindulgence of purine-rich foods and dehydration. Gout is also associated with several medical conditions and screening for these should be undertaken .
The most common presentation of gout is podagra, i.e. monoarthritis of the great toe (1st metatarsophalangeal joint). However, any joint may be affected-the more frequently affected areas are the feet, ankles, knees, wrists and fingers, and 1 in 10 attacks affects more than one joint.
The pain of gout is excruciating, likened to a vice being maximally twisted around the affected joint. Even the weight of the bedclothes resting on the joint may be unbearable. Without treatment, the attack settles spontaneously in 2-3 weeks. This may be the first and only manifestation of the disorder. In others, multiple attacks are followed by an intercritical phase where the paroxysms are less severe but prolonged. Subsequently chronic tophaceous gout may develop ( with tophi being deposited in any joint or bone. Most commonly these occur at the elbow (olecranon bursa), tragus of the ear and extensor surfaces of the limbs.A detailed clinical assessment includes assessment of the frequency of attacks, precipitating factors and screening for associated diseases such as hypertension, hyperlipidaemia, ischaemic heart disease and diabetes.Fever may develop during an attack, mimicking sepsis, and appropriate investigations are mandatory to exclude the possibility of septic arthritis.
Precipitants of acute gout include joint injury/trauma excessive physical exercise alcohol diet rich in purine nucleotides starvation Surgery Medications: diuretics, initiation of uricosuric agents or allopurinol . Differential diagnosis of gout include acute arthritis septic arthritis other crystalline arthritis, traumatic arthritis rheumatoid arthritis seronegative spondylarthritis,chronic arthritis nodular rheumatoid arthritis osteoarthritis with Heberden's and Bouchard's nodes and Xanthomatosis
Full blood count, markers of inflammation, A leukocytosis with raised inflammatory markers (CRP, ESR) frequently develops.
Serum uric acid levels. The blood uric acid level may be raised, normal or even low in an acute attack and cannot be relied upon to help diagnostically. The greater the hyperuricaemia, however, the more likely gout is to develop.
Many cases of gout are presumed due to the classic presentation of podagra, however a definitive diagnosis can only be made by demonstrating gouty crystals in joint aspirates. The uric acid crystals are needle-like when viewed under polarized light microscopy and are strongly negatively birefringent (yellow when aligned with the compensator and blue when perpendicular to the polarizer.
As gout is associated with other medical conditions, screening for these is appropriate with blood glucose level, lipid profile and blood pressure estimation.
X-ray of the joints
Radiography is helpful in chronic cases as the changes of gouty arthropathy are characteristic with 'punched-out' erosions having sclerotic margins and overhanging edges
Non-steroidal anti-inflammatory agents
An acute attack of gout is best treated with NSAIDs. Traditionally indometacin (50 mg 4-hourly until the attack resolves) has been the treatment of choice, however any NSAID may be used. A course should last for 1-2 weeks in full therapeutic doses.
If NSAIDs are contraindicated, colchicine is appropriate starting at 0.5 mg 6-hourly followed by dose reduction depending upon response. The use of this medication is limited by its side effect profile. Diarrhoea, which may be explosive, is the most untoward effect; however, this settles upon withdrawal of the drug.
Diet and patient education
Long-term therapy is aimed at reducing hyperuricaemia by decreasing the intake of purine-rich foods . A high fluid intake is recommended for patients who develop uric acid stones. Foods need to be avoided includes beef, liver, kidney, sweetbreads, meat extracts, gravy, seafood ( Crustaceans), vegetables such as peas, beans, spinach, lentils, alfalfa, citrus fruits, tomatoes, beer and beer products.
Other treatments include oral corticosteroids or intramuscular or intra-articular corticosteroid injections.
Preventative treatment with allopurinol is reserved for patients who have multiple attacks of gout (more than3 per year), for those with tophi and those with renal impairment.
Allopurinol inhibits the enzyme xanthine oxidase, the final enzyme required for the production of uric acid, andis extremely effective at preventing attacks. Successful lowering of plasma urate abolishes the risk of gout and tophi will eventually disappear. The aim is to lower the uric acid as far as possible. Allopurinol is not given in the acute setting as it may precipitate or prolong an attack. It is commenced several weeks following an acute episode concurrently with an NSAID or colchicine for 3 months and then continued indefinitely.
Sulfinpyrazone and probenecid act by blocking renal tubular transport of uric acid, allowing the filtered load to be excreted. They are not as effective as allopurinol and do not help in patients with renal failure. They are rarely used these days.
Treatment of underlying condition The treatment of associated and any underlying conditions that would predispose to hyperuricaemia is an important aspect in the management of patients with gout. Obese patients should lose weight, alcohol should be reduced and the need for diuretics be reconsidered.
Etoricoxib, a COX-2 inhibitor, has been found to have comparable efficacy to indometacin in the treatment of acute gouty arthritis and is generally safe and well tolerated
With effective treatment the prognosis is excellent and recurrences are limited. Complications such as urate calculi are rare. The main cause of mortality in patients with gout is associated disease such as hypertension, ischaemic heart disease and diabetes.
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