Gout

Clinical features, Diagnosis, Management, Prognosis,

The term refers to acute or chronic arthritis of peripheral joints that predominantly affects adults males and results from deposition of monosodium urate crystals (derived from hyperuricaemic body fluids) in the joint or tendons and tendon sheaths. Hyperuricaemia is a necessary but not a sufficient prerequisite for clinical manifestations of gout because asymptomatic hyperuricaemia is 10 times more common. Hyperuricaemia is defined as a serum uric acid level above 0.42 mmol/L in adult males and 0.36 mmol/L in adult females.

Solubility of uric acid drops with temperature, so characteristic needle-shaped crystals of monosodium urate are formed in avascular tissues (e.g., cartilage) or relatively avascular tissues (e.g., tendons, ligaments) around cooler distal peripheral joints and cooler tissues (e.g., ears). In severe ling standing gout deposits can be found in other tissues such as the kidney (uric acid stones).

Two mechanisms of hyperuricaemia have been identified:

• Diminished kidney excretion of uric acid is found more than 75% of patients with gout; these individuals are unable to increase uric acid excretion in response to any event that increases purine load (uric acid is an end product of metabolism of purine nitrogenous bases adenine and guanine found in nucleic acids). Genetically determined defect in urate excretion is probably responsible for hyperuricaemia in most patients in this group, but in others renal failure, diuretic drugs (they compete with uric acid for secretory carriers in kidney tubules) and chronic alcohol abuse may be involved.
• Increased production of uric acid is at least partly responsible for hyperuricaemia in 20-25% of gout patients. Uric acid can be overproduced when there is increased turnover of cells as in certain blood malignancies such as polycythaemia vera and chronic lymphatic leukaemia, and in severe psoriasis. Increased purine synthesis is found in rare enzyme defects such as hypoxanthine-guanine-phosphoribosyl transferase (HGPRT) deficiency and phosphoribosyl pyrophosphate (PRPP) synthetase overactivity. In certain cases enzyme defect is unknown.

Clinical features:  < BACK TO TOP >

1. Acute gout

         The metatarso-phalangeal joint of a great toe is the site of the first attack of acute gouty arthritis in 70% of patients.

         The ankle, the knee, the small joints of the feet and hands, the wrist and elbow follow in decreasing order of frequency.

         The onset is usually explosively sudden without warning, often waking the patient from sleep.

         The affected joint is hot, red and swollen with shiny overlying skin, it is very painful and tender; signs resemble acute infection.

         Very acute attacks may be accompanied by fever, chills, tachycardia, leukocytosis and raised ESR.

         If untreated, the attack lasts for days or weeks but it eventually subsides spontaneously.

         Some patients have only a single attack, or suffer another only after an interval of many months or years, but more often there is a tendency to have recurrent attacks.

         Acute attacks may be precipitated by sudden rises in serum urate following dietary excess (overindulgence in purine-rich food such as meat), alcohol, diuretic drugs, reduction of anti-gout therapy, trauma, unusual physical exercise, surgery or severe systemic illness. 

2. Chronic gout

         First attacks of gouty arthritis are seldom associated with residual disability.

         Recurrent acute attacks may lead to progressive cartilage and bone erosion due to formation of tophi (depositions of white ‘chalk-like?material), followed by secondary degenerative changes.

         Severe functional impairment and gross joint deformities may occur in chronic tophaceous gout.

         Tophi are also frequently found in the cartilage of the ear, bursae and tendon sheaths. 

3. Urate urolithiasis

         This occurs in about 20% of patients with gout.

         All symptoms and signs associated with urolithiasis may appear.

Diagnosis:  < BACK TO TOP >

         Clinical presentation is usually very suggestive of gout.

         The serum urate level is usually raised but does not prove the diagnosis because asymptomatic hyperuricaemia is very common.

         Synovial fluid should be aspirated and examined under special microscope with polarising light when needle-shaped crystals of monosodium urate could be seen.

         Joint radiographs can be useful in later stages of the disease when characteristic erosions may become apparent.

Management  < BACK TO TOP >

         A dramatic response in acute gout follows within 24 hours of colchicine [Colchicine, Colgout] that is given orally or sometimes intravenously.

         NSAIDs are also effective in relief of pain and inflammation, corticosteroids may be used in short courses to suppress severe inflammation.

         Drugs which lower the serum urate level are considered in:

            - recurrent attacks of gouty arthritis

            - tophi or evidence of chronic gouty arthritis

            - associated renal disease (urolithiasis)

            - gout and markedly raised serum urate

         Allopurinol [Capurate, Progout, Zyloprim, Allorin] is the hypouricaemic drug of choice; it lowers the serum urate by inhibiting enzyme xanthine oxidase which is responsible for the conversion of xanthine and hypoxanthine to uric acid; DNA breakdown is then diverted towards other more soluble waste products that can be more readily excreted.

         There is no need for severe dietary restrictions but excessive purine intake in meat and overindulgence in alcohol should be avoided.

         Occasionally surgery for gross joint deformities associated with reduced movements is needed.

         Urolithiasis has to be appropriately treated (lithotripsy may be used).

Prognosis  < BACK TO TOP >

• - - 

Nutrition  < BACK TO TOP >

Nutrition that alleviate or prevent gout :-

Cherry (or Cherry juice)

Herbs  < BACK TO TOP >

Herbs that alleviate or prevent gout :-
Apium graveolens (Celery seed) - Urate excretion stimulant
Arctium lappa (Burdock)
Berberis aquifolium (Oregon Grape)
Berberis vulgaris (Barberry)
Betula pendula (Silver birch)
Eupatorium purpureum (Gravel Root)
Filipendula ulmaria (Meadowsweet)
Galium aparine (Cleavers, Clivers)
Glycyrrhiza glabra (Licorice)
Guaicum officinalis (Guaicum)
Harpagophytum procumbens (Devil's claw)
Urtica dioica (nettle leaf) - Urate excretion stimulant

(source : Dr Zoran Pletikosa)