- Image via Wikipedia
When gout is clinically manifest, however, acute treatment of gouty arthritis should be followed by determination of the cause of hyperuricemia, and long-term treatment to lower the uric acid level is usually necessary.
In addition to reduced consumption of purine-rich foods such as offal and seafood, patients should also limit their consumption of fructose-containing drinks as these reduce the excretion of uric acid.
The diet should be rich in milk and skimmed milk products and in vegetable protein. An important element is limited consumption of alcohol: There should be at least three alcohol-free days a week.
Beer should be avoided because of its high purine content, but a glass of wine is regarded as harmless in gout.
Careful weight loss of less than 1 kg/month with light physical exercise is desirable; more rapid loss of weight could lead to ketoacidosis, provoking gout attacks.
Patients with a history of kidney stones are recommended to drink more than 2 L/d.
These changes in life habits, however, usually make only a moderate contribution to urate reduction.
A consistently purine-poor diet, for example, may be expected to result in a 10% to 15% reduction in serum urate concentration.
Given that for many gout patients the serum urate concentration measured before the start of treatment is 480 µmol/L (8 mg/dL), such a reduction would result in a value of 400 µmol/L (6.7 mg/dL)—still above the required target range for gout patients.
As a general measure, the patient should be given advice on possible changes of life habits that could lead to an improvement in his or her overall metabolic profile.
An extensive interview at the start of therapy often improves the patient‘s understanding and therefore also the compliance. Many patients fail to understand that the treatment for the acute gout attack is not treatment for the actual cause of the gout.
Gout is the name given to the condition when an excess of uric acid (urate) in the body (hyperuricemia) leads to the formation in various tissues of crystals of monosodium urate.
The result is attacks of gout, urate nephropathy, and/or tophi.
Apart from hereditary disorders of uric acid excretion and purine metabolism, the main causes of gout are purine-rich food, alcohol consumption, and overweight.
