Gout (old name: podagra) is a form of arthritis caused by the accumulation of uric acid crystals (due to hyperuricemia) in joints. It is an immensely painful disease, which in most cases affects only one joint, most commonly the big toe. The patient usually suffers from two sources of pain. The crystals inside the joint cause immense pain whenever the affected area is moved. The inflammation of the tissues around the joint also causes the skin to be swollen, tender and sore even if it is slightly touched. For example, a blanket draping over the affected area would cause extreme pain.
Signs and symptoms
The classical picture is of excruciating pain of sudden onset in only one joint, usually the big toe (75% of first attacks affect the first metatarsal-phalangeal joint ), associated with swelling and redness.
Patients with longstanding hyperuricemia (see below) can have tophi (uric acid crystal deposits) in other tissues e.g. the helix of the ear. Uric acid stones can form as one kind of kidney stones in some occasions.
The diagnosis is generally made on a clinical basis, although tests are required to confirm the disease.
Hyperuricemia is a required feature; it is defined as a plasma urate (uric acid) level greater than 420 μmol/L (7.0 mg/dL); despite the above, high uric acid level does not necessarily mean a person will develop gout.
Other blood tests commonly performed are full blood count, electrolytes, renal function and erythrocyte sedimentation rate (ESR). This serves mainly to exclude other causes of arthritis, most notably septic arthritis.
A definitive diagnosis of gout is from light microscopy of joint fluid aspirated from the joint (this test may be difficult to perform) to demonstrate intracellular monosodium urate crystals in synovial fluid polymorphonuclear leukocytes.
Pseudogout (calcium pyrophosphate deposition disease) is very similar disease, but the crystals look differently on light microscopy and the accumulated substance is different.
see uric acid metabolism
People with gout have either an increased production of uric acid or an impaired excretion of uric acid, or a combination of the two.
High uric acid levels are associated with age, obesity, type IV hyperlipidaemia , diabetes mellitus, coronary heart disease and hypertension. Thiazide diuretics (e.g. hydrochlorothiazide) are known to impair the excretion of uric acid. Sometimes, a person can inherit a genetic predisposition from their families.
Acutely, first line treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are indomethacin, other nonsteroidal anti-inflammatory drugs (NSAIDs), or intraarticular glucocorticoids, administered via a joint injection.
Colchicine was previously the drug of choice in acute attacks of gout. It impairs the motility of granulocytes and can prevent the inflammatory phenomena that initiate an attack of gout. Its main side-effects (gastrointestinal upset) can complicate its use. NSAIDs are the preferred form of analgesia for patients with gout.
Before medical help is available, some over the counter medication can provide temporary relief to the pain and swelling. NSAIDs such as ibuprofen can reduce the pain and inflammation slightly. Preparation H hemorrhoidal ointment can be applied to the swollen skin to reduce the swelling temporarily. Professional medical care is needed for long term management of gout.
Long term treatment (in frequent attacks) is antihyperuricemic therapy. Dietary change can make a small contribution to lowering the plasma urate level if a diet low in purines is maintained. The mainstay of this approach, however, is the drug allopurinol, a xanthine oxidase inhibitor, which directly reduces the production of uric acid. However, allopurinol treatment should not be initiated during an attack of gout, as it can then worsen the attack. If a patient is on allopurinol during an attack, it should be continued.
The decision to use allopurinol is often a lifelong one. Patients have been known to relapse into acute arthritic gout when they stop taking their allopurinol, as the changing of their serum urate levels alone seems to cause crystal precipitation.
As arterial hypertension quite often coexists with gout treating it with losartan , an AT receptor antagonist, might have an additional beneficial effect on uric acid plasma levels. This way losartan can for instance offset the negative side-effect of thiazides (a group of diuretics used for high blood pressure) on uric acid metabolism in patients with gout.
Interestingly, the drug fenofibrate (which is used in treating hyperlipidemia) also exerts beneficial uricosuric effect (Bardin 2003).
Low purine diet :
- To lower uric acid:
cherries have been shown to reduce uric acid
strawberries are also reputed to be beneficial
- avoid foods high in purines, that is from protein sources: limit meats to one serving a day
- Food to avoid:
- Foods to use sparingly:
- To avoid dehydration:
- Drink plenty of liquids, especially water, to dilute and assist excretion of urates;
- Use diuretic foods or medicines like aspirin, vitamin C, tea and alcohol sparingly.
- Folk lore has it that Joe-Pye weed flushes uric acid quickly, but continued use can damage the liver or kidneys
Gout was traditionally viewed as a disease of the decadent and indolent, because the foods which contribute to its development were only available in quantity to the wealthy. The stereotypical victim was a lazy, obese middle-aged man who habitually overindulged in rich foods and alcohol. Perhaps due to the traditional relationship between wealth and literacy, gout is one of the most commonly-reported maladies in history.
The Roman gladiatorial surgeon Galen described gout as a discharge of the four humors of the body in unbalanced amounts into the joints. The Latin term for a drop, as a drop of discharge, is gutta -- the term gout descends from this word.
Famous people who had gout
One of the most famous sufferers of gout was Henry VIII. Others include Nostradamus, John Milton, Isaac Newton, Samuel Johnson,Charles V, Alfred Lord Tennyson, Thomas Jefferson, William B. Finneran, and Benjamin Franklin.
- Bardin, T: Fenofibrate and losartan. Annals of the Rheumatic Diseases 2003;62:497-498. Full text. PMID 12759281.
- Kumar and Clark, eds. Clinical Medicine, 4th Edition 1998.
- Harrison's principles of internal medicine.
Last updated: 06-02-2005 03:42:27