Gout Signs And Symptoms Diagnosis Pathogenesis Treatment

The classical picture is of excruciating pain of sudden onset in only one joint, usually the big toe (75% of first attacks are the first metatarsal-phalangeal joint ).

Walking on the gouty foot can result in a sprained ankle, as the foot is twisted, to keep weight off the first toe, in the same way it is twisted when sprained.

Patients with longstanding hyperuricemia (see below) can have tophi (uric acid stones) in other organs, e.g. the cartilage of the ear. This has become a rare phenomenon due to pharmacologic treatment of gout. Uric acid stones can form as one kind of kidney stones in some occasions.

2 Diagnosis

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.

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 intracellularIn cell biology, molecular biology and related fields, the word intracellular means "inside the cell". It is used in contrast to extracellular (outside the cell). The cell membrane (and, in plants, the cell wall) is the barrier between the two, and chemic monosodium urate crystals in synovial fluidSynovial fluid is a thick, stringy fluid found in the the cavities of synovial joints. With its egg-like consistency synovial comes from Latin for " egg") synovial fluid reduces friction between the articular cartilage in joints to lubricate and cushion t polymorphonuclear leukocytes.

3 Pathogenesis

People with gout have either an increased production of uric acid or an impaired excretionExcretion is the biological process by which an organism separates waste products from its body. The waste products are then usually expelled from the body by elimination''. In mammals, for example, the two major excretory processes are the formation of u of uric acid, or a combination of the two.

4 Treatment

Acutely, first line treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are colchicine, indomethacin, nonsteroidal anti-inflammatory drugs ( NSAIDs), or intraarticular glucocorticoids.

Colchicine is 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.

Long term treatment is antihyperuricemic therapy. Dietary change can make a small contribution to lowering the plasma urate level if a diet low in purines is considered. The mainstay of this approach, however, is the drug allopurinol, a xanthine oxidase inhibitor, which directly reduces the production and increases urinary excretion of uric acid. Allopurinol cannot be used during an attack of gout, as it can cause precipitation of uric acid crystals in other joints.

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 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 thizides on uric acid metabolism in patients with gout.

Interestingly, another drug fenofibrate , used in treating hyperlipidemia, also exerts beneficial uricosuric effect (Bardin 2003).

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.

5 Diet

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
- avoid alcohol, especially beer because brewer's yeasts are very rich in purine.
Food to avoid:
- sweetbreads, kidneys, liver, brains, or other offal meats
- sardines
- anchovies
- meat extracts, consommés, and gravies
Foods to use sparingly:
- asparagus, beans, lentils, peas, mushrooms, cauliflower, spinach, rhubarb
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.
Joe-Pye weed flushes uric acid quickly, but continued use can damage the liver or kidneys

6 History

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.

7 Famous people who had gout

One of the most famous sufferers of gout was Henry VIII. Others include John Milton, Isaac Newton, Samuel Johnson, Alfred Lord Tennyson, Thomas Jefferson, William B. Finneran, and Benjamin Franklin.

8 References

Bardin, T: Fenofibrate and losartan. Annals of the Rheumatic Diseases 2003;62:497-498 (full text).
Kumar and Clark, eds. Clinical Medicine, 4th Edition 1998.
Harrison's principles of internal medicine.

9 External link

Purine content in food

Rheumatology

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1 Signs and symptoms