Gout

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 to even the slightly touch, for example, a blanket draping over the affected area would be extremely painful.

Table of contents

1 Signs and symptoms 2 Diagnosis 3 Pathogenesis 4 Treatment 5 Diet 6 Famous people who had gout 7 References

Signs and symptoms

\nThe 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.

Diagnosis

\nThe 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.

Pathogenesis

\nsee 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, ischaemic 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.

Treatment

\nAcutely, first line treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are colchicine, nonsteroidal anti-inflammatory drugs (NSAIDs), or intraarticular glucocorticoids. 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 precipitate uric acid 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. Colchicine 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. Several other agents are used for gout. 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\nhyperlipidemia, 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. Ibuprofen such as Motrin, Advil can reduce the pain and inflamation slightly. Preparation H hemorrhoidal ointment can be applied to the swollen skin to reduce the swelling temporarily. Professional medical care is needed to treat the symptoms for long term relief.

Diet

\nLow Purine Diet :\n* To lower uric acid:\n** cherries have been shown to reduce uric acid\n** strawberries are also reputed to be beneficial\n** avoid foods high in purines, that is from protein sources: limit meats to one serving a day\n* Food to avoid:\n**sweetbreads, kidneys, liver, brains, or other offal meats\n**sardines\n**anchovies\n**meat extracts, consommés, and gravies\n* Foods to use sparingly:\n**asparagus, beans, lentils, peas, mushrooms, cauliflower, spinach, rhubarb\n* To avoid dehydration:\n** Drink plenty of liquids, especially water, to dilute and assist excretion of urates;\n** Use diuretic foods or medicines like aspirin, vitamin C, tea and alcohol sparingly.\n* Joe-Pye weed flushes uric acid quickly, but continued use can damage the liver or kidneys

Famous people who had gout

\nOne of the most famous sufferers of gout was Henry VIII. Others include Isaac Newton, Alfred Lord Tennyson,Thomas Jefferson, William B. Finneran, and Benjamin Franklin.

References

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