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(also called ''metabolic arthritis'') is a disease due to a
Congenital disorder of
Uric Acid metabolism. In this condition, monosodium urate or uric acid
Crystal s are deposited on the articular
Cartilage of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the blood stream. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material.
(1799). The artist memorably illustrates the excruciating pain and swelling that are symptoms of the disease]]
The classic picture is of excruciating, sudden, unexpected, burning
Pain , swelling, redness, warmness and stiffness in the joint. Low-grade fever may also be present. The patient usually suffers from two sources of pain. The crystals inside the joint cause intense 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 if it is even slightly touched. For example, a blanket or even the lightest sheet draping over the affected area could cause extreme pain.
Gout usually attacks the
Big Toe (approximately 75% of first attacks), however it can also affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, and spine. In some cases the condition may appear in the joints of the small toes which have become immobile due to impact injury earlier in life, causing poor blood circulation that leads to gout.
Patients with longstanding ) in other tissues e.g. the
Helix Of The Ear . Uric acid stones can form as one kind of
Kidney Stone in some common occasions.
The diagnosis is generally made on a clinical basis, although tests are required to confirm the disease.
Hyperuricemia is a common feature; however, urate levels are not always raised.
1
Hyperuricemia is defined as a
Plasma urate (uric acid) level greater than 420 ''μ''mol/L (7.0 mg/dL) in males (or 380 ''μ''mol/L in females); however, high
Uric Acid level does not necessarily mean a person will develop gout. Additionally, urate is within the normal range in up to two-thirds of cases.
2
If gout is suspected, the serum urate test should be repeated once the attack has subsided. Other blood tests commonly performed are
Full Blood Count ,
Electrolyte s,
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 . The urate crystal is identified by strong negative bi-refringence under polarised microscopy, and their needle-like morphology. A trained observer does better in distinguishing them from other crystals.
Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues.
Purine Metabolism gives rise to uric acid. This is normally excreted in the urine. Uric acid is more likely to form into crystals when there is a
Hyperuricaemia . Hyperuricaemia is 10 times more common without clinical gout than with it
3
Purines can be generated by the body itself (via the breakdown of cells in normal cellular turnover) or can be ingested in purine-rich foods (e.g. seafood, beer). Most people with gout, however, do not produce more than the normal amount of uric acid, but instead tend to be under-excretors. The kidney is responsible for approximately one third of uric acid excretion, with the gut responsible for the rest. It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.
There are also different racial propensities to develop gout. Gout is high among the peoples of the Pacific Islands, and the Māori of New Zealand, but rare in the Australian aborigine despite the latter's higher mean concentration of serum uric acid.
4 In the United States, gout is twice as prevalent in African American males as it is in Caucasians.
5
Hyperuricemia is considered an aspect of
Metabolic Syndrome , although its prominence has been reduced in recent classifications. This explains the increased prevalence of gout among
Obese individuals.
Gout is a form of arthritis which affects mostly men between the ages of 40 and 50. The high levels of uric acid in the blood are caused by protein rich foods. Alcohol intake often causes acute attacks of gout. There is correlation that there are hereditary factors that contribute to the elevation of uric acid. Typically persons with gout are: obese, predisposed to diabetes and hypertension, and at higher risk of heart disease. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol.
6 It is known that lead sugar was used to sweeten wine, and that chronic
Lead Poisoning is a cause of gout,
78 which condition is then known as because of its association with alcohol and excess.
9
Gout can also develop as co-morbidity of other diseases, including
Polycythaemia ,
Leukaemia , intake of
Cytotoxic s,
Obesity ,
Diabetes ,
Hypertension ,
Renal disorders, and
Hemolytic Anemia . This form of gout is often called secondary gout.
Diuretic s (particularly
Thiazide diuretics) have traditionally been blamed for precipitating attacks of gout, but a Dutch case-control study from 2006 appears to cast doubt on this.
10
The first line of treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are
Indomethacin , other
Nonsteroidal Anti-inflammatory Drugs (NSAIDs), or intra-articular
Glucocorticoids , administered via a
Joint Injection .
Colchicine was previously the drug of choice in acute attacks of gout. It impairs the motility of
Granulocyte s and can prevent the inflammatory phenomena that initiate an attack of gout. Colchicine should be taken within the first 12 hours of the attack and usually relieves the pain within 48 hours. Its main side-effects (gastrointestinal upset such as
Diarrhea and
Nausea ) 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, although
Aspirin should not be used as it can worsen the condition.
Preparation H Hemorrhoid al
Ointment can be applied to the swollen skin to reduce the swelling temporarily. Professional medical care is needed for long term management of gout.
Ice may be applied for 20–30 minutes several times a day. There are concerns that uric acid crystallization is accelerated by low temperature, but in a 2002 study in the ''Journal of Rheumatology''
11 patients who used ice packs had better relief of pain with no negative side effects. Keeping the affected area elevated above the level of the heart may help as well.
Due to swelling around affected joints for prolonged periods, shedding of skin may occur. This is particularly evident when small toes are affected and may promote fungal infection in the web region if dampness occurs; it is usually treated in a similar fashion to
Athlete's Foot .
- Probenecid , a uricosuric drug that promotes the excretion of uric acid in urine, is also commonly prescribed - often in conjunction with Colchicine . The drug Fenofibrate (which is used in treating Hyperlipidemia ) also exerts a beneficial uricosuric effect.13
- It is suspected that in many cases gout may be secondary to untreated Sleep Apnea , when oxygen-starved cells break down and release purines as a by-product. Treatment for apnea can be effective in lessening incidence of acute gout attacks.14
- A study in 2004 suggests that animal flesh sources of purine, such as beef and seafood, greatly increase the risk of developing gout. However, high-purine vegetable sources did not. Low fat dairy products such as skim milk significantly reduced the chances of gout. The study followed over 40000 men over a period of 12 years, in which 1300 cases of gout were reported.15
- PEG-uricase , a polyethylene glycol ("PEG") conjugate of recombinant porcine uricase (urate oxidase), which breaks down the uric acid deposits is being studied in Phase III Clinical Trials for the treatment of severe, treatment-refractory gout in the United States in 2006 . Pipeline
- Sodium Bicarbonate (baking soda) is an old remedy,The British Pharmaceutical Codex. Published by direction of the Council of the Pharmaceutical Society of Great Britain, 1911. Sodium thought to work by raising blood pH (lowering blood acidity). However, the added sodium may be inappropriate for some people.
- Research from the University of British Columbia suggests long-term coffee consumption is associated with a lower risk of gout.
