Gout and Pseudogout
Gout and Pseudogout are inflammatory arthritis that can be caused by monosodium urate and calcium pyrophosphate dihydrate crystal formation in joints. An excess of uric acid in the body causes this conditions. This excess can be caused by an increase in production of uric acid by the body, by under-elimination of uric acid by the kidneys or by increased intake of foods containing purines, which are metabolized to uric acid in the body. With time, elevated levels of uric acid in the blood may lead to deposits around joints. Eventually, the uric acid may form needle-like crystals in joints, leading to acute gout attacks. After a time, this excess of uric acid usually causes painful joint inflammation (arthritis). In addition to the arthritis, gout causes the formation of tophi, which are lumpy
Because of the unpleasant side effects of colchicine, non-steroidal anti-inflammatory drugs (NSAIDs) have become the treatment of choice for most acute attacks of gout. Moreover, eating the diet containing purines, decrease the consumption of alcohol intake, and drinking excessive amount of fluid can lessen the chance of having high levels of uric acid and to prevent this chronic disease. Uric acid-lowering therapy directed at normalizing uric acid levels in the blood should be considered for patients who have had multiple gout attacks. With correct treatment, gout should be well controlled in almost all cases. Clinical presentations and imaging of the affected joints can be helpful for diagnosis of gout and pseudogout. Acute gout episodes affect peripheral joints such as feet and hands, and last up to 10 days, whereas pseudogout affects intermediate joints such as knees, shoulders and wrists, and has more prolonged effects. Geriatric patients who are taking diuretics are also at the high risk of getting gouty attacks. There is no sure way to prevent gout. Colchicine has been the standard treatment for acute gout. The acute attacks can be eliminated with the help of different medications. NSAIDs may also have significant toxicity, but if used for the short-term, are generally well tolerated. Corticosteroids are the other option to decrease the inflammation. The definitive diagnosis of gout is dependent on finding uric acid crystals in the joint fluid during an acute attack. However, uric acid levels in the blood alone are often misleading and may be transiently normal or even low.
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