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 deposits of uric acid crystals. 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.
            
             Prevalence of gout is 6 times more common in men than women. In geriatric patients, women are mainly affected after the menopause. Gout can be suspected if the first toe joint is inflamed or the level of uric acid in the blood is higher than 9mg/100 ml. Geriatric patients who are taking diuretics are also at the high risk of getting gouty attacks. 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. Clinical presentations and imaging of the affected joints can be helpful for diagnosis of gout and pseudogout.
            
             The goals of treatment for gout consist of alleviating pain, avoiding severe attacks in the future, and preventing long-term joint damage. Colchicine has been the standard treatment for acute gout. While colchicine is very effect...