Gout is a common type of arthritis that causes inflammation, swelling and pain of the joints. The disease is caused by the accumulation of uric crystals at the level of the joints and muscular tissues. In many cases, the underlying cause of gout is high serum uric acid concentration. Uric acid is a substance synthesized during the body’s purine metabolism, having no physiological importance inside the organism. In fact, uric acid is a waste product excreted by the kidneys through urine. High serum uric acid levels are the result of either overproduction or inappropriate excretion of uric acid. The great majority of gout cases are caused by under-excretion of uric acid, as a consequence of renal dysfunctions.

Although hyperucemia (high levels of serum uric acid) is considered to be directly related with the development of gout, the disease isn’t always caused by this factor. For instance, people may develop gout even on the premises of normal serum uric acid levels, while many people with hyperucemia don’t actually develop gout. Although the symptoms of gout closely resemble the clinical manifestation of rheumatoid arthritis, there doesn’t seem to be a connection between these two disorders.

Gout is generally diagnosed upon patients’ clinical manifestations. However, in order to confirm the diagnosis, doctors often perform additional tests, such as blood analyses or tissue examinations under the microscope. The process of diagnosing gout involves revealing traces of uric acid accumulation at the level of the joints and soft tissues. Gout sufferers usually have serum uric acid levels above the average of 7 mg per dL. Although hyperucemia isn’t always the primary cause of gout, people affected by the disease generally have elevated serum uric acid concentrations.

Gout is often the result of uric acid overproduction, facilitated by food regimens that contain high levels of purines. However, sometimes the body’ overproduction of uric acid is the consequence of physiological abnormalities. Recently conducted experiments have identified various physiological dysfunctions in people diagnosed with gout, such as abnormal activity of the enzymes that control purine synthesis. Gout is considered to have a pronounced genetic character and it can often be seen in people who have a family history of the disease.

In some cases, gout occurs due to under-excretion of uric acid. This waste product is eliminated by the kidneys, through urine, or by the gastrointestinal tract, through stools. However, the primary cause for the under-excretion of uric acid is abnormal activity of the kidneys. Thus, people with kidney disorders are exposed to a high risk of developing gout.

The symptoms of gout are generally episodic and they often involve intense pain in the joints. Pain attacks tend to intensify at night and they may last anywhere from a few hours to a few days. The medical treatment of gout generally acts on two levels: it normalizes serum uric acid levels and relieves gout attacks. In order to ameliorate pain attacks, doctors usually prescribe gout sufferers non-steroidal anti-inflammatory drugs, colchinide or injections with corticosteroids. Medications such as probenecid, sulfinpyrazone and allopurinol are usually used in the treatment of gout for preventing the recurrence of pain attacks. Corroborated with an appropriate diet and lifestyle improvements, medical treatments available today can in time overcome gout, also minimizing the chances of relapse.