Gout is an ancient disease characterised by uric acid deposits, particularly in the joints and kidneys. In 2640 BCE, the Egyptians classified local foot pain in the big toe as a distinct ailment, long before the term “gout” was used. Hippocrates characterised it, noting that it had a high male-to-female ratio and was associated with alcohol. Based on his own personal experience, Dr. Thomas Sydenham (1624-1689) described the lumps of uric acid (called tophi) that can be seen in gout. Gout was not effectively distinguished from other inflammatory kinds of arthritis until the early nineteenth century. The routes of uric acid generation in the body were only elucidated in the twentieth century, as was the potential of uric acid crystals to cause joint pain.
Gouty arthritis develops when a person produces too much uric acid or is unable to excrete enough of it in their urine (or both). The inability to eliminate enough uric acid in the urine is the most prevalent cause of gout (approximately 90% of cases). This disability might be caused by a variety of factors. The most frequent is a genetic deficiency in organic anion transporters in the kidney, which results in excessive uric acid reabsorption from the kidney – and therefore too much uric acid in the blood. However, medications like diuretics, low-dose aspirin, and alcohol can cause a problem with uric acid excretion. When the kidneys aren't working properly, uric acid excretion becomes faulty.
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