Uric acid is a heterocyclic compound composed of carbon, nitrogen, oxygen, and hydrogen atoms arranged in a ring structure. It results in the formation of urates and acid urates, such as ammonium acid urate, as well as ions and salts. In humans, uric acid is produced as a by-product of the metabolic breakdown of purine nucleotides and is a normal component of urine. Extremely high levels of uric acid in the blood can cause gout and are associated with a number of other medical conditions, including diabetes and the development of ammonium acid urate kidney stones.
GOUT
Inflammatory arthritis of the joints, known as gout, is a metabolic disorder characterised by recurrent acute attacks of severe inflammation in one or more of the joints. Gout is caused by the deposition of uric acid salts in and around the joints, which are present in excessive amounts throughout the body in those who suffer from the condition. Uric acid is produced by the breakdown of purines, which are compounds that are essential components of DNA and RNA as well as many biosynthetic reactions. It is excreted into the urine in a steady stream under normal conditions. It is estimated that gout accounts for at least 5% of all cases of arthritis. Women, on the other hand, are less likely to be affected; the male to female ratio is 20:1. Pseudogout (chondrocalcinosis) is a condition that is similar to osteoarthritis in that it is caused by deposits of calcium pyrophosphate crystals in the joint fluid.
Despite the fact that gout is suspected to be an inborn disorder, the first attack of acute joint inflammation, also known as gouty arthritis, does not usually occur until the middle of a person’s life. An injury to a peripheral joint can occur in any location, but it is particularly common in the joint at the base of the big toe. The most common symptoms are redness of the skin and extreme tenderness, warmth, and pain in the joints that have been affected. Even if left untreated, an attack can subside in a week or two if not sooner. Despite the fact that attacks may come and go without apparent cause, there are a number of factors that can trigger them, including acute infection and emotional upset, excessive alcohol consumption and poor diet, obesity, diuresis, surgery, trauma, and the administration of certain medications. The formation of uric acid crystals in the joint cartilage occurs prior to the onset of the first attack. Knobby deformities may develop in some cases due to the accumulation of uric acid salts in the cartilage, which may also occur in cartilage that is not associated with the joints, for example, on the rim of the ear.
Several people who are affected by gout have family members who are also afflicted; however, it is not known how the disorder is passed down through families. In association with abnormal uric acid metabolism, a number of genetic variations have been discovered. The most striking feature of these variations is found in a gene known as SLC2A9 (solute carrier family 2, member 9), which normally encodes a protein that is involved in maintaining uric acid homeostasis in the body. The exact mechanisms by which SLC2A9 variants increase susceptibility to gout are unknown, but scientists suspect that the variants produce abnormal proteins that interfere with uric acid transport and uptake into cells, thereby increasing the risk of gout. Understanding the genetic mechanisms that contribute to the development of gout may aid in the identification of methods of prevention and the development of drugs for the treatment of the condition.
Acute Gout
Acute gout attacks are treated with nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin and naproxen, to relieve the pain and inflammation. Corticosteroids may also be injected directly into the affected joint to alleviate the swelling and pain. If nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are ineffective, a medication known as colchicine may be prescribed. Recurrent acute attacks are treated with medications such as allopurinol, which reduces urate formation, and probenecid, which promotes the excretion of uric acid through the urine. Additionally, supplementation with vitamin C, which increases excretion of uric acid by the kidneys and, as a result, decreases the amount of uric acid circulating in the body, may help to reduce the frequency and severity of recurrent attacks. Vitamin C has been shown to reduce the frequency and severity of recurrent attacks.
Conclusion
Subjects with obesity, metabolic syndrome, and type 2 diabetes are more likely to have gout and other uric acid related disorders. The effects of insulin resistance on uric acid excretion were attributed to these diseases for a long time, and it was believed that uric acid did not play a causal role in the metabolic syndrome for a long time as well.