Gout is an inflammatory disease in which monosodium urate crystals deposit into a joint, making it red, hot, tender and swollen within hours. When this happens, it’s called a gouty attack. The underlying cause is hyperuricemiaâ€”too much uric acid in the blood, which results in the formation of sharp, needlelike crystals, in areas with slow blood flow like the joints and the kidney tubules. Over time, repeated gouty attacks can cause destruction of the joint tissue which results in arthritis.
To understand where the uric acid comes from, let’s start with purines, which, together with pyrimidines, are nature’s most common nitrogencontaining heterocycles. A heterocycle being any molecular ring or cycle with different types of atoms. Purines, as well as pyrimidines, are key components of nucleic acids like DNA and RNA, and when cells, along with the nucleic acids in those cells, are broken down throughout the body, those purines are converted into uric acidâ€”a molecule that can be filtered out of the blood and excreted in the urine. Uric acid has limited solubility in body fluids, though.
Hyperuricemia occurs when levels of uric acid exceed the rate of its solubility, which is about 6.8mgdL. At a physiologic pH of about 7.4, uric acid loses a proton and becomes a urate ion, which then binds sodium and forms monosodium urate crystals. These crystals can form as a result of increased consumption of purines, like from consuming purinerich foods like shellfish, anchovies, red meat or organ meat. Also, though, they can result from increased production of purines, for example highfructose corn syrup containing beverages could contribute to the formation of uric acid by increasing.
Purine synthesis. Another way crystals could form is from decreased clearance of uric acid, which can result from dehydration from not drinking enough water or from consumption of alcoholic beverages, both of allowing uric acid to precipitate out. Regularly eating these kinds of foods can also lead to obesity and diabetes, both of which are riskfactors for gout. Hyperuricemia can also develop as a result of chemotherapy or radiation treatment, since cells die at a fasterthannormal rate.
Also, some individuals have a genetic predisposition to overproduction of uric acid while others with chronic kidney disease may be unable to excrete the uric acid. Finally, there are some medications like thiazide diuretics and aspirin which can also increase the levels of uric acid and therefore the risk of gout. Now gout most often affects the first metatarsal joint of the footâ€”or the base of the big toe, and when it does, this condition is called podagra. Classically in podagra, a person will wake up from sleep feeling like their big toe is on fire; even the weight of the sheets can be painful.
The pain is most severe in the hours immediately following the attack and then generally lessens over time, but that discomfort and swelling can last for days or weeks. Gout can affect other joints as well like those in the ankles, knees, wrists, and elbows. This inflammation and local pain’s ultimately caused by white blood cells, or leukocytes, which migrate to the site to help eliminate uric acid and release proinflammatory chemicals, including cytokines. Treatment of a gouty attack is typically focused on decreasing the pain and swelling, most often with nonsteroidal antiinflammatory medications, or NSAIDS, like ibuprofen or.
Naproxen sodium, but occasionally with corticosteroids as well. Colchicine which has antiinflammatory effects by inhibiting white blood cell migration has also been used for a long time to treat gouty attacks. To treat the underlying cause of increased uric acid, though, it’s important to modify the diet, doing things like staying well hydrated (with water), reducing or eliminating soda, alcohol, red meat, and seafood, and staying active to ward off obesity. There are also medications that help to decrease uric acid levels, which include xanthine oxidase inhibitors like allopurinol.