gout and uric acid

gout and uric acid

crystal growing is both fascinating and easyto do. simply dissolve a bit of table salt in somewater, place a string inside, and then let the water evaporate over a few days. as less and less water is present, the concentrationof salt will increase. however, water cannot dissolve an infiniteamount of salt, therefore there must be a maximum or saturated concentration. at that maximum concentration, salt will notdissolve but instead will solidify to form crystals on the string. this is an awesome phenomenon to show yourfriends, but imagine if crystallization occurred

within your body. in people who have gouty arthritis, or gout,a compound known as uric acid begins to form crystals inside joints, which leads to intensepain. in fact, the pain is so severe that many whosuffer from a gout attack describe that even the weight of a bedsheet on their affectedjoint causes excruciating pain. what’s the reason for the formation of thesecrystals? in the table salt example, crystallizationonly occurred when the concentration of table salt in water exceeded a certain point. similarly, uric acid crystals form only whenthe concentration of uric acid in the blood

is too high, which is known as hyperuricemia. what causes hyperuricemia? compounds known as purines, for example adenineand guanine, are found in genetic material in both our own cellsand in food. purines are eventually broken down into uricacid. normally, most uric acid is filtered out ofour bloodstream in the kidneys and excreted in the urine. however, damage to the kidneys decreases filtration,causing less uric acid to be removed from the bloodstream, resulting in hyperuricemia.

mutations in membrane proteins in the kidneythat transport uric acid, such as urat1, can also cause hyperuricemia. urat1, which is found on the membrane of cellsthat line the tubes which drain urine, can reabsorb uric acid from the filtrate intothe cell, which then sends uric acid back into the blood. mutations that increase the activity of urat1and other uric acid transporters cause more uric acid to be reabsorbed back into the bloodstream,leading to hyperuricemia. small clumps of uric acid crystals form inthe joints as hyperuricemia continues. despite the crystals looking sharp, they donot directly cause pain.

trauma, such as stubbing one’s toe, or suddenswings in uric acid concentration, for example caused by a meal rich with purines, can causesome of these crystals to dislodge. when large immune cells known as macrophagesswallow up the crystals, they begin to release an inflammatory signal protein known as interleukin1î² which recruits and activates other immune cells to the joint space. this is a natural, built-in response, notan autoimmune response, as uric acid is usually released by dead or dying cells. therefore,crystals of uric acid normally indicate infections that are killing cells and therefore requiresinflammation to kill the pathogens causing the infection.

in gout, even though there is no infection,inflammation occurs anyways. whenever there is inflammation, there is redness,swelling, and pain. acute gout attacks can last for up to a week,but eventually subside. often times, the attacks happen at night,as lower temperatures decrease solubility and increase crystallization. usually, the attacks occur on the foot, particularlythe joint of the big toe, possibly because our feet have a lower temperature comparedto the rest of the body and because our feet are the most likely to get injured, for example,by stubbing your toe, which releases crystals. if nothing is done to treat the hyperuricemia,more episodes of acute gout can occur, which

could eventually lead to continuous or chronicgout. tophi, which are large clumps of uric acid,can form which permanently damages bone and disfigures joints. look up tophi on google images if you dareto see how disfiguring they can be. there are two ways of treating gout – eitherprevent inflammation or treat the underlying hyperuricemia. preventing inflammation can be done by anti-inflammatorydrugs such as ibuprofen or advil, naproxen or aleve, colchicine, and steroids. aspirin, which is also commonly used to preventinflammation, is not recommended at low doses

to treat gout because despite decreasing inflammation,it also decreases uric acid excretion in the kidneys which further contributes to hyperuricemia. treating hyperuricemia often involves changingone’s lifestyle. excess consumption of meat, seafood, alcohol,and fructose such as in candy and pop drinks, are all linked to gout, possibly due to increasedpurine content or activation of purine breakdown. in fact, gout was originally known as the“disease of kings”, since in the past only royalty was able to excessively eat thesefood groups. by eating less of these food groups, uricacid levels in blood can decrease, preventing further crystallization.

other food such as caffeine, cherries, vitaminc, and milk seem to prevent future gout attacks, though their mechanism on how they lower uricacid levels is still unclear. another way to treat hyperuricemia is by usinguricosuric drugs, which can block uric acid transporters such as urat1. this decreases reabsorption and increasesexcretion of uric acid, decreasing uric acid levels in the blood. nowadays, since high purine content foodsare more accessible, gout has been steadily increasing in frequency in developed countriessuch as canada, the us, many european countries, china, and australia, with about 3-5% of thepopulation affected by at least one gout attack

in their lifetime. comparatively, less developed countries haverates of gout less than 1%. over 50 million people are affected by goutworldwide, making it an extremely common ailment. risk factors essentially are anything thatcauses hyperuricemia. impaired kidney function due to increasedage, high blood pressure, and diabetes increase the risk of gout. drugs that cause more water to be excretedcan decrease the amount of water in blood and therefore increase uric acid concentration. gout affects men three times more than women,possibly because estrogen is a natural uricosuric.

of the women that are affected, the majorityis post-menopausal women who have decreased estrogen levels. gout is also found to run in families, likelydue to genetic mutations in uric acid transporters in the kidney. it is important to note that hyperuricemiaincreases the risk of gout but does not guarantee it – a minority of people with hyperuricemianever develop gout, implying that there may be other unknown factors in this disease. hopefully, awareness and knowledge about goutcan lead to more people paying attention to their diet to prevent this painful disease.

to learn more about gout, check out the linksin the description below. thanks for watching, and see you next timefor another explanation of a disease on medicurio.

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