With the exception of , most myeloproliferative disorders increase the risk of hyperuricemia and gout.
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A 55 year-old man comes to the emergency department because of a three-day history of pain, erythema, and swelling in the first metatarsophalangeal joint of his right foot. He is unable to sleep at night because he has severe pain whenever his bed sheet touches the joint. He admits to smoking one pack per day and drinking three to four beers nightly. He denies any previous episodes of pain in this joint and denies trauma to the area. He denies pain in any other joint. His only medication is hydrochlorothiazide for hypertension, and the dose of this medication was recently increased by his primary care provider. Physical examination shows a tender, warm, erythematous right toe. Synovial fluid is removed from the joint, and crystals are seen on microscopy. Which of the following substances is most likely to be seen on analysis?
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 hyperuricemia—too much uric acid in the blood, which results in the formation of sharp, needle-like 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 nitrogen-containing 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 acid—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 6.8mg/dL.
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 purine-rich foods like shellfish, anchovies, red meat or organ meat.
Also, though, they can result from increased production of purines, for example high-fructose 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.
Hyperuricemia can also develop as a result of chemotherapy or radiation treatment, since cells die at a faster-than-normal 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.