Hyperuricemia manifestations

Written by Lin Xiang Dong
Endocrinology
Updated on September 09, 2024
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Most cases of hyperuricemia usually have no obvious clinical symptoms, and it can take years to decades from the increase in blood uric acid to symptom onset, with some individuals never exhibiting obvious clinical symptoms throughout their lifetime. However, as age increases, the incidence of gout becomes higher. When accompanied by acute gouty arthritis, patients may experience severe joint pain. If blood uric acid levels remain high over a long period, this can lead to the formation of gouty tophi and uric acid stones, among other issues.

Other Voices

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Written by Luo Juan
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Can people with hyperuricemia eat wood ear mushrooms?

People with hyperuricemia can eat wood ear mushrooms. As wood ear mushrooms are considered a low-purine food, containing approximately 8.8mg of purines per 100 grams, they can be consumed during hyperuricemia. For hyperuricemia, it is necessary to restrict some high-purine foods, such as animal offal, clams, crabs, oysters, and sardines. Some meats, seafood, peas, and spinach, which also contain a certain amount of purines, can be consumed in moderation. Wood ear mushrooms are a low-purine food and are generally not restricted. Thus, people with hyperuricemia can eat wood ear mushrooms.

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Written by Li Hui Zhi
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What are the symptoms of hyperuricemia?

Some patients with hyperuricemia are asymptomatic, while others may suffer from complications such as gouty arthritis, gouty nephropathy, and tophi. Gouty arthritis is very common clinically and is primarily characterized by localized joint redness, swelling, heat, and pain. The commonly affected joints include the first metatarsophalangeal joint, ankle joint, and wrist joint. In cases of gouty nephropathy, patients may exhibit high levels of uric acid and increased creatinine levels, which may manifest as frequent urination, nocturia, and swelling of the lower limbs. If gout crystals deposit in the joints, they can form tophi, leading to joint deformities and restricted movement.

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Pre-symptomatic hyperuricemia

Hyperuricemia in the preclinical phase can be asymptomatic, only showing fluctuating or persistent hyperuricemia during blood tests. From the increase in uric acid to the onset of symptoms, it can generally take several years to decades. Additionally, some changes in the kidneys due to the deposition of uric acid can cause manifestations of gouty nephropathy. Early stages may present intermittent proteinuria and increased urine foam. As the condition progresses, the kidney's concentrating ability may decrease, resulting in increased nighttime urination. Further progression can lead to renal insufficiency, elevated creatinine and urea nitrogen, and possibly swelling and hypertension. In severe cases, acute renal failure may occur, showing symptoms of oliguria or anuria. This type of uric acid nephropathy is primarily due to the deposition in the kidneys, causing episodes of kidney stones and back pain, with stone episodes also accompanied by hematuria. Therefore, the main presentations are associated with the deposition of uric acid in the kidneys during the preclinical phase of hyperuricemia.

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Written by Li Hui Zhi
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Hyperuricemia Clinical Symptoms

Some patients with hyperuricemia may not have any symptoms, and only discover elevated uric acid levels during a physical examination. However, some patients may experience gouty arthritis, manifesting as redness, swelling, heat, and pain in a localized joint, commonly in the joints of the toes. It may also affect joints like the ankle and elbow. Additionally, some patients may develop gouty nephropathy, leading to renal insufficiency. Therefore, hyperuricemia should be taken seriously to prevent severe conditions such as gouty arthritis and other serious symptoms associated with gout.

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Hyperuricemia treatment agent

Currently, the main treatments for hyperuricemia in clinical practice include the following types. One category is drugs that inhibit uric acid synthesis, primarily allopurinol and febuxostat. Allopurinol is a xanthine oxidase inhibitor, which mainly works by preventing the conversion of hypoxanthine and xanthine into uric acid through the inhibition of xanthine oxidase. Febuxostat, on the other hand, is a newer xanthine oxidase inhibitor and may be more effective than allopurinol in lowering blood uric acid levels. Another category includes drugs that promote the excretion of uric acid, suitable for patients with normal renal function and hyperuricemia. These mainly include probenecid, benzbromarone, and some use of thiazide diuretics, though their effectiveness for hyperuricemia is somewhat controversial. (Specific medications should be taken under the guidance of a physician.)