Pre-symptomatic hyperuricemia

Written by Zhang Jun Jun
Endocrinology
Updated on October 28, 2024
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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
Endocrinology
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What foods to eat for hyperuricemia?

Dietary requirements for hyperuricemia primarily include a low-purine diet, avoiding foods high in purines. It's important to recognize which foods are high in purines, such as seafood and certain fish, which should be avoided. Secondly, some mushrooms and soy products also have higher levels of purines and should be consumed less frequently. Thirdly, alcohol, especially spirits and beer, must be avoided. Fourthly, one should avoid consuming rich, slow-cooked broths as they also contain high levels of purines. Lastly, it is recommended to drink more water, typically between 1500ml to 2000ml daily.

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Written by Li Hui Zhi
Endocrinology
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Hyperuricemia Complications

Common complications, the first is the effect on joints, manifested as local joint redness, swelling, heat, and pain, and even mobility impairment, usually referring to gouty arthritis. The second complication is the effect on the kidneys, resulting in hyperuricemic nephropathy, where the patient will experience abnormal kidney function. The third complication is the formation of gouty tophi, where many patients have deposits in the joints, leading to the occurrence of tophi and causing joint mobility impairment. Therefore, hyperuricemia needs to be treated promptly to prevent these complications.

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Written by Lin Xiang Dong
Endocrinology
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Hyperuricemia standards

The diagnostic criteria for hyperuricemia specify that under normal purine diet conditions, if the fasting serum uric acid level on non-consecutive days exceeds 420 micromoles/liter for males and 360 micromoles/liter for females, hyperuricemia can be diagnosed. Hyperuricemia is typically classified into primary hyperuricemia and secondary hyperuricemia, with most patients showing no clear clinical symptoms.

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Written by Luo Juan
Endocrinology
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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.)

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Written by Lin Xiang Dong
Endocrinology
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Hyperuricemia Typing

Hyperuricemia can usually be divided into two types: primary hyperuricemia and secondary hyperuricemia. The first type, primary hyperuricemia, is mainly due to congenital purine metabolic disorders, leading to excessive production of uric acid in the body, which then causes hyperuricemia. Secondary hyperuricemia is caused by a variety of acute and chronic diseases, such as common chronic renal failure, and hematological tumors, among others.