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 Luo Juan
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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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How is hyperuricemia treated?

The treatment of hyperuricemia mainly includes the following points: 1. Improve lifestyle primarily, including a low-purine diet, appropriate exercise, smoking cessation, and increased water intake. 2. Alkalize urine using sodium bicarbonate to maintain urine pH value between 6.2 and 6.9, which facilitates the excretion of uric acid. 3. Avoid drugs that increase uric acid levels, such as diuretics, corticosteroids, and insulin. 4. Use medications that lower uric acid levels; drugs that increase uric acid excretion mainly include probenecid and sulfinpyrazone, and drugs that inhibit uric acid synthesis mainly include febuxostat and allopurinol. However, the treatment with these drugs has specific indications, contraindications, and related side effects. It is advised to use medication under the guidance of a doctor and avoid choosing drugs for treatment arbitrarily.

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What should be noted for hyperuricemia?

Firstly, hyperuricemia is just found during routine physical examinations or blood tests, showing an increase in blood uric acid levels without the occurrence of gout attacks, meaning there are no symptoms of joint pain. At this time, there is no need for special medication, which means uric acid-lowering drugs are not required. However, you need to be cautious and change your lifestyle habits. For example, abstaining from alcohol, controlling the intake of animal organs, seafood, and barbecued foods. Additionally, drinking more water is necessary, and for overweight individuals, controlling weight and losing weight are important considerations. Also, you should avoid intense physical activities as they can trigger gout attacks, but this doesn't mean no exercise at all; slow walking and swimming are fine.

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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.

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Can hyperuricemia be cured?

Hyperuricemia is a metabolic disease caused by disorders in purine metabolism and is clinically divided into primary and secondary categories. Primary hyperuricemia is caused by congenital abnormalities in purine metabolism and is often associated with obesity, dyslipidemia, hypertension, atherosclerosis, and coronary heart disease. Secondary hyperuricemia, on the other hand, is caused by certain systemic diseases or medications. Therefore, whether hyperuricemia can be cured depends on the underlying condition, and the efficacy of treatment cannot be generalized. For hyperuricemia caused by medications or systemic diseases, it can be cured by treating the disease or discontinuing the medication. However, for hyperuricemia caused by congenital abnormalities in purine metabolism, it can be clinically managed by controlling diet and medication, but it is not curable.