Can people with hyperuricemia eat eggs?

Written by Li Lang Bo
Endocrinology
Updated on November 28, 2024
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In the case of hyperuricemia, we primarily recommend a low-purine diet to prevent the onset of gouty arthritis. As for the nutritional content of eggs, they are considered a food with a moderate level of purines. Therefore, when uric acid levels are relatively high, it is still possible to consume them in moderation. Aside from diet, it is also necessary to drink plenty of water or to alkalize the urine using baking soda tablets even if there is a transient increase in blood uric acid levels. If sufficient water is consumed, it is less likely for deposits to form in the joints. If deposits do not easily form, it also relatively reduces the possibility of triggering inflammatory responses, thus preventing the occurrence of gouty arthritis. Therefore, it is possible to consume an appropriate amount of eggs, but it is also important to drink plenty of water and appropriately alkalize the urine.

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The causes of hyperuricemia

The causes of hyperuricemia can currently be divided into two categories: primary and secondary. The cause of most primary hyperuricemia is not yet clear. A few cases are due to enzyme deficiencies, which are related to either excessive production or reduced excretion of uric acid. There is also idiopathic hyperuricemia, such as familial kidney diseases that are associated with hyperuricemia, among others. Some secondary hyperuricemias, for example, are secondary to some congenital metabolic diseases, such as glycogen storage disease. It can also be due to certain systemic diseases, such as leukemia, multiple myeloma, lymphoma, polycythemia vera, hemolytic anemia, etc. Some cases are physiological increases, such as the intake of foods rich in purines, long-term eating and fasting states can also cause increased blood uric acid. Some medications can also lead to hyperuricemia, such as thiazide diuretics, furosemide, ethanol, immunosuppressants, aspirin, etc., which can also cause hyperuricemia. Therefore, the causes of hyperuricemia are diverse, and some causes are still unclear.

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Are hyperuricemia and high uric acid the same thing?

Firstly, hyperuricemia and high uric acid levels refer to the same concept, defined as blood uric acid levels greater than 420. This condition is described as asymptomatic hyperuricemia, which does not require special treatment at this stage, but it does necessitate changes in lifestyle habits such as abstaining from alcohol, avoiding eating animal organs, seafood, and high-protein foods, not drinking carbonated beverages, and losing weight if obese, to help control body weight. After changing these lifestyle habits, a recheck of the uric acid levels should be done in two weeks to see if there has been a decrease. If the levels have not decreased at that time, sodium bicarbonate tablets can be used to alkalinize the urine. Additionally, increasing water intake to promote the excretion of uric acid and monitoring the dynamic changes in uric acid levels are needed. Once joint pain occurs, which indicates an acute gout attack, proper uric acid-lowering medication is required. (Please undergo medication under the guidance of a professional physician, and do not self-medicate blindly.)

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How is hyperuricemia treated?

The treatment of hyperuricemia mainly includes: First, improving lifestyle, including healthy eating with a low-purine diet, quitting smoking, drinking more water, exercising regularly, and controlling weight. Second, alkalinizing the urine using sodium bicarbonate to maintain urine pH between 6.2 and 6.9, which facilitates the excretion of uric acid. Third, avoiding medications that increase blood uric acid levels, such as diuretics, corticosteroids, and insulin, among others. Fourth, using medications that lower uric acid, including drugs that increase uric acid excretion, mainly benzbromarone and probenecid, and drugs that inhibit uric acid synthesis, such as allopurinol and febuxostat. The choice of medication has specific indications, contraindications, and side effects, and it is advised to use these medications under the guidance of a specialist and not to self-medicate.

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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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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.