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Hyperuricemia
Is hyperuricemia contagious?
Hyperuricemia is not contagious. Hyperuricemia refers to a condition where the concentration of uric acid in the blood exceeds the normal upper limit. Typically, for males and post-menopausal females, a blood uric acid concentration greater than 420 µmol/L, or pre-menopausal females with more than 348 µmol/L, is considered hyperuricemia. Most severe cases of hyperuricemia are due to deficiencies in uric acid metabolism enzymes and fall under the category of liver metabolism disorders. Moreover, mild to moderate hyperuricemia is often associated with obesity, type 2 diabetes, hyperlipidemia, hypertension, arteriosclerosis, and coronary heart disease, among others. It is a type of nucleic acid metabolic disease, and therefore, it is not contagious.
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.
How is hyperuricemia caused?
Hyperuricemia is mostly asymptomatic, meaning there are no uncomfortable symptoms. It is usually discovered during physical examinations or blood tests when the uric acid level is found to be elevated, around 420, which is considered hyperuricemia. What causes it? It is mainly caused by poor lifestyle habits, such as long periods of drinking alcohol, excessive intake of animal organs, seafood, barbecue, and too much protein intake. Additionally, some people may develop high uric acid levels due to prolonged use of diuretics. When hyperuricemia occurs, it is essential to change lifestyle habits, but at this time, no special medication treatment is needed.
Is hyperuricemia dangerous?
Hyperuricemia is generally diagnosed when the blood uric acid level in males exceeds 420 micromoles per liter and in females exceeds 360 micromoles per liter. Some patients with hyperuricemia are asymptomatic, but others may develop gouty arthritis, characterized by local joint redness, swelling, heat, and pain, and even limited mobility. Some patients may develop gouty nephropathy, leading to abnormal kidney function. There are also instances of patients developing tophi, which can cause joint deformity and even limited mobility. Therefore, if hyperuricemia is not controlled promptly, it poses certain risks and may lead to complications such as tophi, gouty arthritis, and gouty nephropathy.
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.)
What fruits to eat for hyperuricemia?
For patients with hyperuricemia, we generally need to limit the intake of high-purine foods, such as crab and animal offal. Moderate consumption of medium-purine foods, such as meats and fish, is acceptable. Low-purine foods like vegetables, fruits, milk, and eggs can be safely consumed. For example, fruits like grapes, pears, grapefruits, kiwis, and dragon fruits are all acceptable to eat. However, many patients with hyperuricemia also have other metabolic abnormalities, such as high blood sugar. In such cases, it is important to monitor the quantity of fruit intake because excessive consumption can lead to fluctuations in blood sugar levels. Therefore, fruits can be safely consumed by those with hyperuricemia, but attention must be paid to any additional metabolic abnormalities that may be present.
Can people with hyperuricemia eat eggs?
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.
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.
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.
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.