Hyperuricemia is a disease closely related to age and lifestyle, which can not only cause gout attacks but also interact with chronic diseases such as hypertension, coronary heart disease, metabolic syndrome and diabetes, and is one of the causes of renal insufficiency. Hyperuricemia should be treated by maintaining a healthy lifestyle and using reasonable uric acid-lowering drugs when necessary.
I. What is hyperuricemia?
Uric acid is a product of purine metabolism in the body. Purines and pyrimidines are important raw materials for the synthesis of DNA (deoxyribonucleic acid) and RNA (ribonucleic acid), the genetic material of life. Under normal circumstances, the daily production and excretion of uric acid in human body basically maintain a dynamic balance, the total amount of uric acid in the body is about 1200mg, the daily new production of uric acid is about 750mg, excretion of about 800-1000mg, 30% from the intestinal tract and bile duct excretion, 70% by the kidney excretion. When uric acid is filtered through the glomerulus, about 90% of it is reabsorbed in the renal tubules, and only 6-12% of uric acid is excreted with urine. Therefore, increased production and/or decreased excretion of uric acid can lead to increased blood uric acid levels, which in turn can cause gouty arthritis, gout and gouty nephropathy. Xing Yongsheng, Department of Cardiovascular Medicine, Xinxiang Central Hospital, Henan Province, China
What factors can cause hyperuricemia?
The secondary reduction of uric acid excretion due to various causes is the most important reason for the development of hyperuricemia. Age-related physiological renal hypofunction; combined with hypertension, diabetes, atherosclerosis, metabolic syndrome, heart failure and other diseases, can cause renal arteriosclerosis, intrarenal microcirculation blood insufficiency, decreased glomerular filtration rate and reduced uric acid secretion function of the renal tubules, resulting in impaired uric acid excretion and hyperuricemia; the use of diuretics, high-dose aspirin, anti-tuberculosis drugs (pyrazinamide, ethambutol Butanol), pancreatic enzyme preparations, levodopa, nicergoline, niacin, sulfonylurea hypoglycemic agents, immunosuppressant cyclosporine A and quinolones can not only increase the incidence of hyperuricemia, but also induce acute attacks of gout.
In addition, excessive exogenous purine intake (consumption of purine-rich foods, alcohol consumption, etc.) is also an important cause of hyperuricemia and increased incidence of gout.
What are the clinical manifestations of gout?
Gout often starts acutely, mostly with severe pain in the first joint of the thumb and metatarsophalangeal joint, with the thumb and the first metatarsophalangeal joint being most commonly involved. It can also involve the ankle, hand, wrist, knee, elbow and small joints of the foot. The affected joints have redness, swelling, heat, pain and limited movement, often in a single joint, but after repeated attacks, multiple joints may be involved.
In elderly patients, acute gouty arthritis rarely occurs, and the pain symptoms may not be severe; it mostly starts as subacute or chronic polyarthritis, mainly involving the small joints of the hands, and some patients are easily misdiagnosed as arthritis or osteoarthrosis. Patients with hyperuricemia who have impaired renal function due to long-term use of diuretics and non-steroidal anti-inflammatory drugs (NSAIDs) may develop gouty stone deposits at an early stage without a history of acute gouty arthritis attacks.
Fourth, how is hyperuricemia diagnosed?
Normal blood uric acid level: 150-350µmol/L (2.5-6mg/dl) in men;
For women, it is 100-300µmol/L (1.7-5mg/dl).
Hyperuricemia can be diagnosed when blood uric acid levels are >420µmol/L (7mg/dl) in men and >360µmol/L (6mg/dl) in women.
It is classified as decreased secretion and excessive production of uric acid. If creatinine clearance >60ml/min, uric acid excretion <800mg/24h with normal diet and <600mg/24h with purine-free diet, it can be defined as decreased secretion type; conversely, overproduction type can be diagnosed. Some patients have both decreased secretion and increased production, which is called mixed type.
V. What are the dangers of hyperuricemia?
It can cause gout attacks and urinary stones (uric acid stones), and if left untreated, it can cause kidney damage. Uric acid and its salts deposited in the kidneys can lead to uric acid nephropathy, which can lead to kidney failure. Renal failure in turn can cause an increase in blood uric acid, forming a vicious circle. In addition, high uric acid can directly damage vascular endothelial function, activate platelets to induce thrombosis, deposit uric acid crystals in the vascular wall, promote inflammatory reactions, promote lipid peroxidation, increase oxygen radical generation, and promote the development of atherosclerosis.
Sixth, how to treat hyperuricemia?
Treatment of hyperuricemia not only prevents the occurrence of gout, but also contributes to the treatment of chronic diseases such as hypertension, coronary heart disease, diabetes and metabolic syndrome.
Asymptomatic hyperuricemia is defined as patients with elevated blood uric acid levels but no history of gout attacks. In this case, the cause of the patient’s elevated uric acid should be actively sought. Restriction of high purine diet, low protein and low sugar diet, alcohol cessation, exercise and weight reduction are recommended to help reduce blood uric acid levels. At the same time, drugs that inhibit uric acid excretion (such as diuretics and anti-tuberculosis drugs) should be avoided, and various diseases that affect uric acid metabolism should be actively treated.
When the blood uric acid concentration is >12-13mg/dl (714.3-773.8μmol/L) in men and >10mg/dl (595.2μmol/L) in women, uric acid-lowering drugs should be used to control the blood uric acid level.
1. How to control the diet in patients with hyperuricemia?
(1) Low purine diet (avoid animal viscera);
(2) Control protein intake (<1.0g/kg/d);
(3) Eat more fresh vegetables and fruits;
(4) Avoid alcoholic beverages;
(5) Drink more water: maintain more than 1.5-2 liters of fluid intake per day;
(6) Urinate 2000-2500ml per day to help uric acid excretion.
2. Drugs for hyperuricemia
According to the kidney function and 24-hour uric acid excretion, for patients with reduced secretion (normal diet, uric acid excretion <800mg/24h; purine-free diet, uric acid excretion <600mg>60ml/min) and no gouty kidney stones, drugs can be used to promote uric acid excretion; for patients with excessive uric acid production and daily uric acid excretion higher than 800mg, drugs are used to inhibit uric acid synthesis. For patients with excessive uric acid production and uric acid excretion above 800 mg per day, drugs that inhibit uric acid synthesis should be used.
Adjusting the urine pH to 6.2-6.9 in patients with hyperuricemia is conducive to the dissolution of uric acid crystals and their excretion from the urine, reducing the formation of uric acid stones. Sodium bicarbonate can be used to adjust urine pH, usually 0.5-1g each time, 3 times a day.
(1) Benzbromarone (Ligarixen): It is the most used drug to promote uric acid excretion. It can be used in patients with hyperuricemia with normal renal function or mild renal insufficiency. 25~100mg each time, once a day. However, it should be noted that: ① do not use the drug during acute gout attack; ② it is necessary to drink a lot of water during the treatment period to keep the urine volume above 2000ml per day as appropriate. Some patients have gastrointestinal reactions, which may induce renal colic and acute arthritis attacks.
(2) Benzenesulfonazolone and carbenzene sulfonamide (propofol): due to the large side effects, they are less used in clinical practice.
Allopurinol: mainly used in patients with hyperuric acid production (uric acid excretion >800 mg/24h), can be used in patients with renal insufficiency, gout stone deposition, renal calculi, and patients for whom uric acid excretory agents are ineffective or contraindicated. The starting dose is 50-100 mg every other day in the elderly, and then increased by 50-100 mg/day every two weeks until the blood uric acid concentration is below 6 mg/dl.
Drink plenty of water to ensure adequate urine output (>2000ml per day) during the dosing period. Individual patients may have fever, allergic rash, abdominal pain, diarrhea, leukocyte and platelet reduction, and even liver function impairment and other side effects, which can be recovered by stopping the drug and giving appropriate treatment. The side effects such as fever, allergic rash, abdominal pain, diarrhea, leukocytopenia and thrombocytopenia, and even hepatic impairment can be recovered after stopping the drug and giving corresponding treatment.
3. Treatment of hyperuricemia with gout
(1) Non-steroidal anti-inflammatory drugs
They have good anti-inflammatory properties to relieve painful symptoms caused by acute gout, and should be used with caution for patients with peptic ulcer because they are used according to medical advice.
(2) Colchicine: Treatment of acute gouty arthritis, mainly controls the acute inflammation of gout, but does not reduce blood uric acid concentration or increase uric uric acid excretion. It is administered 0.5-1.0mg per dose, 1-2 times/d. However, the therapeutic window is narrow and its application is limited. The most common adverse reactions are diarrhea, vomiting, and may even cause hepatic, renal and cardiac insufficiency, cardiac arrhythmias, peripheral neuropathy and rhabdomyolysis. Monitoring should be strengthened during the drug administration.
(3) Sodium bicarbonate: alkalinize urine, 3-6g/day, divided into three oral doses to adjust urine PH value to 6.2-6.9, which is conducive to the dissolution of urate crystals and their discharge from urine and reduce uric acid stone formation.
(4) Glucocorticoid (prednisone): It can be considered for patients with acute gouty arthritis and renal damage who have poor treatment results, and should be decided by experienced specialists, and bacterial arthritis must be excluded before use. Glucocorticoids have side effects such as water and sodium storage, hypokalemia, hypertension, abnormal blood glucose and osteoporosis, etc. Attention should be paid to monitoring blood glucose, blood pressure, electrolytes and psychoneurological symptoms when using them.
2) How to apply uric acid-lowering drugs in gout patients?
If uric acid-lowering treatment is started during the acute gouty arthritis attack will affect the control of gout symptoms or even aggravate the symptoms and damage caused by gout, uric acid-lowering treatment can be started after 1 to 2 weeks of pain relief from the acute attack.
If the patient has already applied uric acid-lowering medication before the gout attack, he or she should continue to take it.