Overview.
The international diagnosis of hyperuricemia is defined as: two fasting SUA levels on non-same day under normal purine diet status: >420 μmol/L in men and >360 μmol/L in women. with the rapid economic development, people’s living standard has improved greatly than before, the diet structure has changed, the incidence of hyperuricemia ((hyperuricemia, HUA)) in The incidence of hyperuricemia (HUA) in China is not only gradually increasing, but also the age of the disease is advanced…. The number of patients with asymptomatic hyperuricemia in China is increasing rapidly, and the incidence is becoming younger. At present, there are about 120 million patients with hyperuricemia and about 17 million patients with gout in China.
Uric acid is the end metabolite of purine compounds in humans, and disorders of purine metabolism lead to hyperuricemia. Basic research has confirmed that 90% of hyperuricemia is due to a decrease in uric acid excretion and 10% is related to an increase in uric acid synthesis. Gout is a group of syndromes in which disorders of purine metabolism and/or impaired uric acid excretion result in elevated blood uric acid and deposition of urate from supersaturated extracellular fluid in tissues or organs. Enhanced purine anabolism and/or decreased uric acid excretion are the primary mechanisms of increased serum uric acid levels in patients with gout.
Gender differences in hyperuricemia
There are very significant gender differences in hyperuricemia. The prevalence of hyperuricemia has been reported to be 21.6% in men compared to 8.6% in women. The prevalence of hyperuricemia in men and women has been reported to be as high as 10:1. The prevalence of hyperuricemia in women increases gradually with age, and the detection rate of hyperuricemia in postmenopausal women is almost equal to that of men. The detection rate of hyperuricemia in men is higher than that in women because men have more social and poor dietary habits than women; secondly, androgens promote the reabsorption of uric acid by the kidneys. In women, the rate of hyperuricemia increases significantly after menopause, probably due to the decrease in estrogen levels, which in turn leads to the weakening of the kidney’s removal of uric acid.
Dangers of hyperuricemia
More and more studies have shown that hyperuricemia is closely related to hypertension, insulin resistance, obesity, hyperlipidemia, etc. It is an important factor that aggravates atherosclerosis and promotes the development and progression of cardiovascular and cerebrovascular diseases. Uric acid is a predictor of the development of type 2 diabetes in patients with risk factors for diabetes. HUA significantly increases the risk of stroke incidence and mortality. The effect of high uric acid levels on the incidence of vascular events is more pronounced when diabetes is present. Therefore, HUA is an independent predictor of poor outcome (death or life dependence) in acute ischemic stroke and high incidence of post-stroke vascular events. HUA is closely related to multiple risk factors of cerebrovascular disease and is an important risk factor for ischemic stroke. Therefore, attention should be paid to HUA and reasonable and standardized treatment should be given early.
Therapeutic drugs.
1. Xanthine oxidase inhibitors that inhibit uric acid production are the first choice of medication, and allopurinol or febuxostat monotherapy is recommended. Allopurinol is a competitive xanthine oxidase inhibitor, which produces uric acid lowering effect by inhibiting uric acid synthesis. The use of allopurinol in patients with chronic kidney disease and with thiazide diuretics requires caution for the possible development of hypersensitivity syndrome, although a significant proportion of patients with hyperuricemia treated with allopurinol fail to achieve the recommended control of serum uric acid concentrations. In addition, although allopurinol has a good safety profile, it has an increased incidence and severity of side effects in patients with impaired renal function, so that the dose should be adjusted downward according to the creatinine profile. In some countries, allopurinol is often used as a first-line drug for long-term uric acid-lowering therapy in guidelines. If the blood uric acid does not reach the standard after monotherapy, it can be combined with oral drugs for hyperuricemia, such as a xanthine oxidase inhibitor drug and a drug for uric acid excretion.
2, drugs that promote uric acid excretion such as propofol and benzbromarone are also commonly used to lower uric acid in clinical practice. Drink more water during the use of these drugs to alkalize the urine, and they should not be used together with salicylic acid, thiazide diuretics, furosemide, diuretic acid and other drugs that inhibit uric acid excretion. The application of these drugs is limited because they can cause the deposition of uric acid crystals in the urinary tract, resulting in adverse reactions such as renal colic, kidney stones and renal function impairment.
Note: Drugs commonly used in clinical practice for the treatment of gout include allopurinol tablets, propofol, and benzbromarone. These drugs should be taken 2 weeks after the acute phase of gout and should be taken in small doses, otherwise the blood uric acid level will decrease too quickly and the difference in uric acid concentration between joint fluid and blood will promote the precipitation of uric acid crystals deposited in synovial membrane, cartilage and soft tissues such as joints, thus triggering the onset of acute arthritis;
3, uric acid oxidase: can catalyze uric acid into water-soluble, easy to be excreted by the kidneys of allantoin, due to the lack of uric acid enzyme in humans can not achieve this transformation process, so prone to hyperuricemia or gout, through the supplementation of uric acid oxidase is another strategy for the treatment of hyperuricemia. Uricase has a strong uric acid-lowering effect, and intravenous administration can reduce blood uric acid to 0. Therefore, adrenocorticosteroids need to be used simultaneously to prevent acute attacks of gout. The representative drugs are rasburicase and pegloticase. The latter is a recombinant modified mammalian uric acid oxidase produced by Escherichia coli and monomethoxy polyethylene glycol covalently combined to form a biological agent. It was first approved in the United States in September 2010 for the treatment of adults with chronic gout who have not achieved the recommended control of serum uric acid concentration despite conventional uric acid-lowering drugs.
4. In clinical studies, a single tablet combination of cloxacin 50 mg and dihydrocoumarotide 12.5 mg was found to lower uric acid levels while better lowering blood pressure, especially in patients with poorly controlled blood pressure and concomitant hyperuricemia. Micronized fenofibrate was effective in improving lipid and uric acid metabolism in patients with hypertriglyceridemia and hyperuricemia, independent of baseline uric acid levels and gender.
5. In recent years, studies have also confirmed that the commonly used drug compound Danshin Drops has the effect of reducing UA because the active ingredient of Chinese medicine Danshin, Tanshinone IIA, has the effect of inhibiting xanthine oxidase (XO) activity. The research on the use of active ingredients of Chinese medicine for the treatment of hyperuricemia is still in the exploratory stage. Preliminary studies have shown that herbs with xanthine oxidase inhibition include: cinnamon, onion, honeysuckle, chicken yam vine, genistein, qinpi, salvia, sea cucumber, corn mullein, scutellaria, scutellaria, burdock root, fu ling, moneywort, etc. The Chinese herbs that have the effect of lowering uric acid include: Atractylodes, Phellodendron, Cornu Cervi Pantotrichum, Plantain, Tianjihuang, Scorpion grass, Wailing, Dioscorea, and Tiger stick. Commonly used formulas include: 加味茵陈五苓散, 当归拈痛丸二妙丸, 三妙丸, 四妙散, etc.
Diet and lifestyle taboos
1, drink a lot of water: make the habit of drinking more water, or eat fruits and foods containing more water, and maintain the amount of liquid at more than 2000ml/day, preferably up to 3000ml/day, to ensure the discharge of uric acid. In case of renal insufficiency, water consumption should be appropriately restricted. The excretion of uric acid is also related to the acidity of urine, acidic urine is not conducive to the excretion of uric acid. At present, the market supply of pure water pH value is generally about 6.0, towards the weak acidity, for gout patients, this is undoubtedly a disadvantage.
2, supply sufficient vitamins, especially vitamin B and vitamin C.
3, supply more vegetables and fruits into alkaline food, because the body in alkaline can improve the solubility of uric acid salt, conducive to uric acid discharge. In addition, vegetables and fruits are rich in vitamin C, which can promote the dissolution of uric acid salts in the tissue. Generally require a daily supply of vegetables and fruits 1000g, fruits 4 to 5 times.
4, abstain from alcohol: including white wine beer and red wine should not drink more. Long-term heavy alcohol consumption for gout patients can lead to increased blood uric acid and increased blood lactate. Can stimulate purine increase, drinking alcohol often eat high purine food, wine can accelerate the metabolism of purine, leading to increased blood uric acid levels in the body and induce acute attacks of gouty arthritis.
5, do not eat animal offal z such as liver, kidney, brain, heart, intestines, etc. { and meat soup, eat less seafood.
6.Choose low purine diet・According to the amount of purine content, the daily food can be divided into: no or very little content; little content (75mg/100g); high content; very high content four levels.
a Very little content: cereals, most vegetables, cream of wheat, eggs, milk, fruits, candy, beverages, fats and oils, etc.
b Very little content (75mg/100g): string beans, green beans, spinach, peas, flat mushrooms, asparagus, cauliflower, cereals, mackerel, salmon, tuna, white fish, lobster, wheat bran bread, etc.
cHigher content: lentils, sea bass, pike, halibut, carp,, sturgeon, shellfish, lavender ham, pork, beef, chicken broth, pigeon, duck, goose, rabbit, broth, shiitake mushrooms, portobello mushrooms and liver and intestines and other offal.
The d content is extremely high (greater than 150mg/100g): anchovies, sardines, pancreas, beef liver, beef loin, brains, gravy, beer, ha crab, bone marrow, etc.
7, pay attention to life conditioning. Patients with hyperuricemia should pay attention to excessive mental tension in daily life, pay attention to avoid staying up late as much as possible, develop regular living habits, quit drinking and smoking, and play outdoor sports appropriately. To pay attention to weight loss, not to let the weight is too overweight.
8, to pay attention to uric acid monitoring. Patients with hyperuricemia who have a family history of gout should pay attention to blood uric acid monitoring every other month to prevent the development of the disease. If combined with obesity, hypertension, hyperlipidemia and other metabolic diseases, patients should actively reduce uric acid while treating the comorbidities, and if necessary, carry out drug therapy.