Some gout patients always have this question: Why is it that the more I lower my uric acid, the more severe my gout attacks become? Can I continue to take this medicine to lower uric acid? Gout is like the first love, abused me a thousand times High uric acid is the main culprit of gout, in order not to suffer from the kind of pain brought by gout, must lower uric acid. However, there are always gout patients will have this question: why the more I lower the uric acid, the more gout attacks instead? Can I continue to take this medicine to lower uric acid? Some common chronic diseases such as diabetes, cardiovascular disease and other drugs can raise uric acid, do you know? Why eat uric acid medicine gout to offend? Many gout patients are reluctant to take uric acid-lowering drugs, because after eating uric acid-lowering drugs instead of gout will attack. Professor Liu Xiangyuan said, this is a normal reaction of uric acid-lowering drugs. The uric acid drops quickly after using the medicine, just like the snowman in winter, after the sun comes out and the temperature rises, the snowman will start to melt, and the snow crumbs will fall down piece by piece after melting. The snowman can be compared to the urate crystals in the body of a gout patient, and the snow crumbs can be compared to the urate particles that are dissolved. These urate particles that fall off from a large piece of urate crystals will be deposited on other joints in the body, creating a new round of pain, but Professor Liu Xiangyuan says they will slowly dissolve away in the long run. This is precisely the process by which the drug works. How can we lower uric acid without triggering gout? Scientific usage of uric acid-lowering drugs It is very common for gout patients to have gout attacks during uric acid-lowering, especially the more effective drugs, such as benzbromarone and febuxostat. This is normal and what should be done? Many patients think that since the attack is induced by uric acid-lowering drugs, they should stop using the drug as soon as possible. This is completely wrong. If this continues, the patient’s blood uric acid will not be effectively controlled for a long time, and the gout will continue to attack for a long time, eventually leading to uremia and death. The correct approach is to not stop using uric acid-lowering drugs (repeated fluctuations in uric acid are also the reason for attacks and not easy to get well), while adding anti-inflammatory and analgesic drugs such as Fotarine, Fenbendazole, Loxone or Ankangxin, etc., orally with topical Qingpeng cream, etc. If such drugs are contraindicated, other drugs such as colchicine, prednisone, Medrol, Depo-Provera, Tramadol, Ixepro, and Prednisone may be used. For patients with frequent attacks, these drugs need to be combined with uric acid-lowering drugs for several months until no more attacks occur. If the blood uric acid level is maintained below 360umol/L for more than a few years, the gout stones deposited in the body will gradually dissolve and disappear, and then the attack will no longer occur. For patients with gout combined with cardiovascular disease, there are some medications that can cause an increase in uric acid. Extra attention is needed. Small doses of aspirin can cause an increase in uric acid. It is recommended to switch to Bolivar, which also has the ability to reduce platelet aggregation, to prevent cardiovascular disease. Calcium hydroxybenzoate capsules are used for diabetic microangiopathy and should have no effect on uric acid and can continue to be used. The scientific name of Hale capsule is tamsulosin hydrochloride extended-release capsule, which can treat benign prostatic hyperplasia. It is a highly selective alpha1A adrenergic receptor blocker, which has been reported to raise blood uric acid, while non-selective alpha1 receptor blockers such as prazosin, bunazosin and doxazosin have no significant effect on blood uric acid. prazosin is particularly suitable for patients suffering from hypertension and gout with prostatic hyperplasia, with milder side effects. It is the same as amlodipine, which is a calcium antagonist and has almost no effect on blood uric acid, so it can continue to be used. The same calcium antagonist antihypertensive drugs nifedipine, nicardipine, nifurtimox and nisoldipine have the effect of raising blood uric acid, and should be used with caution. If the above treatment still cannot control blood pressure, angiotensin II receptor antagonists can be added, which is the drug of choice for hypertension combined with gout, whose representative is coxsartan, which can increase uric acid excretion and raise urinary pH, while valsartan and irbesartan can also reduce blood uric acid, with valsartan relatively weaker and irbesartan stronger. Angiotensin-converting enzyme inhibitors (ACEI) such as Benazepril and Lenopril have inconsistent effects on blood uric acid. β-blockers such as propranolol and nadolol (hydroxynaphthacin) can increase blood uric acid, while metoprolol (medrolol, betaxolol) and betaxolol (lentaxin) have minimal effects on blood uric acid and can be used in patients with gout combined with hypertension. Diuretics such as furosemide, etanercept, hydrochlorothiazide, aminoglutethimide and compound preparations have the effect of raising blood uric acid and increasing uric acid deposition in the kidneys, so patients with gout accompanied by hypertension, kidney stones and diabetes should not use them for a long time. Gout patients combined with diabetes medication rules Diabetic patients take Bysampin, the scientific name is acarbose, belongs to the glucosidase inhibitor, mainly to lower postprandial blood sugar, does not affect the blood uric acid, can continue to use. Among all hypoglycemic drugs, only biguanides (such as hypoglycemic tablets) can increase blood uric acid, gout patients generally do not use. The uric acid is not that abominable and is actually beneficial to the body when it is well controlled. Professor Liu Xiangyuan said that uric acid also has certain benefits to the body, it is the body’s natural antioxidants. Large-scale epidemiological studies around the world have found that uric acid is associated with degenerative lesions in brain tissue. Below normal levels of uric acid can cause diseases such as Alzheimer’s and multiple sclerosis. The researchers used five years to compare 59,204 gout patients with 238,805 non-gout patients in the United Kingdom. The average age of this group was 65 years. Their conditions were similar. The study found that there were 309 cases of Alzheimer’s disease among gout patients and 1,942 cases among non-gout patients. The rate of Alzheimer’s disease was 24 percent lower in the gout patients than in the other group. The reason why such results occurred is not clear. But gout is due to too much uric acid in the blood, and uric acid prevents oxidative stress. It may help slow down neurological aging. When Professor Liu Xiangyuan visited the neurology consultation, he found that many patients with Alzheimer’s disease have low blood uric acid. Therefore, it is important to grasp the blood uric acid value, and it is generally advocated to control the blood uric acid level between 200μmol/L-300μmol/L. Too high or too low is not good for the body.