Diabetes and hyperuricemia are common metabolic diseases in the clinic, so when diabetes suffers from hyperuricemia, how can we send medicines to lose one another and achieve a win-win situation?Diabetes and hyperuricemia are related siblings, and they can coexist and affect each other.On the one hand, diabetes can lead to an increase in serum uric acid, the possible mechanisms are as follows: (1) In the state of insulin resistance (IR), the intermediate products of the glycolysis process are transferred to 5-phosphate ribose and phosphoribosyl pyrophosphate, resulting inIncreased blood uric acid production.(2) Patients with type 2 diabetes often have hyperinsulinemia.Hyperinsulinemia can promote Na +-H + exchange in the renal proximal tubules, increase anion (including uric acid) reabsorption, and reduce uric acid excretion.(3) Type 2 diabetes and its complications increase the level of oxidative stress in the body, and uric acid is one of the main endogenous water-soluble antioxidants in the human body. In order to protect the body from harmful oxidative free radicals, blood uric acid levelsRise.(4) Patients with diabetes often have factors such as hypertension and renal arteriosclerosis. Arteriosclerosis leads to glomerular hypoxia, increased lactic acid production, and excretion due to competition with uric acid, resulting in increased blood uric acid.(5) For severe diabetic nephropathy and renal insufficiency, the effective nephron decreases, uric acid filtration from the glomerulus decreases, and the kidney’s ability to excrete uric acid weakens.On the other hand, hyperuricemia is an independent risk factor for the occurrence and development of diabetes complications. According to statistics, the incidence of microangiopathy, macrovascular disease, and neuropathy in diabetic patients with hyperuricemia is significantly higher than uric acid levels.Normal diabetics.(1) Increase the risk of diabetic nephropathy: Diabetic nephropathy is a serious complication of type 2 diabetes. Hyperuricemia not only causes uric acid crystal deposition to cause renal arterioles and chronic interstitial inflammation to aggravate kidney damage, but uric acid can directly cause kidney damage.Microvessel disease occurs in the afferent bulbous artery, leading to chronic kidneys and end-stage development of uremia, but a major cause of death in patients with diabetes.(2) Increase the risk of diabetic retinopathy: Diabetic retinopathy is a major cause of blindness and disability in diabetic patients.Increased blood uric acid can cause urate crystals to deposit on the walls of arterial blood vessels, cause vascular intimal damage, and also cause vascular smooth muscle proliferation, leading to retinal vascular disease.These can cause microcirculation disorders, which promote the occurrence of diabetic retinopathy.(3) Increasing the risk of diabetic macroangiopathy: Especially in elderly patients with type 2 diabetes, the increase in blood uric acid levels is significantly related to the occurrence and development of coronary heart disease and cerebrovascular disease.Macrovascular disease is the leading cause of death in patients with type 2 diabetes.(4) Hyperuricemia is related to hypertension in patients with type 2 diabetes: Hyperuricemia can also lead to the occurrence of hypertension and difficult to control hypertension in patients with type 2 diabetes.Because hyperuricemia can increase insulin resistance and promote the production of angiotensin II, these factors can lead to increased blood pressure.Therefore, when the type of diabetic patients with hypertension is difficult to control, blood uric acid levels need to be monitored to exclude the effect of high uric acid on blood pressure.(5) Hyperuricemia is related to other metabolic abnormalities of type 2 diabetes: Hyperuricemia is closely related to dyslipidemia, obesity, etc. Those with abnormal uric acid levels have higher levels of dyslipidemia and obesity, and with theIncreased and showed an increasing trend, so patients with type 2 diabetes and hyperuricemia are more likely to have metabolic abnormalities such as obesity, increased abdominal circumference, and increased blood lipids.The cause may be related to the increase of insulin resistance in patients with type 2 diabetes with hyperuricemia.In general, diabetes and hyperuricemia have a common pathogenesis, they are related to each other, cause and effect, and affect each other.Therefore, in the prevention and treatment of type 2 diabetes and chronic complications, we must not only pay attention to the control of blood glucose, blood pressure, blood lipids, weight, etc., but also pay attention to the risk factor of hyperuricemia and give relevant treatment in time.So when diabetes suffers from hyperuricemia, how should the medicine be used?On this issue, we divide into two angles to discuss in detail.1 Selection of uric acid lowering and anti-gout drugs ▎Uric acid lowering glucose metabolism patients with blood uric acid> 480μmol / L should immediately start uric acid lowering drug treatment.In theory, lowering blood uric acid can improve insulin resistance, increase insulin sensitivity, and protect pancreatic β-cell function, which is conducive to blood glucose control.Therefore, the currently used uric acid-lowering drugs have no adverse effect on blood sugar, but pay close attention to the adverse reactions of the drugs during use.▎Anti-gout drugs clinically hyperuricemia often causes gout, and gout attacks may be induced during uric acid lowering treatment. Therefore, the application of anti-gout drugs has to be considered during the treatment of diabetes combined with hyperuricemia.The commonly used drugs for gout attacks are: colchicine, non-steroidal anti-inflammatory drugs (NSAIDs) or glucocorticoids.Glucocorticoids may significantly increase blood sugar. Therefore, when diabetes occurs with gout, we should try to avoid using glucocorticoids.However, on the other hand, the gout treatment guidelines suggest that in order to avoid worsening renal function, gout should be used to control the onset of gout.If a diabetic patient is associated with renal insufficiency and gout at the same time, we need to consider the use of glucocorticoids as appropriate according to the patient’s blood glucose or renal function, and closely monitor changes in blood glucose and renal function during the medication.2 The choice of hypoglycemic drugs The goal of hypoglycemic treatment is not only to control blood sugar, but also to reduce the complications of diabetes and reduce the risk of death, thereby improving the long-term prognosis of patients.When diabetes encounters the special case of hyperuricemia, choose a hypoglycemic drug. In addition to paying attention to the efficacy of hypoglycemic agents, attention should also be paid to the effect of hypoglycemic drugs on uric acid. In principle, it does not affect the metabolism of uric acid and does not increase or induce it.Gout hypoglycemic drugs are preferred.The following briefly introduces the characteristics of current hypoglycemic drugs and their effects on uric acid▎α-glucosidase inhibitors: Delays the absorption of carbohydrates by inhibiting intestinal α-glucosidase activity, which is suitable for carbohydrate-basedAnd postprandial blood sugar rise.Domestically listed are acarbose, voglibose and miglitol.Among them, acarbose can reduce the increase of blood uric acid level caused by sucrose decomposition.▎thiazolidinediones (TZDs): Reduce blood glucose mainly by increasing the sensitivity of target cells to insulin action and reducing insulin resistance.There are mainly rosiglitazone and pioglitazone, which can reduce fasting and postprandial blood glucose, reduce glycated hemoglobin, and improve lipid metabolism disorders.May reduce blood uric acid levels by reducing insulin resistance and improving lipid metabolism.▎Metformin: Metformin can inhibit glycogen breakdown, promote glucose utilization, and increase the sensitivity of the body’s insulin to reduce blood sugar, while also having a weight loss effect.It is generally believed that metformin reduces weight and reduces triglycerides by suppressing appetite, increases insulin sensitivity, reduces renal tubular epithelial cell apoptosis, thereby improving renal function, promoting blood uric acid metabolism, and thereby lowering blood uric acid levels.▎SGLT2 inhibitor: By inhibiting the sodium glucose cotransporter 2 (SGLT2) activity of the renal proximal tubule reabsorbs glucose, it increases urine glucose excretion and lowers blood sugar.Studies have shown that SGLT2 inhibitors can reduce blood uric acid by 10% to 15%.Blood uric acid, like blood glucose, is also absorbed in the proximal tubules.SGLT2 inhibitors increase urinary glucose excretion and increase uric acid secretion in response to the reabsorption of glucose, resulting in increased uric acid excretion. DDP-4 inhibitors and GLP-1 receptor agonists: dipeptidyl peptidase-4Although (DPP-4) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists have different sites of action, they are both drugs that promote insulin secretion indirectly through intestinal insulinotropin.It promotes insulin secretion in a glucose concentration-dependent manner. As the blood glucose increases, the amount of insulin secretion increases, but when the blood glucose concentration is too low, it no longer promotes insulin secretion.These two drugs can improve islet function, reduce insulin resistance, do not cause elevated blood uric acid, and even reduce serum uric acid by reducing serum insulin levels and weight.Sulfonylureas: Reduce blood sugar by stimulating islet β-cell secretion of insulin, increasing insulin levels in the body.Among them, glibenclamide, glimepiride, gliclazide and other drugs that are mainly excreted by the kidney may affect kidney function and reduce the excretion of uric acid, but the overall effect is not significant.Gliquidone has little effect on uric acid mainly through bile excretion.Glinate: It is a blood glucose regulator for meals. It can increase serum insulin concentration to reduce glucose. It is mainly metabolized by the liver and has little effect on uric acid. However, it is also believed to cause hyperinsulinemia, and insulin can promote kidney to uric acid.Reabsorption, causing an increase in blood uric acid.▎Insulin is a good medicine for treating various types of diabetes, but the drug can increase the reabsorption of uric acid and increase the blood uric acid level in the metabolic process of the body.Although hyperinsulinemia is the main cause of elevated blood uric acid levels, other studies have found that short-term intensive insulin therapy can effectively improve insulin resistance and reduce blood uric acid levels in patients with type 2 diabetes.Therefore, insulin can affect the level of blood uric acid from multiple levels. It cannot be simply said that the use of insulin must increase or decrease blood uric acid, which is closely related to the dose of insulin used by the patient and the pancreas and pancreas function of the patient..From the characteristics of the above-mentioned hypoglycemic agents, metformin, TZDs, α-glucosidase inhibitors, GLP-1 receptor agonists, and DPP-4 inhibitors can improve islet function, reduce insulin resistance, and reduce blood uric acid to some extent.Role, SGLT-2 inhibitors can directly promote the excretion of uric acid. If there is no contraindication, these types of hypoglycemic agents are preferred for patients with diabetes and hyperuricemia; insulin secretagogues (sulfonylureas and glienafil) are generallyIt is said that it has little effect on uric acid, but after all, insulin secretagogues can increase serum insulin concentration and may not be conducive to uric acid excretion, so it is not recommended; insulin can promote renal reabsorption of uric acid and adversely affect uric acid excretion, so it is useful for diabetesPatients with high uric acid are not suitable.For insulin secretagogues and exogenous insulin, if it must be used, it is best to use it in combination with metformin or insulin sensitizers, alpha glucosidase inhibitors, and reduce the amount of insulin as much as possible.In short, diabetes combined with hyperuricemia requires a combination of both and comprehensive treatment.In terms of drug selection schemes, drugs that lower blood uric acid theoretically, lowering blood uric acid can help lower blood sugar, and have no effect on blood sugar as a whole; however, some blood glucose lowering drugs may cause uric acid to increase.As far as possible, you should choose a hypoglycemic agent that is beneficial to uric acid excretion..
When diabetes suffers from high uric acid, what is the combination of the two?