After the occurrence of diabetes in patients, with the increase of the course of disease and the increase of the age of patients, the incidence of other combined diseases in patients is also increasing. Diabetes combined with hyperuricemia is a common clinical disease, and 40% of patients with diabetes will develop hyperuricemia and other complications, which not only makes the treatment of the disease more difficult, but also increases the burden of the hospital. Therefore, to analyze the metabolic factors related to hyperfatemia, and to provide a reference for the clinical exploration of active and effective treatment

Ren, Yanming

Zhang, Min

English

Advanced Emergency Medicine (E-Journal)

Volume 11 | Issue 4 -163-Analysis of Metabolic Factors Associated with Hyperuricemia inDiabetes MellitusMin Zhang, Yanming RenQinghai University, Xining 810016, China.Abstract:After the occurrence of diabetes in patients, with the increase of the course of disease and the increase of the age ofpatients, the incidence of other combined diseases in patients is also increasing. Diabetes combined with hyperuricemia is acommon clinical disease, and 40% of patients with diabetes will develop hyperuricemia and other complications, which notonly makes the treatment of the disease more difficult, but also increases the burden of the hospital. Therefore, to analyze themetabolic factors related to hyperfatemia, and to provide a reference for the clinical exploration of active and effectivetreatment.Keywords: Diabetes Mellitus; Hyperuricemia; Metabolic FactorsIntroductionDiabetes mellitus is a common chronic disease in clinical practice, and patients are often complicated withhyperglycemia, hyperuricemia and other complications. Related studies have shown that there is a certain relationshipbetween hyperuricemia and diabetes[1]. This paper studies the internal pathogenesis and rules of diabetes combined withhyperuricemia, providing a new basis for the clinical prevention and treatment of diabetes combined with hyperuricemia.1. Overview of the correlation between hyperuricemia and diabetesmellitusHyperuricemia refers to the hypersaturated state of urate in the extracellular fluid. It is characterized by the disorder ofpurine metabolism and the increase of uric acid in the body. It is generally believed that hyperuricemia should be consideredwhen blood uric acid ≥420umol/L(7mg/L) in males and ≥360umol/L(6mg/L) in females.Uric acid (UA) is the end product of purine metabolism in the human body. One third of purines in the body come fromfood breakdown, two thirds are synthesized by the body itself, and most purines are oxidized and metabolized by the liverinto uric acid. The daily production is approximately equal to the excretion, 1/3 is excreted by the intestine, and 2/3 isexcreted by the kidney. The kidney is the main way of uric acid excretion. After blood uric acid is filtered from the glomeruli,98% of uric acid is reabsorbed by the proximal tubules, and finally, less than 10% of uric acid is excreted into the urine bythe distal convoluted tubules. Blood uric acid (SUA) concentration depends on the balance between the amount of purinesynthesis, the amount of ingested and the amount of uric acid excreted. If uric acid is generated too much or excreted toolittle, uric acid metabolism will lose balance, and uric acid will accumulate in the body, leading to elevated blood uric acid,hyperuricemia (HUA), and a series of pathophysiological changes.With the rapid development of economy in recent years, the occurrence of hyperuricemia not only gradually increases,but also tends to occur at an earlier age. At present, it is clinically found that the age of 30 to 39 years old is prone tohyperuricemia, which may be related to genetic factors, mental factors, lifestyle (diet, alcohol consumption, physical-164- Advanced Emergency Medicineexercise). After puberty, serum uric acid levels increase more rapidly in men than in women and peak at age 50. The serumuric acid level of females does not rise significantly after puberty, but rapidly rises to a level similar to that of males aftermenopause, possibly because estrogen can promote the excretion of uric acid by the kidney. In the 40 to 59 age group,hyperuricemia is associated with a cluster of diseases, such as hyperuricemia with hyperuricemia, hypertension, obesity, anddiabetes. This is mainly related to metabolic risk factors such as renal excretory dysfunction and insulin resistance. It isworth exploring the relationship between diabetes mellitus combined with hyperuricemia and these metabolic diseases.2. Analysis of metabolic factors related to hyperuricemia in diabetesmellitusUric acid is the end product of purine metabolism in the body. In the body, uric acid is mainly degraded by urateoxidase (uricase) in the liver to produce allantoin, and then excreted by the kidney. Uric acid levels in the body is mainlyaffected by two aspects, on the one hand is to make increased uric acid to produce factors (10%), such as high purine orprotein diet is taken, alcohol consumption, the high level of cell metabolism, and the shortcomings of the purine metabolicenzymes, etc., on the other hand is reduce uric acid excretion factor (90%), two-thirds of renal excretion by the blood uricacid, a third by the bowels, After glomerular filtration, 98% of uric acid is reabsorbed by proximal tubules, and less than10% is finally excreted into urine by distal convoluted tubules[3]. For example, the renal excretion capacity decreases, theglomerular filtration rate decreases, the renal tubular reabsorption increases (such as the use of thiazide diuretics), and theblood uric acid increases.The occurrence of hyperuricemia in diabetic patients is the result of increased production or decreased excretion. Thereasons may be as follows :① Microangiopaplasia is common in diabetic patients, and renal microangiopaplasia leads torenal ischemia and decreased renal blood flow, while uric acid excretion is directly proportional to renal blood flow, so blooduric acid increases. ② Uric acid, as one of the most widely distributed water-soluble antioxidants in the human body, has theproperty of iron as a mixture, which can reduce the incidence of lipid peroxidation and stabilize the serum ascorbic acid fromoxidation. In some patients, oxidative stress is aggravated and large blood vessels are damaged. Uric acid compensativelyincreases to counter this oxidative reaction, resulting in hyperuricemia. ③ Elevated serum uric acid can further damage isletB cells. Hyperuricemia is also one of the clinical manifestations of metabolic syndrome. The pathogenesis of diabetichyperuricemia is also related to hyperinsulinemia caused by insulin resistance. Because it increases urinary sodium excretionin proximal convoluted tubules, it competitively inhibits uric acid excretion. It is known that glucose and uric acid arecompetitively reabsorbed in the proximal convoluted tubules of the kidney. Increased excretion of urine sugar willcompetitively inhibit uric acid reabsorption, resulting in a decrease in blood uric acid level. When blood glucose is wellcontrolled, urine sugar decreases, uric acid reabsorption increases, and blood uric acid increases. It is suggested that thedecrease of renal function can increase the serum uric acid level, 8 but the blood glucose level is not the cause of theabnormal uric acid metabolism. Studies have shown that body weight is an independent risk factor for diabetes mellituscomplicated with hyperuricemia. The mechanism of association between obesity and hyperuricemia may be the decreasedexpression or clearance of leptin gene in serum of patients with hyperuricemia. Atherosclerosis induced by high level ofserum uric acid in patients with diabetes may be deposited directly in the arteriolar wall through uric acid stones, and thendamage the intima through purine metabolism and lipid metabolism. Hyperuric acid, hyperglycemia and hyperlipidemiahave superposed pathogenic effects to accelerate the process of atherosclerosis, while hypertension can also cause renalmicrovascular sclerosis, increase the concentration of angiotensin and catecholamines, reduce renal blood flow, andaccumulate hypoxic lactic acid in local tissues, which compete with blood uric acid for excretion, and increase blood uricacid[4].On the other hand, uric acid crystals in diabetes can promote blood pressure by stimulating renin angiotensin systemVolume 11 | Issue 4 -165-and inhibiting nitric oxide synthesis[5]. At the same time, uric acid crystals are deposited in the vessel wall, which promotelipid peroxidation, increase the generation of oxygen free radicals, and participate in the inflammatory reaction. Recentstudies have also found that hypertension is related to genes related to vascular proliferation and sclerosis, such asupregulation of uric acid transporter I and cyclooxygenase-2 genes on vascular wall. It can be seen that hyperuricemia isclosely related to hypertension and its atherosclerotic complications. Stepwise regression analysis showed that Ccr, bodyweight and LDL-C were independent risk factors for diabetes mellitus complicated with hyperuricemia. These resultsindicated that the increase of serum uric acid level in diabetes mellitus was closely related to obesity, lipid metabolismdisorder, elevated blood pressure, IR and metabolic syndrome. Elevated serum uric acid level is an important characteristicof insulin resistance syndrome.3. The prevention of hyperuricemiaFor asymptomatic hyperuricemia patients with family history of gout or blood uric acid >535umol/L and 24h urine uricacid >5.9mmol/L, drugs should be used to reduce uric acid. At present, drugs to reduce uric acid are mainly divided into twokinds: uric acid excreting drugs (benbromarone) and uric acid inhibiting drugs (allopurinol), the former can inhibit uric acid.Reabsorption of uric acid by renal tubules increases uric acid excretion. Generally applicable to the type of uric acidexcretion reduction, taking method :50mg, once a day. Allopurinol can inhibit the activity of xanthine oxidase, therebyreducing the biosynthesis of uric acid and decreasing the concentration of blood uric acid. Allopurinol is commonly used inpatients with increased uric acid production. How to take: Starting dose 50mg, 3 times a day, gradually increased to300-600mg/d. It is worth pointing out that the above two types of drugs must be used after the control of acute inflammationin gouty arthritis (2 weeks after the acute attack). Colchicine or non-steroidal anti-inflammatory drugs should be used inacute gout attacks.4. SummaryTo sum up, high uric acid hematic disease is common complications of diabetes, are caused by lipid metabolismdisorders in body, is in patients with atherosclerosis, stroke and other chronic cardiovascular disease risk factors, treatmentand prevention of diabetic high blood uric acid is an important content of current medical research, is of great significance toreduce chronic cardiovascular disease clinically. Since hyperuric acid, hyperglycemia, dyslipidemia and hypertensioncomplement each other and promote the formation of atherosclerosis and the aggravation of insulin resistance, it is necessaryto not only control fasting blood glucose, blood pressure, blood lipids and obesity, but also pay attention to the risk factor ofhyperuric acid in patients with T2DM and give timely treatment relevant interventions.References[1] Marco Meloni, Valentina Izzo, Erika Vainieri, Laura Giurato,Valeria Ruotolo,Luigi Uccioli.Management of negativepressure wound therapy in the treatment of diabetic foot ulcers[J]. World Journal of Orthopedics: 2015,6(4):387-393.[2] Liu JC, Tang CY, Lu SY et al., a famous Chinese medicine practitioner in China, discusses the pathogenesischaracteristics of adolescent central obesity based on "qi change theory"[J].Journal of Hainan MedicalCollege,2020(8):56-60.[3] Pan LB, Han P, Ma SR, et al. Abnormal metabolism of gut microbiota reveals the possible molecular mechanism ofnephropathy induced by hyperuricemia [J]. Journal of pharmaceutical sciences, 2020,0(2):249-261.[4] Cappuuio FP, Strazzullo P, Farinaro E, et al. Reduction of serum uric acid by hormonal replacement therapy inpostmenopausal with hyperuricemia. Lancet, 1999, 354: 650.

Analysis of Metabolic Factors Associated with Hyperuricemia in Diabetes Mellitus

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Analysis of Metabolic Factors Associated with Hyperuricemia in Diabetes Mellitus

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