Briefly talk about the impact of hyperuricemia.(Part. 1)😎😎😎

Uric acid is a catabolite of purine nucleotides in the human body. It is a weakorganic acid. 80% of purine nucleotides are produced by human cell metabolism and 20% are obtained from food. The main cause of the increase in uric acid is excessive uric acid production and decreased uric acid excretion. 90% of hyperuricemia is related to decreased renal uric acid excretion.

1. Uric acid metabolism.

Synthesis:

The catabolism of purine nucleotides in the body is mainly carried out in the liver, small intestine and kidney. The abnormality of various key enzymes in the metabolic process will lead to an increase in uric acid synthesis, which accounts for about 10%.

Excretion:

Uric acid is mainly excreted through the kidneys and intestines. Normally, the amount of uric acid excreted into the intestinal cavity through the liver every day is about 1/4 to 1/3 of that produced, and then it is decomposed by bacteria in the intestinal cavity and then excreted from the body. The remaining 3/4 to 2/3 are excreted in urine by the kidneys. The abnormality of uric acid transporter located in the glomerulus and renal tubules and intestinal tract can affect the excretion of uric acid.

2. Causes of hyperuricemia.

Hyperuricemia is a metabolic syndrome caused by a disorder of purine metabolism. At a body temperature of 37 ℃, the saturated solubility of monosodium urate (MSU) in serum is 404.5 umol/L (6.8 mg/dL). It is usually defined as hyperuricemia when the serum uric acid level is> 420 umol/L (about 7 mg/dL). According to the cause, hyperuricemia is mainly divided into two categories: primary and secondary.

Primary hyperuricemia is mainly caused by abnormal enzyme activity during purine metabolism.

Secondary urinary hyperuricemia is characterized by defects in enzyme structure, excessive purine intake, alcohol consumption, enhanced nucleic acid metabolism (such as leukemia, anemic hemolysis, and malignant tumors) and accelerated purine decomposition (such as type I glycogen accumulation disease, hypoglycemia, hunger or exercise). The main causes of secondary hyperuricemia are: blood system disease, kidney disease, drug-induced, and excessive production of organic acids.

3. The effect of hyperuricemia on the body.

When uric acid or urate exceeds the normal solubility limit in body fluids, it will form crystals and deposit in any soft tissues except nerve tissues, which will cause different pathological changes.

Gout:

Hyperuricemia is the main risk factor for gout. Uric acid crystals deposit on joints and cause gout attacks. It causes bone and joint damage. Studies have shown that about 5% to 12% of hyperuricemia eventually develops into gout.

Hypertension:

Hyperuricemia can activate the renin-angiotensin system. It reduces the synthesis of nitric oxide in vascular endothelial cells and stimulates the proliferation of vascular smooth muscle. This can lead to increased blood pressure through various mechanisms such as vascular remodeling. In addition, long-term hypertension also affects uric acid metabolism through glomerular arteriosclerosis and other pathways, thereby aggravating hyperuricemia.

Abnormal blood lipid metabolism:

There is a mutual influence between uric acid metabolism and fat metabolism. Hyperuricemia and blood lipids can cause a decrease in lipoproteinase activity. At the same time, hyperlipidemia will also increase the rise of uric acid. In addition, hyperuricemia and hyperlipidemia are risk factors for arteriosclerosis and hypertension.

Diabetes:

Hyperuricemia can directly damage the function of pancreatic β-cells, thereby affecting insulin secretion and leading to diabetes. It can also aggravate metabolic disorders and insulin resistance in diabetic patients. It promotes the occurrence of macrovascular and microvascular complications in diabetic patients. At the same time, diabetic nephropathy and insulin resistance can also lead to aggravation of hyperuricemia.

Arteriosclerosis:

Uric acid crystals stimulate the blood vessel wall and induce an inflammatory response that damages vascular endothelial cells. In addition, hyperuricemia can also promote the formation of atherosclerosis together with hypertension, hyperlipidemia and hyperglycemia.

Heart failure:

Most cardiovascular diseases eventually lead to heart failure. Hyperuricemia is a risk factor for heart failure. This is closely related to its occurrence, development and prognosis.

Kidney damage:

Uric acid crystals are deposited in the kidneys. It causes uric acid nephropathy, increases the incidence of kidney stones and the risk of kidney failure.

Androgenetic alopecia:

Studies have shown that there is a significant correlation between hyperuricemia and androgenic alopecia, especially in patients with early-onset androgenic alopecia (< 30 years).