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*For reference only for medical professionals, I have quit drinking, and I also try to avoid seafood and meat.
Why is uric acid still high? In the last issue (Are you a high-risk group of gout? 6 major living habits teach you to prevent it!), our endocrinology team of the Southern Theater General Hospital helped everyone identify the high-risk groups of gout, the incentives for gout, and prevent gout through six major life>
.
So, a gout patient came to ask our team: I have quit drinking, and I also try to avoid seafood and meat.
Why is uric acid still high? In fact, once you enter gout, simply relying on diet control or exercise cannot effectively reduce the level of uric acid, nor can it replace the treatment of uric acid-lowering drugs
.
Today, our endocrinology team will continue to take you to understand the source and destination of uric acid in your body, the cause of hyperuricemia, and the treatment options for different stages of gout
.
The source and destination of uric acid 1 Source of uric acid There are two main sources of uric acid in the human body.
One is endogenous, which is mainly metabolized from substances in the body, accounting for 80% of the total uric acid in the body; the other is exogenous, which is rich in uric acid.
Nucleotides are decomposed in food and account for 20% of the total uric acid in the body
.
That is to say, even if you don't eat or drink, you can only reduce blood uric acid by 60-120 μmol/L
.
Therefore, for gout patients, adjusting the diet can only be used as an adjuvant therapy
.
2.
Where to go for uric acid Uric acid is mainly excreted through the kidneys and intestines.
The normal human body excretes about 1/4 to 1/3 of uric acid into the intestinal cavity through the liver every day, and then is decomposed and excreted by bacteria in the intestinal cavity
.
The remaining 2/3 to 3/4 are excreted in the urine through the kidneys
.
The main causes of elevated uric acid are excessive uric acid production and decreased uric acid excretion, of which 90% of hyperuricemia is related to decreased renal uric acid excretion
.
The etiology of hyperuricemia Hyperuricemia is mainly divided into two categories: primary and secondary according to the etiology
.
1.
The cause of primary hyperuricemia Primary hyperuricemia is an increase in serum uric acid concentration caused by congenital purine metabolism disorder on the basis of excluding other diseases
.
More than 90% of patients with primary hyperuricemia are caused by decreased renal uric acid excretion, mainly due to decreased renal tubular excretion of uric acid
.
Less than 10% of primary hyperuricemia is caused by increased uric acid production, and congenital defects in purine metabolizing enzymes are the main reason
.
When purine-restricted diet for 5 days, uric acid/24h>600mg indicates increased uric acid production
.
2.
The etiology of secondary hyperuricemia Secondary hyperuricemia is characterized by defects in enzyme structure, excessive purine intake, alcohol consumption, enhanced nucleic acid metabolism (such as leukemia, anemia hemolysis and malignant tumors and other diseases) and purine of accelerated decomposition (type I glycogen storage disease, hypoglycemia, starvation or exercise)
.
The following reasons can also be seen: acute and chronic leukemia, polycythemia, multiple myeloma, hemolytic anemia, lymphoma and various solid tumors in the blood system diseases, due to the massive decomposition of intracellular nucleic acid, resulting in excessive uric acid production
.
Taking drug diuretics, compound antihypertensive tablets, pyrazinamide and other anti-tuberculosis drugs, anti-Parkinson's disease drugs, low-dose aspirin, vitamin B12, tobacco acid, cytotoxic drugs, immunosuppressants,
etc.
Organic acids produce too much lactic acidosis, diabetic ketoacidosis, excessive exercise, starvation, and alcohol intake inhibit uric acid excretion
.
Various types of kidney diseases Renal insufficiency and renal tubular disease cause decreased uric acid excretion and increased serum uric acid
.
Under normal circumstances, the production and clearance of uric acid are in a dynamic balance, so that the serum uric acid level maintains the normal range
.
Any cause of increased uric acid production or decreased excretion, or the presence of both mechanisms, will result in increased serum uric acid levels, leading to gout
.
According to the principle of uric acid generation and metabolism, there are two types of commonly used uric acid-lowering drugs, one can inhibit the production of uric acid, and the representative drug is allopurinol; the other can promote uric acid excretion, and the representative drug is benzbromarone
.
Table 1 Drug therapy for lowering uric acid It is better to teach him to fish than to teach him to fish
.
In the last issue, we mentioned that the treatment plans for lowering uric acid in different stages are different, which is mainly reflected in the difference in the timing and target value of lowering uric acid
.
Patients with pure hyperuricemia, even if they have no symptoms of gout, still need uric acid-lowering treatment, as follows: Figure 1 Differences in the target value of uric acid lowering in different stages 1.
Simple hyperuricemia has one of the following complications: hypertension, Abnormal lipid metabolism, diabetes, obesity, stroke, coronary heart disease, cardiac insufficiency, uric acid nephrolithiasis, renal function impairment (≥CKD stage 2); 2.
Gout has one of the following combined conditions: the number of gout attacks ≥ 2 times/ years, tophi, chronic gouty arthritis, kidney stones, chronic kidney disease, hypertension, diabetes, dyslipidemia, stroke, ischemic heart disease, heart failure, age of onset <40 years old; it is recommended to control serum uric acid at <40 years old 300µmol/L
.
Consult your doctor for specific medication choices! After reading this, are you using the right uric acid-lowering drug? Has the target value been reached? If we let it go, what kind of harm will hyperuricemia cause to our human body? Please look forward to our endocrinology team of the Southern Theater General Hospital to answer the dangers of hyperuricemia for you! Expert introduction Li Jia Deputy Chief Physician of the Department of Endocrinology, Southern Theater General Hospital, MD, Postdoctoral, Master Supervisor Chairman (preparation) of the Osteoporosis Prevention and Rehabilitation Committee of Guangdong Geriatrics Health Association Chairman (preparation) Published more than 40 papers in SCI and core journals Editor-in-chief, co-editing, and translation of 5 monographs In recent years, he has hosted more than 5 national natural and provincial and ministerial-level funds Served as the simultaneous translation of several SCI magazine reviewers at the conference
Why is uric acid still high? In the last issue (Are you a high-risk group of gout? 6 major living habits teach you to prevent it!), our endocrinology team of the Southern Theater General Hospital helped everyone identify the high-risk groups of gout, the incentives for gout, and prevent gout through six major life>
.
So, a gout patient came to ask our team: I have quit drinking, and I also try to avoid seafood and meat.
Why is uric acid still high? In fact, once you enter gout, simply relying on diet control or exercise cannot effectively reduce the level of uric acid, nor can it replace the treatment of uric acid-lowering drugs
.
Today, our endocrinology team will continue to take you to understand the source and destination of uric acid in your body, the cause of hyperuricemia, and the treatment options for different stages of gout
.
The source and destination of uric acid 1 Source of uric acid There are two main sources of uric acid in the human body.
One is endogenous, which is mainly metabolized from substances in the body, accounting for 80% of the total uric acid in the body; the other is exogenous, which is rich in uric acid.
Nucleotides are decomposed in food and account for 20% of the total uric acid in the body
.
That is to say, even if you don't eat or drink, you can only reduce blood uric acid by 60-120 μmol/L
.
Therefore, for gout patients, adjusting the diet can only be used as an adjuvant therapy
.
2.
Where to go for uric acid Uric acid is mainly excreted through the kidneys and intestines.
The normal human body excretes about 1/4 to 1/3 of uric acid into the intestinal cavity through the liver every day, and then is decomposed and excreted by bacteria in the intestinal cavity
.
The remaining 2/3 to 3/4 are excreted in the urine through the kidneys
.
The main causes of elevated uric acid are excessive uric acid production and decreased uric acid excretion, of which 90% of hyperuricemia is related to decreased renal uric acid excretion
.
The etiology of hyperuricemia Hyperuricemia is mainly divided into two categories: primary and secondary according to the etiology
.
1.
The cause of primary hyperuricemia Primary hyperuricemia is an increase in serum uric acid concentration caused by congenital purine metabolism disorder on the basis of excluding other diseases
.
More than 90% of patients with primary hyperuricemia are caused by decreased renal uric acid excretion, mainly due to decreased renal tubular excretion of uric acid
.
Less than 10% of primary hyperuricemia is caused by increased uric acid production, and congenital defects in purine metabolizing enzymes are the main reason
.
When purine-restricted diet for 5 days, uric acid/24h>600mg indicates increased uric acid production
.
2.
The etiology of secondary hyperuricemia Secondary hyperuricemia is characterized by defects in enzyme structure, excessive purine intake, alcohol consumption, enhanced nucleic acid metabolism (such as leukemia, anemia hemolysis and malignant tumors and other diseases) and purine of accelerated decomposition (type I glycogen storage disease, hypoglycemia, starvation or exercise)
.
The following reasons can also be seen: acute and chronic leukemia, polycythemia, multiple myeloma, hemolytic anemia, lymphoma and various solid tumors in the blood system diseases, due to the massive decomposition of intracellular nucleic acid, resulting in excessive uric acid production
.
Taking drug diuretics, compound antihypertensive tablets, pyrazinamide and other anti-tuberculosis drugs, anti-Parkinson's disease drugs, low-dose aspirin, vitamin B12, tobacco acid, cytotoxic drugs, immunosuppressants,
etc.
Organic acids produce too much lactic acidosis, diabetic ketoacidosis, excessive exercise, starvation, and alcohol intake inhibit uric acid excretion
.
Various types of kidney diseases Renal insufficiency and renal tubular disease cause decreased uric acid excretion and increased serum uric acid
.
Under normal circumstances, the production and clearance of uric acid are in a dynamic balance, so that the serum uric acid level maintains the normal range
.
Any cause of increased uric acid production or decreased excretion, or the presence of both mechanisms, will result in increased serum uric acid levels, leading to gout
.
According to the principle of uric acid generation and metabolism, there are two types of commonly used uric acid-lowering drugs, one can inhibit the production of uric acid, and the representative drug is allopurinol; the other can promote uric acid excretion, and the representative drug is benzbromarone
.
Table 1 Drug therapy for lowering uric acid It is better to teach him to fish than to teach him to fish
.
In the last issue, we mentioned that the treatment plans for lowering uric acid in different stages are different, which is mainly reflected in the difference in the timing and target value of lowering uric acid
.
Patients with pure hyperuricemia, even if they have no symptoms of gout, still need uric acid-lowering treatment, as follows: Figure 1 Differences in the target value of uric acid lowering in different stages 1.
Simple hyperuricemia has one of the following complications: hypertension, Abnormal lipid metabolism, diabetes, obesity, stroke, coronary heart disease, cardiac insufficiency, uric acid nephrolithiasis, renal function impairment (≥CKD stage 2); 2.
Gout has one of the following combined conditions: the number of gout attacks ≥ 2 times/ years, tophi, chronic gouty arthritis, kidney stones, chronic kidney disease, hypertension, diabetes, dyslipidemia, stroke, ischemic heart disease, heart failure, age of onset <40 years old; it is recommended to control serum uric acid at <40 years old 300µmol/L
.
Consult your doctor for specific medication choices! After reading this, are you using the right uric acid-lowering drug? Has the target value been reached? If we let it go, what kind of harm will hyperuricemia cause to our human body? Please look forward to our endocrinology team of the Southern Theater General Hospital to answer the dangers of hyperuricemia for you! Expert introduction Li Jia Deputy Chief Physician of the Department of Endocrinology, Southern Theater General Hospital, MD, Postdoctoral, Master Supervisor Chairman (preparation) of the Osteoporosis Prevention and Rehabilitation Committee of Guangdong Geriatrics Health Association Chairman (preparation) Published more than 40 papers in SCI and core journals Editor-in-chief, co-editing, and translation of 5 monographs In recent years, he has hosted more than 5 national natural and provincial and ministerial-level funds Served as the simultaneous translation of several SCI magazine reviewers at the conference
