To treat gout well, these two indicators are indispensable

The diagnosis, treatment and even prevention of gout are inseparable from these two indicators - uric acid and uric acid

Uric acid is a product of purine metabolism in humans

The daily production and excretion of uric acid in the human body basically maintains a dynamic balance, and any factors that affect the production and (or) excretion of blood uric acid can lead to changes in blood uric acid and uric acid

Detailed explanation of blood uric acid

Serum uric acid is associated with renal, cardiovascular, cerebrovascular and peripheral vascular target organ damage

If there is tophi in the body, whether it is on the joints or in the organs, the concentration of blood uric acid is the concentration of "uric acid saturated solution", which varies with the pH of the blood

Increased serum uric acid is more common in:

① Serum uric acid in acute and chronic nephritis was significantly increased, which was more significant and earlier than blood urea nitrogen (BUN) and serum creatinine (Cr)

②Gout, caused by nucleoprotein and purine metabolism disorder, serum uric acid >595μmol/L

③ Leukemia, multiple myeloma, polycythemia vera, etc.

④Others: chloroform, carbon tetrachloride, lead poisoning, eclampsia, pregnancy reaction, strenuous exercise,

Detailed explanation of uric acid

In clinical practice, the total uric acid excretion in 24-hour urine is usually detected.

Increased uric acid is more common in:

① gout;

② Mass destruction of tissues, excessive nucleoprotein decomposition, such as pneumonia, eclampsia, etc.

③ renal tubular reabsorption disorders, such as Fanconi syndrome, hepatolenticular degeneration, the use of adrenocorticotropic hormone (ACTH) and adrenocortical hormone, etc.

④ enhanced nuclear protein metabolism, such as myeloid leukemia, myeloid dysplasia, hemolytic anemia, pernicious anemia, lymphoma and hypothyroidism

The relationship between uric acid and hyperuricemia

The combined calculation of serum uric acid and uric acid can be used to classify hyperuricemia and give targeted treatment

Uric acid excretion can be expressed by two indicators: urinary uric acid excretion rate (urinary uric acid excretion, UEua) and uric acid excretion fraction (factional excetion of uric acid, FEua)

Poor excretion type: UEUA＜3600umol/d/(1.

Hyperplasia: UEUA>3600umol/d/(1.
73m2)[600mg/d/1.
73m2] and FEUA≥5.
5%
.

Mixed type: UEUA>3600umol/d/(1.
73m2)[600mg/d/l.
73m2] and FEUA<5.
5%
.

Among them, UEUA[umol/d/(1.
73m2]=uric acid (umol/d/body surface area (1.
73m2));

FEUA(%)=(uric acid X serum creatinine)/(serum uric acid X urine creatinine)
.

Among patients with hyperuricemia, 10%-25% of the patients are hyperuricemic type, and most of them can be combined with the type of poor excretion.
The main reasons include high uric acid diet, drinking and diseases that increase blood uric acid (myeloproliferative diseases, hemolytic anemia, psoriasis),
etc.
And more than 90% are poor excretion, including chronic kidney disease, genetic diseases (URAT 1, GLUT 9, ABCG 2 mutations), hyperuricemia, metabolic syndrome, lead poisoning, drugs (aspirin, diuretics, calcineurin inhibition) drugs, anti-tuberculosis drugs, etc.
)
.

treat

The treatment of hyperuricemia can be divided into drug treatment and non-drug treatment
.
The gout treatment guidelines published by the American College of Rheumatology (ACR) in 2012 included non-drug therapy as the basis for gout treatment
.
The guidelines recommend that patients quit smoking, exercise, control their weight, have a balanced nutrition, and classify their food; it is recommended to eat fat-free or low-fat dairy products and vegetables; and to limit or avoid the intake of purine-rich foods, sucrose, salt, and alcoholic beverages
.

However, clinical research reports show that non-drug therapy can only reduce blood uric acid levels by about 10% to 18%
.
Therefore, drug treatment of hyperuricemia is very necessary
.

Promote uric acid excretion

For the type with poor uric acid excretion, it is more likely to occur in the early stage of the disease, and drugs that promote uric acid excretion can be used
.
Uric acid excretion drugs promote uric acid excretion by inhibiting renal tubular reabsorption or increasing secretion of uric acid, and are mostly used when xanthine oxidase inhibitors are intolerant or contraindicated
.

Common drugs such as probenecid, sulfinpyrazone, benzbromarone,
etc.
It is suitable for patients with normal or mildly impaired renal function, uric acid <600 mg/24 h, and no kidney stones
.

Inhibit uric acid production

For the hyperuricemic type, diet and drugs that inhibit the production of uric acid can be combined with each other.
Common drugs such as febuxostat and allopurinol can interfere with purine metabolism and affect uric acid synthesis, resulting in a decrease in uric acid levels and causing hyperuricemia.
It is suitable for patients with impaired renal function, history of urinary calculi, uric acid > 1000 mg/24 h, and ineffective treatment with drugs to promote uric acid excretion
.

For patients with mixed type, the combination of drugs can be used according to the patient's own conditions
.

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.
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