-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
*It is only for medical professionals to read for reference.
Even among people with severe hyperuricemia, less than 50% of people will get gout in 15 years.
The prevalence rate of gout in my country is 1%~3%, and it is increasing year by year.
It is estimated that there are about 80 million gout patients in my country, and present different regional characteristics, such as higher prevalence in coastal areas.
However, the standardization of gout treatment is not satisfactory.
Data from my country's National Rheumatism Data Center (CRDC) shows that the 3-month blood uric acid level compliance rate of gout patients is only 29.
12%, and the 6-month compliance rate is only 38.
2%.
, The follow-up rate of 1 month after the acute attack is only about 20%.
How to deal with gout attacks? What are the precautions for long-term management? How to prevent it? Recently, "The Lancet" published a review article comprehensively summarizing the latest developments in the clinical features, pathophysiology and treatment of gout.
The Lancet-01-From "high uric acid" to "tophi", there are only 4 steps! Clinically, you must pay attention to patients who come with a "meeting ceremony" like tophi in the picture below.
Common sites for tophi are elbow joints, auricles, fingers, Achilles tendons, toes, etc.
; it can also be found in tissues and organs, including eyes, heart valves, kidneys, skin, and even feces.
The long-term existence of tophi can affect the patient's limb function, causing pain in the affected limb, limited joint mobility and joint deformity.
In severe cases, it may be combined with ulceration and infection.
Figure 1: A review of "The Lancet" in a patient with ruptured tophi pointed out that there are four pathophysiological stages in the progression of hyperuricemia and gout: the development of hyperuricemia, the deposition of urate crystals, and the deposition of crystals.
Acute inflammatory reaction caused by gout attacks, and advanced disease characterized by tophi.
Figure 2: The 4 pathophysiological stages of gout.
Clinically, gout is also divided into four different stages, but no matter which stage it is, great attention should be paid. The first stage is the period of hyperuricemia, which can be maintained for a long time, and some patients with hyperuricemia will not have any symptoms for life; the second stage is the acute attack period of gout, that is, patients with hyperuricemia have certain incentives Acute gouty arthritis appears in the lower part, which is manifested as redness, swelling, heat, and pain in the joints; the third stage is the remission period of gout, during this period the patient returns to the original asymptomatic period; if the patient does not have standardized treatment, it will enter In the chronic stage (stage 4), the patient has recurrent arthritis during this period, even involving multiple organs such as kidneys.
If you do not want to develop gout, you must first avoid gout attacks, and the continuous increase of blood uric acid level is the main risk factor for gout.
Therefore, many factors that induce hyperuricemia are also related to the increased risk of gout, such as medical conditions, obesity, life>
For gout patients, elevated blood uric acid levels are also a risk factor for future gout attacks.
In addition, joint trauma, acute illness, dehydration and other factors can also trigger an acute attack of gout.
Figure 3: The progression of hyperuricemia to gout.
However, you may ask, from the rheology data, patients with hyperuricemia are far lower than those with gout.
Why? In fact, most patients with hyperuricemia are asymptomatic and will not develop gout.
Even among people with severe hyperuricemia (≥600 µmol/L), less than 50% of people will develop gout in 15 years.
How far is hyperuricemia from the appearance of "tophi"? Generally speaking, the deposition of urate crystals in patients with hyperuricemia is considered an important node in the occurrence and development of gout.
Approximately 25% of patients with hyperuricemia have urate crystal deposits, which can be confirmed by imaging studies.
Figure 4: The activation of NLRP3 inflammasomes in macrophages and monocytes by tophi urate crystals under gout attacks and dual-energy CT is particularly related to gout attacks.
The activation of NLRP3 inflammasomes depends on two signaling systems.
The inflammatory response caused by urate crystals is only one step, which is why there may be no obvious clinical inflammation in the early stage of urate deposition. Once gout attacks, the predominant site is often accompanied by redness and swelling, which may cause the patient to have limited mobility and difficulty walking.
However, the time from the onset to the peak of the pain is usually less than 12 hours, and most patients will have repeated attacks.
Moreover, with continuous exposure to higher levels of serum urate, the burden of urate continues to increase, and each gout attack may last longer.
Over time, some people with persistent hyperuricemia will also develop tophi.
-02-Different stages, the treatment plan for gout is very different! The overall principle of non-drug treatment of gout is life>
It is particularly emphasized here that once you enter gout, diet control or exercise alone cannot effectively reduce the level of uric acid, and cannot replace the treatment of uric acid-lowering drugs.
▎So, when should uric acid lowering treatment be started? Current domestic general recommendations: Gouty arthritis attacks ≥2 times; or 1 gouty arthritis attack and any of the following at the same time: age <40 years old, blood uric acid >480 μmol/L, tophi, uric acid kidney Stone disease or renal impairment [estimated glomerular filtration rate (eGFR) <90 ml/min], high blood pressure, impaired glucose tolerance or diabetes, dyslipidemia, obesity, coronary heart disease, stroke, cardiac insufficiency, start immediately Drug treatment for lowering uric acid.
▎Medication in the acute phase: The principle of acute phase treatment is to quickly control the symptoms and pain of arthritis.
In the acute phase, bed rest should be used, and the affected limb should be raised.
It is best to start to use drugs to control acute inflammation within 24 hours of the onset.
The first-line treatment drugs are colchicine and non-steroidal anti-inflammatory drugs.
There are also applications of interleukin-1 (IL-1) receptor antagonists abroad as the treatment of acute second-line gout.
▎Medications in chronic phase: 1) Uric acid-lowering drugs: Category 1: drugs that inhibit uric acid synthesis, are xanthine oxidase inhibitors (XO1), the most classic is allopurinol, due to liver damage and hypersensitivity reactions (such as exfoliation The use of dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis, etc.
) has been reduced; the new drug febuxostat has a stronger and lasting uric acid-lowering effect, and has less liver and kidney damage, and is more suitable for chronic renal insufficiency The second category: drugs that promote uric acid excretion, such as benzbromarone, inhibit the active reabsorption of urate in the renal tubules and increase uric acid excretion; during medication, a lot of drinking water and alkalization of urine are required to avoid the formation of urinary stones; It should be used with caution in patients with ulcers or renal insufficiency, and those with 24h uric acid >3.
54mmol or urinary calculi should not be used; 2) Alkalizing urine drugs: the best morning urine pH is 6.
2-6.
9; when morning urine pH<6.
0, Especially when taking uric acid excretion drugs to alkalize urine; sodium bicarbonate is suitable for patients with chronic renal insufficiency and metabolic poisoning, and citrate preparations are suitable for those with uric acid kidney stones; 3) Uric acid oxidase: this category The drug promotes the oxidation of uric acid to allantoin, which is easier to excrete, and reduces the blood uric acid level.
For example, Rasburidase is suitable for patients with hyperuricemia caused by radiotherapy and chemotherapy.
For patients with tophus, etc.
; 4) Biological agents: such as IL-1 antagonist, anakinra, Kanazumab, Linazep, suitable for patients with refractory gout.
▎When will the uric acid drop to be relieved? Fluctuations in blood uric acid can cause an acute attack of gout.
Most gout guidelines do not recommend the use of uric acid lowering drugs at the beginning of the acute attack of gout.
They must be used as appropriate after 2 weeks of anti-inflammatory and analgesic treatment.
The goal of lowering uric acid treatment for gout patients is blood uric acid <360 μmol/L and long-term maintenance; if the patient has frequent attacks of tophi, chronic gouty arthritis or gouty arthritis, the goal of lowering uric acid treatment is blood uric acid <300 μmol/ L, until the tophi is completely dissolved and the symptoms of frequent episodes of arthritis improve, the treatment goal can be changed to blood uric acid <420 μmol/L and maintained for a long time.
However, blood uric acid is not as low as possible, and usually should not be less than 180 μmol/L.
With the continuous advancement of the guidelines for diagnosis and treatment of gout, "controlling acute inflammation + lowering uric acid" has become a well-known "knowledge of martial arts", "colchicine/non-steroidal drugs/glucocorticoids" and other three conventional acute-phase control drugs and "Allopurinol/benzbromarone/febuxostat" three uric acid-lowering drugs have become doctors' "three tricks" to effectively combat gout in different periods, but they need to be carefully combined in daily use to balance efficacy and safety.
References: [1]https://doi.
org/10.
1016/S0140-6736(21)00569-9[2] Dehlin M, Jacobsson L, Roddy E.
Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors [published online ahead of print, 2020 Jun 15].
Nat Rev Rheumatol.
2020;10.
1038/s41584-020-0441-1.
doi:10.
1038/s41584-020-0441-1.
[3] Barnett R.
Gout.
Lancet .
2018;391(10140):2595.
doi:10.
1016/S0140-6736(18)31366-7.
[4] Dalbeth N, Merriman TR, Stamp LK.
Gout.
Lancet.
2016;388(10055):2039-2052 .
doi:10.
1016/S0140-6736(16)00346-9.
[5] Liu R, Han C, Wu D, et al.
Prevalence of Hyperuricemia and Gout in China from 2000 to 2014: A Systematic Review and Meta-Analysis.
Biomed Res Int.
2015;2015:762820.
doi:10.
1155/2015/762820
Even among people with severe hyperuricemia, less than 50% of people will get gout in 15 years.
The prevalence rate of gout in my country is 1%~3%, and it is increasing year by year.
It is estimated that there are about 80 million gout patients in my country, and present different regional characteristics, such as higher prevalence in coastal areas.
However, the standardization of gout treatment is not satisfactory.
Data from my country's National Rheumatism Data Center (CRDC) shows that the 3-month blood uric acid level compliance rate of gout patients is only 29.
12%, and the 6-month compliance rate is only 38.
2%.
, The follow-up rate of 1 month after the acute attack is only about 20%.
How to deal with gout attacks? What are the precautions for long-term management? How to prevent it? Recently, "The Lancet" published a review article comprehensively summarizing the latest developments in the clinical features, pathophysiology and treatment of gout.
The Lancet-01-From "high uric acid" to "tophi", there are only 4 steps! Clinically, you must pay attention to patients who come with a "meeting ceremony" like tophi in the picture below.
Common sites for tophi are elbow joints, auricles, fingers, Achilles tendons, toes, etc.
; it can also be found in tissues and organs, including eyes, heart valves, kidneys, skin, and even feces.
The long-term existence of tophi can affect the patient's limb function, causing pain in the affected limb, limited joint mobility and joint deformity.
In severe cases, it may be combined with ulceration and infection.
Figure 1: A review of "The Lancet" in a patient with ruptured tophi pointed out that there are four pathophysiological stages in the progression of hyperuricemia and gout: the development of hyperuricemia, the deposition of urate crystals, and the deposition of crystals.
Acute inflammatory reaction caused by gout attacks, and advanced disease characterized by tophi.
Figure 2: The 4 pathophysiological stages of gout.
Clinically, gout is also divided into four different stages, but no matter which stage it is, great attention should be paid. The first stage is the period of hyperuricemia, which can be maintained for a long time, and some patients with hyperuricemia will not have any symptoms for life; the second stage is the acute attack period of gout, that is, patients with hyperuricemia have certain incentives Acute gouty arthritis appears in the lower part, which is manifested as redness, swelling, heat, and pain in the joints; the third stage is the remission period of gout, during this period the patient returns to the original asymptomatic period; if the patient does not have standardized treatment, it will enter In the chronic stage (stage 4), the patient has recurrent arthritis during this period, even involving multiple organs such as kidneys.
If you do not want to develop gout, you must first avoid gout attacks, and the continuous increase of blood uric acid level is the main risk factor for gout.
Therefore, many factors that induce hyperuricemia are also related to the increased risk of gout, such as medical conditions, obesity, life>
For gout patients, elevated blood uric acid levels are also a risk factor for future gout attacks.
In addition, joint trauma, acute illness, dehydration and other factors can also trigger an acute attack of gout.
Figure 3: The progression of hyperuricemia to gout.
However, you may ask, from the rheology data, patients with hyperuricemia are far lower than those with gout.
Why? In fact, most patients with hyperuricemia are asymptomatic and will not develop gout.
Even among people with severe hyperuricemia (≥600 µmol/L), less than 50% of people will develop gout in 15 years.
How far is hyperuricemia from the appearance of "tophi"? Generally speaking, the deposition of urate crystals in patients with hyperuricemia is considered an important node in the occurrence and development of gout.
Approximately 25% of patients with hyperuricemia have urate crystal deposits, which can be confirmed by imaging studies.
Figure 4: The activation of NLRP3 inflammasomes in macrophages and monocytes by tophi urate crystals under gout attacks and dual-energy CT is particularly related to gout attacks.
The activation of NLRP3 inflammasomes depends on two signaling systems.
The inflammatory response caused by urate crystals is only one step, which is why there may be no obvious clinical inflammation in the early stage of urate deposition. Once gout attacks, the predominant site is often accompanied by redness and swelling, which may cause the patient to have limited mobility and difficulty walking.
However, the time from the onset to the peak of the pain is usually less than 12 hours, and most patients will have repeated attacks.
Moreover, with continuous exposure to higher levels of serum urate, the burden of urate continues to increase, and each gout attack may last longer.
Over time, some people with persistent hyperuricemia will also develop tophi.
-02-Different stages, the treatment plan for gout is very different! The overall principle of non-drug treatment of gout is life>
It is particularly emphasized here that once you enter gout, diet control or exercise alone cannot effectively reduce the level of uric acid, and cannot replace the treatment of uric acid-lowering drugs.
▎So, when should uric acid lowering treatment be started? Current domestic general recommendations: Gouty arthritis attacks ≥2 times; or 1 gouty arthritis attack and any of the following at the same time: age <40 years old, blood uric acid >480 μmol/L, tophi, uric acid kidney Stone disease or renal impairment [estimated glomerular filtration rate (eGFR) <90 ml/min], high blood pressure, impaired glucose tolerance or diabetes, dyslipidemia, obesity, coronary heart disease, stroke, cardiac insufficiency, start immediately Drug treatment for lowering uric acid.
▎Medication in the acute phase: The principle of acute phase treatment is to quickly control the symptoms and pain of arthritis.
In the acute phase, bed rest should be used, and the affected limb should be raised.
It is best to start to use drugs to control acute inflammation within 24 hours of the onset.
The first-line treatment drugs are colchicine and non-steroidal anti-inflammatory drugs.
There are also applications of interleukin-1 (IL-1) receptor antagonists abroad as the treatment of acute second-line gout.
▎Medications in chronic phase: 1) Uric acid-lowering drugs: Category 1: drugs that inhibit uric acid synthesis, are xanthine oxidase inhibitors (XO1), the most classic is allopurinol, due to liver damage and hypersensitivity reactions (such as exfoliation The use of dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis, etc.
) has been reduced; the new drug febuxostat has a stronger and lasting uric acid-lowering effect, and has less liver and kidney damage, and is more suitable for chronic renal insufficiency The second category: drugs that promote uric acid excretion, such as benzbromarone, inhibit the active reabsorption of urate in the renal tubules and increase uric acid excretion; during medication, a lot of drinking water and alkalization of urine are required to avoid the formation of urinary stones; It should be used with caution in patients with ulcers or renal insufficiency, and those with 24h uric acid >3.
54mmol or urinary calculi should not be used; 2) Alkalizing urine drugs: the best morning urine pH is 6.
2-6.
9; when morning urine pH<6.
0, Especially when taking uric acid excretion drugs to alkalize urine; sodium bicarbonate is suitable for patients with chronic renal insufficiency and metabolic poisoning, and citrate preparations are suitable for those with uric acid kidney stones; 3) Uric acid oxidase: this category The drug promotes the oxidation of uric acid to allantoin, which is easier to excrete, and reduces the blood uric acid level.
For example, Rasburidase is suitable for patients with hyperuricemia caused by radiotherapy and chemotherapy.
For patients with tophus, etc.
; 4) Biological agents: such as IL-1 antagonist, anakinra, Kanazumab, Linazep, suitable for patients with refractory gout.
▎When will the uric acid drop to be relieved? Fluctuations in blood uric acid can cause an acute attack of gout.
Most gout guidelines do not recommend the use of uric acid lowering drugs at the beginning of the acute attack of gout.
They must be used as appropriate after 2 weeks of anti-inflammatory and analgesic treatment.
The goal of lowering uric acid treatment for gout patients is blood uric acid <360 μmol/L and long-term maintenance; if the patient has frequent attacks of tophi, chronic gouty arthritis or gouty arthritis, the goal of lowering uric acid treatment is blood uric acid <300 μmol/ L, until the tophi is completely dissolved and the symptoms of frequent episodes of arthritis improve, the treatment goal can be changed to blood uric acid <420 μmol/L and maintained for a long time.
However, blood uric acid is not as low as possible, and usually should not be less than 180 μmol/L.
With the continuous advancement of the guidelines for diagnosis and treatment of gout, "controlling acute inflammation + lowering uric acid" has become a well-known "knowledge of martial arts", "colchicine/non-steroidal drugs/glucocorticoids" and other three conventional acute-phase control drugs and "Allopurinol/benzbromarone/febuxostat" three uric acid-lowering drugs have become doctors' "three tricks" to effectively combat gout in different periods, but they need to be carefully combined in daily use to balance efficacy and safety.
References: [1]https://doi.
org/10.
1016/S0140-6736(21)00569-9[2] Dehlin M, Jacobsson L, Roddy E.
Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors [published online ahead of print, 2020 Jun 15].
Nat Rev Rheumatol.
2020;10.
1038/s41584-020-0441-1.
doi:10.
1038/s41584-020-0441-1.
[3] Barnett R.
Gout.
Lancet .
2018;391(10140):2595.
doi:10.
1016/S0140-6736(18)31366-7.
[4] Dalbeth N, Merriman TR, Stamp LK.
Gout.
Lancet.
2016;388(10055):2039-2052 .
doi:10.
1016/S0140-6736(16)00346-9.
[5] Liu R, Han C, Wu D, et al.
Prevalence of Hyperuricemia and Gout in China from 2000 to 2014: A Systematic Review and Meta-Analysis.
Biomed Res Int.
2015;2015:762820.
doi:10.
1155/2015/762820
