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*For medical professionals to read only for reference, dry goods are full, fast forward! ~Gout is a crystal-related arthropathy caused by monosodium uric acid deposition, which is directly related to hyperuricemia caused by purine metabolism disorder and/or decreased uric acid excretion.
As the standard of living is getting higher and higher, more and more people are suffering from this "richness disease", and they are getting younger and younger! 20% of purines come from outside the body, which is specifically caused by eating and drinking.
Diet can reduce uric acid by 10%-18%.
It sounds like diet has a little effect, and diet alone has limited uric acid reduction.
And 80% is produced endogenously, this part of purine still needs drugs to reduce.
At present, allopurinol and benzbromarone are widely used clinically for lowering uric acid, but how to choose? The following author summarized it for everyone, hoping to help everyone have a better understanding of the choice of uric acid lowering drugs.
1.
Inhibit the production of VS and promote excretion.
The mechanism of action is very different.
1.
Allopurinol: inhibits the production of uric acid.
Both allopurinol and its metabolite oxypurine can inhibit xanthine, and prevent hypoxanthine and xanthine by inhibiting xanthine oxidase.
Metabolized to uric acid, thereby reducing the production of uric acid.
Reduce the uric acid content in blood and urine to below the solubility level, prevent the formation of uric acid crystals and deposit in joints and other tissues, and also help the re-dissolution of uric acid crystals in the tissues of gout patients.
2.
Benzbromarone: promotes uric acid excretion, acts on the proximal convoluted tubules S1 and S3 of the kidney, strongly inhibits the activity of uric acid-anion transporter 1 (URAT-1), inhibits the reabsorption of uric acid in the renal tubules, and promotes uric acid It is excreted from urine to reduce high uric acid [1].
2 Treatment indications Allopurinol: It can be used to treat primary and secondary hyperuricemia, hyperuricemia secondary to malignant tumors, hyperuricemia after organ transplantation, and calcium oxalate stone disease.
Benzbromarone: suitable for primary and secondary hyperuricemia, gout caused by various reasons, and non-acute episodes of gouty arthritis.
3 Beware of Adverse Reactions Of course, "it is a three-point drug" I believe everyone is very clear.
There is no guarantee that any medicine will have no side effects, and the same is true for allopurinol and benzbromarone.
Adverse reactions of allopurinol: 1.
Skin rash: It can be pruritic papules or urticaria.
If the rash is widespread and long-lasting, and symptomatic treatment is ineffective, and the drug must be discontinued when it tends to aggravate; 2.
Gastrointestinal reactions: including diarrhea, nausea, vomiting and abdominal pain, etc.
; 3.
Leukopenia, or thrombocytopenia, or anemia, Or bone marrow suppression, both should be considered for discontinuation; 4.
Other hair loss, fever, lymphadenopathy, hepatotoxicity, interstitial nephritis and allergic vasculitis, etc.
; 5.
Several foreign patients have been reported to have occurred during the period of taking this product.
Sudden death of unknown cause.
Benzbromarone adverse reactions: 1.
Gastrointestinal damage: vomiting, abdominal pain, gastrointestinal bleeding, etc.
; 2.
Liver and gallbladder damage: abnormal liver biochemical indicators, liver cell damage, etc.
; 3.
Systemic damage: fatigue, edema, chest pain, Fever, etc.
; 4.
Nervous system damage: dizziness, headache, etc.
; 5.
Urinary system damage: hematuria, oliguria, frequent urination, abnormal renal function, acute renal failure, etc.
; 6.
Immune dysfunction: allergic reactions, allergic-like reactions, etc.
; 7.
Others: conjunctivitis, thrombocytopenia, leukopenia, palpitations, impotence, etc.
In 2003, benzbromarone withdrew from the European market due to hepatotoxicity.
Studies believe that most cases of liver damage (75%) occur within 1 month, while fatal liver failure occurs in the 11th week to 5 months after the medication, which may mean that the longer the medication, the more severe the liver damage and the better the prognosis.
Poor [2,3].
Some time ago, the Food and Drug Administration revised the instructions for benzbromarone, which in general emphasized the monitoring of liver and kidney function during the use of benzbromarone to prevent liver and kidney toxicity.
After understanding the mechanism, indications and adverse reactions of allopurinol and benzbromarone, let’s talk about which drug is the first choice for uric acid-lowering treatment? 4 Allopurinol is the first choice for lowering uric acid! The 2020 American College of Rheumatology (ACR) guidelines mention allopurinol as a first-line drug.
Patients with chronic kidney disease stage 3 and above should choose xanthine oxidase inhibitors-allopurinol or febuxostat instead of uric acid Excretion of drugs.
No matter what type of blood uric acid is high, allopurinol can achieve the goal of lowering blood uric acid satisfactorily.
Before using uric acid excretion drugs, the patient’s renal uric acid excretion function must be clarified.
For those with higher uric acid excretion, only drugs that inhibit uric acid production can be used.
Allopurinol lowering uric acid treatment can protect the kidneys [4].
In 2017, the latest Chinese kidney disease hyperuricemia guidelines believe that the use of allopurinol can have a protective effect if the therapeutic dose is strictly controlled.
Allopurinol can reduce blood uric acid levels, thereby reducing the further damage of uric acid to the kidneys.
With the long-term use of allopurinol, its protective effect on the kidneys has gradually been paid attention, especially for patients with chronic kidney disease (CKD).
However, due to the decreased excretion of allopurinol in patients with CKD, some researchers believe that it is easier to take the drug Cause serious adverse reactions.
Allopurinol has a good cardioprotective effect.
Animal models of heart failure showed that long-term allopurinol treatment improved left ventricular function and prevented left ventricular remodeling.
In addition, allopurinol treatment can improve endothelial function and local blood flow in patients with heart failure with hyperuricemia.
Allopurinol has fewer side reactions.
Practices in Europe and the United States have confirmed that the risk of serious side effects caused by allopurinol is 1/56,000, which is lower than the 1/17,000 risk of benzbromarone.
Although Chinese Han, Thai and Korean patients have a higher fatal risk of allopurinol, they can be screened for the HLA-B*5801 allele to avoid this risk.
After the gene is screened out, the fatal risk of allopurinol will hardly occur.
5Why not recommend benzbromarone? Allopurinol is the first choice for uric acid-lowering therapy, and it is recommended that Asians undergo HLA-B*5801 genetic testing before using allopurinol; patients who fail allopurinol therapy should prefer febuxostat instead of uric acid excretion drugs.
It is considered related to the following reasons: the 24-hour uric acid excretion should be measured before the use of benzbromarone.
If the patient’s 24-hour uric acid excretion is >3.
54 mmol, such drugs should be banned [5].
Because of excessive uric acid excretion, benzbromarone may form uric acid crystals, which can promote the occurrence or development of obstructive nephropathy and eventually lead to end-stage renal disease.
Therefore, it is very important to determine the patient's uric acid excretion before using benzbromarone.
Those with a large amount of uric acid excretion are not suitable for uric acid excretion drugs.
Although benzbromarone is effective for patients with mild to moderate renal insufficiency, there is a serious risk of liver toxicity.
This is the reason why benzbromarone has not been listed in the United States and many other countries.
Uric acid excretion drugs can increase the risk of stones and uric acid nephropathy.
Therefore, uric acid excretion treatment is not suitable for patients with kidney stones and uric acid nephropathy.
In summary, allopurinol has a better effect on lowering uric acid and has fewer side effects, but patients still need to be closely monitored during treatment.
References: [1] Yang Huijun, Li Zhaofu, Wan Chunping, et al.
Research progress of urate transporter in primary gout and hyperuricemia［J］.
Chinese Journal of Traditional Chinese Medicine, 2013, 31(9) ：1891-1894[2] Liu Yangcong, Li Yan, Zhang Geng.
Analysis of 18 cases of benzbromarone adverse reactions/events[J].
Chinese Journal of Hospital Pharmacy, 2016, 36 (6 ): 507-510.
DOI: 10.
13286 / j.
cnki.
chinhosppharmacyj.
2016.
06.
20.
[3]Suzuki T,Suzuki T,Kimura M,et al.
A case of fulminant hepatitis, possibly caused by benzbromarone[ J].
Nihon Shokakibyo GakkaiZasshi,2001,98 (4):421-425.
[4]LYONS AB,HASBOLD J,HODGKIN P D.
Flow cytometric analysis of cell division history using dilution of carboxyfluorescein diacetate succinimidyl ester,a stably integrated fluorescent probe［J］.
Methods Cell Biol, 2001 ,63:375-398.
[5] Chinese Medical Association Endocrinology Branch.
Chinese expert consensus on the treatment of hyperuricemia and gout[ J].
Chinese Journal of Endocrinology and Metabolism, 2013, 29 (11 ): 913-920.
As the standard of living is getting higher and higher, more and more people are suffering from this "richness disease", and they are getting younger and younger! 20% of purines come from outside the body, which is specifically caused by eating and drinking.
Diet can reduce uric acid by 10%-18%.
It sounds like diet has a little effect, and diet alone has limited uric acid reduction.
And 80% is produced endogenously, this part of purine still needs drugs to reduce.
At present, allopurinol and benzbromarone are widely used clinically for lowering uric acid, but how to choose? The following author summarized it for everyone, hoping to help everyone have a better understanding of the choice of uric acid lowering drugs.
1.
Inhibit the production of VS and promote excretion.
The mechanism of action is very different.
1.
Allopurinol: inhibits the production of uric acid.
Both allopurinol and its metabolite oxypurine can inhibit xanthine, and prevent hypoxanthine and xanthine by inhibiting xanthine oxidase.
Metabolized to uric acid, thereby reducing the production of uric acid.
Reduce the uric acid content in blood and urine to below the solubility level, prevent the formation of uric acid crystals and deposit in joints and other tissues, and also help the re-dissolution of uric acid crystals in the tissues of gout patients.
2.
Benzbromarone: promotes uric acid excretion, acts on the proximal convoluted tubules S1 and S3 of the kidney, strongly inhibits the activity of uric acid-anion transporter 1 (URAT-1), inhibits the reabsorption of uric acid in the renal tubules, and promotes uric acid It is excreted from urine to reduce high uric acid [1].
2 Treatment indications Allopurinol: It can be used to treat primary and secondary hyperuricemia, hyperuricemia secondary to malignant tumors, hyperuricemia after organ transplantation, and calcium oxalate stone disease.
Benzbromarone: suitable for primary and secondary hyperuricemia, gout caused by various reasons, and non-acute episodes of gouty arthritis.
3 Beware of Adverse Reactions Of course, "it is a three-point drug" I believe everyone is very clear.
There is no guarantee that any medicine will have no side effects, and the same is true for allopurinol and benzbromarone.
Adverse reactions of allopurinol: 1.
Skin rash: It can be pruritic papules or urticaria.
If the rash is widespread and long-lasting, and symptomatic treatment is ineffective, and the drug must be discontinued when it tends to aggravate; 2.
Gastrointestinal reactions: including diarrhea, nausea, vomiting and abdominal pain, etc.
; 3.
Leukopenia, or thrombocytopenia, or anemia, Or bone marrow suppression, both should be considered for discontinuation; 4.
Other hair loss, fever, lymphadenopathy, hepatotoxicity, interstitial nephritis and allergic vasculitis, etc.
; 5.
Several foreign patients have been reported to have occurred during the period of taking this product.
Sudden death of unknown cause.
Benzbromarone adverse reactions: 1.
Gastrointestinal damage: vomiting, abdominal pain, gastrointestinal bleeding, etc.
; 2.
Liver and gallbladder damage: abnormal liver biochemical indicators, liver cell damage, etc.
; 3.
Systemic damage: fatigue, edema, chest pain, Fever, etc.
; 4.
Nervous system damage: dizziness, headache, etc.
; 5.
Urinary system damage: hematuria, oliguria, frequent urination, abnormal renal function, acute renal failure, etc.
; 6.
Immune dysfunction: allergic reactions, allergic-like reactions, etc.
; 7.
Others: conjunctivitis, thrombocytopenia, leukopenia, palpitations, impotence, etc.
In 2003, benzbromarone withdrew from the European market due to hepatotoxicity.
Studies believe that most cases of liver damage (75%) occur within 1 month, while fatal liver failure occurs in the 11th week to 5 months after the medication, which may mean that the longer the medication, the more severe the liver damage and the better the prognosis.
Poor [2,3].
Some time ago, the Food and Drug Administration revised the instructions for benzbromarone, which in general emphasized the monitoring of liver and kidney function during the use of benzbromarone to prevent liver and kidney toxicity.
After understanding the mechanism, indications and adverse reactions of allopurinol and benzbromarone, let’s talk about which drug is the first choice for uric acid-lowering treatment? 4 Allopurinol is the first choice for lowering uric acid! The 2020 American College of Rheumatology (ACR) guidelines mention allopurinol as a first-line drug.
Patients with chronic kidney disease stage 3 and above should choose xanthine oxidase inhibitors-allopurinol or febuxostat instead of uric acid Excretion of drugs.
No matter what type of blood uric acid is high, allopurinol can achieve the goal of lowering blood uric acid satisfactorily.
Before using uric acid excretion drugs, the patient’s renal uric acid excretion function must be clarified.
For those with higher uric acid excretion, only drugs that inhibit uric acid production can be used.
Allopurinol lowering uric acid treatment can protect the kidneys [4].
In 2017, the latest Chinese kidney disease hyperuricemia guidelines believe that the use of allopurinol can have a protective effect if the therapeutic dose is strictly controlled.
Allopurinol can reduce blood uric acid levels, thereby reducing the further damage of uric acid to the kidneys.
With the long-term use of allopurinol, its protective effect on the kidneys has gradually been paid attention, especially for patients with chronic kidney disease (CKD).
However, due to the decreased excretion of allopurinol in patients with CKD, some researchers believe that it is easier to take the drug Cause serious adverse reactions.
Allopurinol has a good cardioprotective effect.
Animal models of heart failure showed that long-term allopurinol treatment improved left ventricular function and prevented left ventricular remodeling.
In addition, allopurinol treatment can improve endothelial function and local blood flow in patients with heart failure with hyperuricemia.
Allopurinol has fewer side reactions.
Practices in Europe and the United States have confirmed that the risk of serious side effects caused by allopurinol is 1/56,000, which is lower than the 1/17,000 risk of benzbromarone.
Although Chinese Han, Thai and Korean patients have a higher fatal risk of allopurinol, they can be screened for the HLA-B*5801 allele to avoid this risk.
After the gene is screened out, the fatal risk of allopurinol will hardly occur.
5Why not recommend benzbromarone? Allopurinol is the first choice for uric acid-lowering therapy, and it is recommended that Asians undergo HLA-B*5801 genetic testing before using allopurinol; patients who fail allopurinol therapy should prefer febuxostat instead of uric acid excretion drugs.
It is considered related to the following reasons: the 24-hour uric acid excretion should be measured before the use of benzbromarone.
If the patient’s 24-hour uric acid excretion is >3.
54 mmol, such drugs should be banned [5].
Because of excessive uric acid excretion, benzbromarone may form uric acid crystals, which can promote the occurrence or development of obstructive nephropathy and eventually lead to end-stage renal disease.
Therefore, it is very important to determine the patient's uric acid excretion before using benzbromarone.
Those with a large amount of uric acid excretion are not suitable for uric acid excretion drugs.
Although benzbromarone is effective for patients with mild to moderate renal insufficiency, there is a serious risk of liver toxicity.
This is the reason why benzbromarone has not been listed in the United States and many other countries.
Uric acid excretion drugs can increase the risk of stones and uric acid nephropathy.
Therefore, uric acid excretion treatment is not suitable for patients with kidney stones and uric acid nephropathy.
In summary, allopurinol has a better effect on lowering uric acid and has fewer side effects, but patients still need to be closely monitored during treatment.
References: [1] Yang Huijun, Li Zhaofu, Wan Chunping, et al.
Research progress of urate transporter in primary gout and hyperuricemia［J］.
Chinese Journal of Traditional Chinese Medicine, 2013, 31(9) ：1891-1894[2] Liu Yangcong, Li Yan, Zhang Geng.
Analysis of 18 cases of benzbromarone adverse reactions/events[J].
Chinese Journal of Hospital Pharmacy, 2016, 36 (6 ): 507-510.
DOI: 10.
13286 / j.
cnki.
chinhosppharmacyj.
2016.
06.
20.
[3]Suzuki T,Suzuki T,Kimura M,et al.
A case of fulminant hepatitis, possibly caused by benzbromarone[ J].
Nihon Shokakibyo GakkaiZasshi,2001,98 (4):421-425.
[4]LYONS AB,HASBOLD J,HODGKIN P D.
Flow cytometric analysis of cell division history using dilution of carboxyfluorescein diacetate succinimidyl ester,a stably integrated fluorescent probe［J］.
Methods Cell Biol, 2001 ,63:375-398.
[5] Chinese Medical Association Endocrinology Branch.
Chinese expert consensus on the treatment of hyperuricemia and gout[ J].
Chinese Journal of Endocrinology and Metabolism, 2013, 29 (11 ): 913-920.
