Milurit® (Allopurinol) 100 mg, 50 tablets
One tablet contains
- active ingredient – allopurinol 100 mg, 300 mg
- Excipients: lactose monohydrate, potato starch, povidone K-25, talc, magnesium stearate, sodium carboxymethyl starch (type A) ( for a dosage of 100 mg) microcrystalline cellulose, sodium carboxymethyl starch (type A), gelatin, anhydrous colloidal silicon dioxide, magnesium stearate ( for a dosage of 300 mg)
Allopurinol is active when administered orally. It is rapidly absorbed from the upper gastrointestinal tract. Allopurinol is determined in the blood plasma 30-60 minutes after ingestion. The bioavailability of allopurinol varies from 67% to 90%. The maximum concentration of allopurinol and its metabolite, oxypurinol, is reached in the blood plasma, respectively, 1.5 and 3-5 hours after administration. Then the concentration of allopurinol rapidly decreases. 6 hours after ingestion, only a trace concentration of the drug is determined in the blood plasma. Plasma levels of oxypurinol decrease much more slowly.
Allopurinol hardly binds to plasma proteins, so changes in the level of protein binding should not significantly affect the clearance of the drug. The apparent volume of distribution of allopurinol is about 1.6 l / kg, which indicates a fairly pronounced absorption of the drug by tissues. The content of allopurinol in various tissues of the body has not been studied, however, it is very likely that allopurinol and oxypurinol accumulate in the maximum concentration in the liver and intestinal mucosa, where high xanthine oxidase activity is recorded.
The main metabolite of allopurinol is oxypurinol. Other metabolites of allopurinol include allopurinol-riboside and oxypurinol-7-riboside.
About 20% of the dose taken is excreted through the intestine unchanged within 48-72 hours. Under the action of xanthine oxidase and aldehyde oxidase, allopurinol is metabolized to form oxypurinol, which is the main route of elimination of allopurinol. About 10% of the daily dose is excreted by the glomerular apparatus of the kidneys in the form of unchanged allopurinol. The half-life of allopurinol in plasma is 0.5 – 1.5 hours.
Oxypurinol is not as potent a xanthine oxidase inhibitor as allopurinol, but its half-life is significantly longer, ranging from 13 to 30 hours. Due to these properties, after taking a single daily dose of allopurinol, effective suppression of xanthine oxidase activity is maintained for 24 hours. In patients with normal renal function, the content of oxypurinol in the blood plasma slowly increases until an equilibrium concentration is reached. After taking allopurinol at a dose of 300 mg per day, the concentration of allopurinol in blood plasma is usually 5-10 mg / l. Oxypurinol is excreted unchanged by the kidneys, but due to tubular reabsorption, it has a long half-life. The half-life of allopurinol is 1-2 hours, while the half-life of oxypurinol varies from 13, 6 to 29 hours. These significant differences are likely due to differences in study design and/or creatinine clearance in patients.
Special patient groups
Patients with impaired renal function
In patients with impaired renal function, the excretion of allopurinol and oxypurinol can be significantly slowed down, which, with prolonged therapy, leads to an increase in the concentration of these compounds in the blood plasma. In patients with impaired renal function and creatinine clearance of 10-20 ml/min, after long-term therapy with allopurinol at a dose of 300 mg per day, the plasma concentration of oxypurinol was approximately 30 mg/l. This concentration of oxypurinol can be determined in patients with normal renal function during therapy with allopurinol at a dose of 600 mg per day. Therefore, when treating patients with impaired renal function, the dose of Milurit should be reduced.
In elderly patients, significant changes in the pharmacokinetic properties of allopurinol are unlikely. The exception is patients with concomitant kidney pathology.
Allopurinol is a structural analogue of hypoxanthine. Allopurinol, as well as its main active metabolite, oxypurinol, inhibit xanthine oxidase, an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid. Allopurinol reduces the concentration of uric acid, both in the blood serum and in the urine. Thus, it prevents the deposition of uric acid crystals in the tissues and (or) promotes their dissolution. In addition to inhibition of purine catabolism in some (but not all) patients with hyperuricemia, a large amount of xanthine and hypoxanthine becomes available for the re-formation of purine bases, which leads to inhibition of de novo purine biosynthesis by a feedback mechanism mediated by inhibition of the enzyme hypoxanthine-guanine phosphoribosyl- transferase.
Indications for use
– all types of hyperuricemia that cannot be controlled by diet, including secondary hyperuricemia of various origins, and clinical complications of hyperuricemia, in particular, severe gout, uric nephropathy, as well as the dissolution and prevention of the formation of uric acid crystals (kidney stones)
– treatment of recurrent, mixed calcium oxalate crystals accompanied by hyperuricemia, if fluid intake, diet and similar measures fail
Children and teenagers:
– secondary hyperuricemia of various origins
– uric acid-induced nephropathy in the treatment of leukemia
– congenital enzyme deficiency, Lesch-Nyhan syndrome (complete or partial hypoxanthine-guanine phosphoribosyltransferase deficiency) and adenine phosphoribosyl transferase deficiency.
Dosage and administration
The drug is used strictly according to the doctor’s prescription!
Tablets for oral administration. Milurit should be taken after meals with plenty of water. Allopurinol is generally well tolerated, especially when taken after meals. At daily doses exceeding 300 mg, patients may experience complaints from the gastrointestinal tract, so such doses must be divided into several doses.
To reduce the risk of side effects, treatment should begin with an initial dose of 100 mg once daily.
If necessary, if the level of uric acid in the blood serum does not decrease enough, the initial dose is gradually increased.
When selecting a dose of the drug, it is recommended to use the following dosing regimens:
– 100-200 mg per day for mild disease
– 300-600 mg per day for moderate
– 700-900 mg per day in severe cases.
If when calculating the dose it is necessary to proceed from the patient’s body weight, then the dose of Milurit should be from 2 to 10 mg / kg / day.
Children and adolescents under 15 years of age
The recommended dose is 10-20 mg/kg/day. For low doses, 100 mg tablets are used, which can be divided into two equal doses of 50 mg with the help of risks. The maximum daily dose is 400 mg divided into three doses.
Allopurinol is rarely used in pediatric therapy for malignant oncological diseases (especially leukemia) and certain enzymatic disorders (for example, Lesch-Nyhan syndrome).
In the absence of specific data, the minimum effective dose should be used to provide a sufficient reduction in the concentration of uric acid in the blood serum. Particular attention should be paid to recommendations on the selection of the dose of the drug for patients with impaired renal function and some other conditions.
Since allopurinol and its metabolites are excreted from the body by the kidneys, impaired renal function can lead to retention of the active substance and its metabolites in the body, with a subsequent prolongation of the plasma half-life of these compounds.
The following scheme can serve as a guideline for dose adjustment in case of renal insufficiency:
Creatinine clearance Daily dose
>20 ml/min Normal dose
10-20 ml/min 100-200 mg/day
<10 ml/min 100 mg/day or longer dosing intervals
In severe renal insufficiency, Milurit is recommended to be used at a dose not exceeding 100 mg per day, or to use single doses of 100 mg with an interval of more than one day.
If it is possible to control the concentration of oxypurinol in the blood plasma, then the dose of Milurit should be adjusted so that the level of oxypurinol in the blood plasma is below 100 µmol/l (15.2 mg/l).
Allopurinol and its metabolites are removed from the body during hemodialysis. If hemodialysis sessions are carried out 2-3 times a week, then it is advisable to determine the need to switch to an alternative therapy regimen – taking 300-400 mg of allopurinol immediately after the end of the hemodialysis session (the drug is not taken between hemodialysis sessions).
In patients with impaired renal function, the simultaneous use of the drug Milurit with thiazide diuretics requires special care. In this case, allopurinol should be used at the lowest effective dose with careful monitoring of renal function.
In case of impaired liver function, the dose of the drug must be reduced. At an early stage of therapy, it is recommended to monitor laboratory parameters of liver function.
Conditions accompanied by an increase in the metabolism of uric acid salts (for example, tumor diseases, Lesch-Nyhan syndrome)
Correction of existing hyperuricemia and/or hyperuricosuria with allopurinol is recommended prior to initiating cytotoxic drug therapy. Of great importance is adequate hydration, which contributes to maintaining optimal diuresis, as well as alkalization of urine, due to which the solubility of uric acid and its salts increases. The dose of allopurinol should be close to the lower end of the recommended dose range.
If impaired renal function is due to the development of acute uric acid nephropathy or other renal pathology, then treatment should be continued in accordance with the recommendations presented in the section “Impaired renal function”.
The described measures can reduce the risk of xanthine and/or uric acid accumulation complicating the course of the disease.
To establish the optimal dose of the drug, it is necessary to periodically evaluate the concentration of uric acid salts in the blood serum, as well as the level of uric acid and urate in the urine.
Dosing recommendations for skin reactions
In the event of skin reactions, the use of allopurinol should be discontinued immediately. Upon return to normal after mild reactions, allopurinol may be restarted at a low dose (such as 50 mg/day) after careful consideration of the risks. Thereafter, the dose can be gradually increased while monitoring for skin reactions and other possible adverse events. If the rash recurs, allopurinol should be permanently discontinued, given the possibility of more severe hypersensitivity reactions.
There are no current clinical data to determine the incidence of side effects. Their frequency may vary depending on the dose and whether the drug was prescribed as monotherapy or in combination with other drugs. The following frequency categories assigned to adverse drug reactions are estimates: for most reactions, suitable data are not available to calculate the frequency. Adverse drug reactions identified during post-registration surveillance are considered rare or very rare.
Allopurinol-related adverse reactions in the general population of treated patients have been rare or very rare, and are mostly minor. A higher frequency is observed in the presence of impaired renal and / or liver function.
Common (>1/100 to <1/10)
– increased levels of thyroid-stimulating hormone (TSH)9
Uncommon (>1/1000 to <1/100)
– hypersensitivity reactions2
– change in liver function test results5
– vomiting4, nausea4, diarrhea
Rare (>1/10000 to <1/1000)
– hepatitis (including necrotic and granulomatous forms)5
– severe skin reactions (Stevens-Johnson syndrome (SSD) and toxic epidermal necrolysis (TEN))6, urolithiasis
Very rare (<1/10000)
– agranulocytosis1, aplastic anemia1, thrombocytopenia1, granulocytosis, leukopenia, leukocytosis, eosinophilia and true erythrocyte aplasia
– angioimmunoblastic T-cell lymphoma3
– diabetes mellitus, hyperlipidemia
– coma, paralysis, ataxia, peripheral neuropathy, paresthesia, drowsiness, headache, taste perversion
– cataracts, visual disturbances, macular changes
– dizziness (vertigo)
– angina pectoris, bradycardia
– arterial hypertension
– hematemesis, stomatitis, steatorrhea, changes in bowel frequency
– angioedema7, local drug rash, alopecia, hair color change
– hematuria, azotemia
– male infertility, erectile dysfunction, gynecomastia
– edema, general malaise, general weakness, fever8
Frequency unknown (cannot be determined from the available data).
– abdominal pain
1 Thrombocytopenia, agranulocytosis and aplastic anemia have been reported very rarely, especially in individuals with impaired renal and/or hepatic function, highlighting the need for special care in these patient groups.
2Severe hypersensitivity reactions, including skin reactions with epidermal detachment, fever, lymphadenopathy, arthralgia and/or eosinophilia (including Stevens-Johnson syndrome and toxic epidermal necrolysis). Associated vasculitis or tissue reactions may have a variety of manifestations, including hepatitis, renal involvement, acute cholangitis, xanthine calculi, and, in very rare cases, seizures. The development of anaphylactic shock was very rarely observed. With the development of severe adverse reactions, allopurinol should be stopped immediately and not resumed.
Delayed multiorgan hypersensitivity (known as drug hypersensitivity syndrome /DRESS/) may develop the following symptoms in various combinations: fever, skin rash, vasculitis, lymphadenopathy, pseudolymphoma, arthralgia, leukopenia, eosinophilia, hepato-splenomegaly, abnormal liver function tests, syndrome disappearing bile ducts (destruction or disappearance of the intrahepatic bile ducts). Other organs (eg, liver, lungs, kidneys, pancreas, myocardium, and colon) may also be affected. With the development of such reactions at any time during treatment, allopurinol should be immediately discontinued and never resumed. Milurit should not be re-administered to patients with hypersensitivity syndrome and SJS/TEN.
Generalized hypersensitivity reactions have developed in patients with impaired renal and (or) liver function, especially in cases with a fatal outcome.
3Angioimmunoblastic T-cell lymphoma has very rarely been diagnosed following lymph node biopsy for generalized lymphadenopathy. Angioimmunoblastic lymphadenopathy is reversible and regresses after discontinuation of allopurinol therapy.
4 Nausea and vomiting have been observed in previous clinical studies, but more recent observations have confirmed that these reactions are not clinically significant and can be avoided by administering Milurit after meals.
5 Liver dysfunction may develop without overt signs of generalized hypersensitivity
6 Skin reactions are the most common in patients taking allopurinol. Against the background of drug therapy, these reactions can develop at any time. Skin reactions can be manifested by itching, maculopapular and scaly rashes. In other cases, purpura may develop. Rarely, exfoliative skin lesions (SSD/TEN) have been observed. With the development of such reactions, allopurinol therapy should be stopped immediately. If the skin reaction is mild, then after the disappearance of these changes, you can resume taking allopurinol at a lower dose (for example, 50 mg per day). Subsequently, the dose can be gradually increased.
The HLA-B*5801 allele has been shown to be associated with the risk of allopurinol-dependent hypersensitivity syndrome and SJS/TEN. If a skin reaction occurs repeatedly, the use of allopurinol should be immediately and permanently discontinued, taking into account the possibility of developing more severe hypersensitivity (see subsection “Disorders from the immune system”). If SJS/TEN or other serious hypersensitivity reactions cannot be ruled out, DO NOT restart allopurinol due to the possibility of a severe or even fatal reaction. The basis for the decision is the presence of a clinical diagnosis of SJS/TEN. If such reactions develop at any time during treatment, the use of allopurinol must be immediately and permanently discontinued.
7 Angioedema has been described with or without signs and symptoms of a more generalized hypersensitivity reaction.
8 Fever has been described with or without signs and symptoms of a more generalized hypersensitivity reaction (see Immune System Disorders).
9 The increase in TSH levels observed in the relevant studies did not affect the T4 level and did not indicate the onset of subclinical hypothyroidism.
Reports of suspected adverse reactions
The provision of data on suspected adverse drug reactions is very important to enable continuous monitoring of the risk/benefit ratio of the medicinal product. Health care professionals should be provided with information about any suspected adverse reactions through the contacts listed at the end of the instructions, as well as through the national information collection system.
– hypersensitivity to the active substances or any of the components
– galactose intolerance, lactase deficiency, glucose-galactose malabsorption syndrome – only for 100 mg tablets
– pregnancy and lactation
6-mercaptopurine and azathioprine
Azathioprine is metabolized to 6-mercaptopurine, which is inactivated by xanthine oxidase. In cases where therapy with 6-mercaptopurine or azathioprine is combined with Milurit, patients should be given only one quarter of the usual dose of 6-mercaptopurine or azathioprine, since inhibition of xanthine oxidase activity increases the duration of action of these compounds.
Vidarabine (adenine arabinoside)
With simultaneous use with the drug Milurit, the half-life of vidarabine increases. With the simultaneous use of these drugs, special caution must be observed regarding the enhanced toxic effects of therapy.
Salicylates and uricosuric agents
The main active metabolite of allopurinol is oxypurinol, which is excreted by the kidneys similarly to uric acid salts. Therefore, drugs with uricosuric activity, such as probenecid or high doses of salicylates, may increase the excretion of oxypurinol. In turn, increased excretion of oxypurinol is accompanied by a decrease in the therapeutic activity of allopurinol, however, the significance of this type of interaction must be assessed individually in each case.
With the simultaneous use of the drug Milurit and chlorpropamide, in patients with impaired renal function, the risk of developing prolonged hypoglycemia increases, since allopurinol and chlorpropamide compete with each other at the stage of tubular excretion.
Coumarin derivatives anticoagulants
With simultaneous use with allopurinol, an increase in the effects of warfarin and other anticoagulants of coumarin derivatives was observed. In this regard, it is necessary to carefully monitor the condition of patients receiving concomitant therapy with these drugs.
Allopurinol is able to inhibit the oxidation of phenytoin in the liver, but the clinical significance of this interaction has not been established.
Allopurinol is known to inhibit the metabolism of theophylline. Such an interaction can be explained by the participation of xanthine oxidase in the process of theophylline biotransformation in the human body. Serum levels of theophylline should be monitored at the start of concomitant therapy with allopurinol, as well as when the dose of the latter is increased.
Ampicillin and amoxicillin
Patients receiving ampicillin or amoxicillin and allopurinol concomitantly experienced an increased incidence of skin reactions compared with patients who did not receive such concomitant therapy. The reason for this type of drug interaction has not yet been established. However, in patients receiving allopurinol, it is recommended to prescribe other antibacterial drugs instead of ampicillin and amoxicillin.
With the simultaneous use of allopurinol with cytostatic drugs (such as cyclophosphamide, doxorubicin, bleomycin, procarbazine, alkyl halides), blood dyscrasias develop more often than when these drugs are used separately.
You should regularly count the number of blood cells.
According to some reports, the concentration of cyclosporine in plasma may increase during concomitant therapy with allopurinol. With the simultaneous use of these drugs, it is necessary to take into account the possibility of increasing the toxicity of cyclosporine.
With the simultaneous use of allopurinol with aluminum hydroxide, the effect of allopurinol may be reduced. Between taking both drugs, you must take a break of at least 3 hours.
In healthy volunteers and HIV-infected patients receiving didanosine, against the background of concomitant therapy with allopurinol (300 mg per day), an increase in Cmax (maximum plasma concentration of the drug) and AUC (area under the concentration-time curve) of didanosine was observed by approximately 2 times. The half-life of didanosine did not change. As a rule, the simultaneous use of these drugs is not recommended. If concomitant therapy is unavoidable, dose reduction of didanosine and careful monitoring of the patient may be required.
The concomitant use of ACE inhibitors with allopurinol is associated with an increased risk of leukopenia, so these drugs should be combined with caution.
An increased risk of hypersensitivity has been described with the concomitant use of allopurinol with ACE inhibitors, especially in cases of impaired renal function.
The simultaneous use of allopurinol with captopril may increase the risk of skin reactions, especially in chronic renal failure.
An interaction has been reported between allopurinol and furosemide leading to an increase in serum urate and plasma oxypurinol.
There are reports of an increased risk of developing hypersensitivity reactions with the simultaneous use of allopurinol with diuretics, especially thiazides and in patients with impaired renal function.
Hypersensitivity Syndrome, Stevens-Johnson Syndrome (SSD), and Toxic Epidermal Necrolysis (TEN)
The manifestation of hypersensitivity reactions to allopurinol can be very diverse, including maculopapular exanthema, drug hypersensitivity syndrome (DRESS) and SJS/TEN. These reactions are a clinical diagnosis and their clinical manifestations serve as the basis for making appropriate decisions. Therapy with Milurit should be discontinued immediately if a skin rash or other manifestations of a hypersensitivity reaction occur. Therapy should not be restarted in patients with hypersensitivity syndrome and SJS/TEN. Corticosteroids may be used to treat hypersensitivity skin reactions.
Chronic kidney dysfunction
Patients with chronic renal impairment concomitantly taking diuretics, especially thiazides, have a greater risk of developing hypersensitivity reactions associated with allopurinol, including SJS / TEN.
The development of hypersensitivity syndrome or SJS/TEN should be monitored very carefully. Patients should be informed that at the first appearance of such symptoms, treatment should be immediately and permanently discontinued.
The presence of the HLA-B*5801 allele has been found to be a risk factor for allopurinol-induced SJS/TEN (and possibly other hypersensitivity reactions), as indicated by the results of a retrospective case-control pharmacogenetic study in Han Chinese, Taiwanese, Korean populations. , Japanese and Europeans. The frequency of the presence of the HLA-B*5801 allele can be as high as 20% in the Han Chinese population, 8-15% in the Thai population, about 12% in the Korean population, and 1-2% in the Japanese and Europeans.
Consideration should be given to screening for the HLA-B*5801 allele prior to initiation of allopurinol treatment in subgroups of patients with a known high prevalence of the HLA-B*5801 allele. Chronic kidney disease may further increase this risk in these patients. If genotyping is not possible in Han Chinese, Thai, or Korean patients, then allopurinol should only be given if the benefit outweighs the possible increased risk. The use of genotyping for allopurinol therapy decisions has not been studied in other patient populations.
If a patient is known to be a carrier of the HLA-B*5801 allele (especially in Han Chinese, Thais, Koreans), allopurinol therapy should not be started unless there are no other possible adequate treatment options.
Special alertness is required for signs of hypersensitivity syndrome or SJS/TEN, and patients should be advised to immediately discontinue allopurinol treatment at the first appearance of symptoms.
In the treatment of patients with impaired renal or hepatic function, the dose of allopurinol should be reduced. Patients treated for hypertension or heart failure (eg, patients taking diuretics or ACE inhibitors) may experience concomitant renal dysfunction, so allopurinol should be used with caution in this group of patients.
Allopurinol is not indicated in all cases of hyperuricemia that occurs without clinical manifestations. By itself, asymptomatic hyperuricemia is not an indication for the use of allopurinol. In such cases, improvement in patients’ condition can be achieved through changes in diet and fluid intake, along with the elimination of the underlying cause of hyperuricemia.
Acute attack of gout
You should not start the use of allopurinol until the acute attack of gout is completely relieved, since this can provoke an additional exacerbation of the disease.
Similar to uricosuric therapy, initiation of allopurinol treatment can also provoke an acute attack of gouty arthritis. To avoid this complication, prophylactic therapy with appropriate anti-inflammatory drugs or colchicine is recommended for at least one month prior to allopurinol. Detailed information on recommended doses, warnings and precautions can be found in the relevant literature.
If an acute attack of gout develops during allopurinol therapy, then the drug should be continued at the same dose, and an appropriate non-steroidal anti-inflammatory drug should be prescribed to treat the attack.
Azathioprine or 6-mercaptopurine
Allopurinol should not be administered to patients receiving treatment with azathioprine or 6-mercaptopurine unless the dose of these drugs is reduced to 25% of the originally prescribed dose.
In cases where the formation of urate is significantly increased (for example, malignant tumor and corresponding anticancer therapy, Lesch-Nyhan syndrome), the absolute concentration of xanthine in the urine only in rare cases can reach levels that contribute to the accumulation of xanthine in the tissues of the urinary tract. The likelihood of xanthine accumulation in tissues can be minimized by adequate hydration, which ensures optimal urine dilution.
Intrusion on uric acid stones.
Adequate therapy with allopurinol can lead to the dissolution of large uric acid calculi, however, the likelihood of these calculi in the ureters is small.
In the treatment of gouty kidney disease and urate stones, the daily volume of urine should be at least 2 liters, and the pH value of the urine should be in the range of 6.4-6.8.
The main effect of allopurinol in the treatment of gout is to suppress the activity of the enzyme xanthine oxidase. Xanthine oxidase may be involved in the reduction and excretion of iron deposited in the liver. There are no studies demonstrating the safety of allopurinol therapy in patients with hemochromatosis. In patients with hemochromatosis, as well as their blood relatives, allopurinol should be administered with caution.
Elevated TSH (thyroid stimulating hormone) values (>5.5 μIU / ml) were observed in patients treated with allopurinol for a long time (5.8%) in a long open additional clinical study.
Milurit tablets 100 mg contains lactose
Each tablet of the drug Milurit 100 mg contains 50 mg of lactose. Patients with rare hereditary problems of galactose intolerance, lactase deficiency or glucose-galactose malabsorption should not take this medicine.
Pregnancy and lactation
There is insufficient data on the safety of allopurinol therapy during pregnancy, although this drug has been widely used for many years without apparent adverse effects.
Milurit should not be taken during pregnancy, unless there is no less dangerous alternative treatment and the disease poses a greater risk to the mother and fetus than taking the drug.
According to existing reports, allopurinol and oxypurinol are excreted in breast milk. In women taking allopurinol at a dose of 300 mg / day, the concentration of allopurinol and oxypurinol in breast milk reached, respectively, 1.4 mg / l and 53.7 mg / l. However, there are no data on the effect of allopurinol and its metabolites on breastfed infants. Therefore, the drug Milurit tablets is not recommended during breastfeeding.
Features of the effect of the drug on the ability to drive vehicles and potentially dangerous mechanisms
During allopurinol therapy, the development of such undesirable reactions as drowsiness, dizziness with a sensation of rotation (vertigo) and ataxia, which can affect the ability to drive vehicles and potentially dangerous mechanisms, was observed. Patients taking the drug Milurit should not drive vehicles and mechanisms until they are sure that allopurinol does not adversely affect these abilities.
Symptoms: nausea, vomiting, diarrhea, dizziness were observed in a patient who took 20 g of allopurinol.
There is a report on the intake of 22.5 g of allopurinol without the development of side effects.
Severe overdose can lead to significant inhibition of xanthine oxidase activity. By itself, this effect should not be accompanied by unwanted reactions. An exception is the effect on concomitant therapy, in particular treatment with 6-mercaptopurine and/or azathioprine.
Treatment: No specific antidote known. Adequate hydration, maintaining optimal diuresis, promotes the excretion of allopurinol and its derivatives in the urine. If clinically indicated, hemodialysis is indicated.
Store at a temperature not exceeding 30 °C
Keep out of the reach of children!
Shelf life – 5 years
Do not use after the expiration date.
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