Allopurinol, tablets 100 mg 50 pcs
€3.84 €3.49
Pharmacotherapeutic group
An antipodagric agent – xanthine oxidase inhibitor
ATC code: M04AA
Pharmacodynamics:
Allopurinol is a structural analog of hypoxanthine. Allopurinol and its main active metabolite, oxypurinol, inhibit xanthine oxidase, the enzyme that ensures the conversion of hypoxanthine to xanthine and xanthine to uric acid.
Allopurinol reduces the concentration of uric acid in the blood serum and 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 large amounts of xanthine and hypoxanthine become available for reformation of purine bases, leading to inhibition of purine biosynthesis by a feedback mechanism that is mediated by inhibition of the enzyme hypoxanthine-guanine phosphoribosyl-transferase. Other metabolites of allopurinol are allopurinol riboside and oxypurinol-7 riboside.
Pharmacokinetics:
Assimilation
Allopurinol is active when administered orally. It is rapidly absorbed from the upper gastrointestinal tract. According to pharmacokinetic studies allopurinol is determined in the blood within 30-60 minutes after intake. Allopurinol bioavailability varies from 67% to 90%. Maximum plasma concentration of the drug is usually registered about 15 hours after oral administration. Then the allopurinol concentration decreases rapidly. Six hours after oral administration, only trace concentrations of the drug are detected in plasma. Maximum concentration of the active metabolite – oxypurinol is usually registered 3-5 hours after oral administration of allopurinol. The plasma level of oxypurinol decreases much slower.
Distribution
Allopurinol almost does not bind to plasma proteins so changes in the level of binding to proteins should not have a significant effect on the clearance of the drug. Apparent volume of allopurinol distribution is approximately 16 liters/kg that indicates quite pronounced absorption of the drug by tissues. Content of allopurinol in various human tissues is not studied; however, it is very likely that allopurinol and oxypurinol accumulate at maximum concentration in the liver and intestinal mucosa, where high xanthine oxidase activity is recorded.
Biotransformation
Allopurinol is metabolized under the action of xanthine oxidase and aldehydoxidase to form oxypurinol. Oxipurinol inhibits the activity of xanthine oxidase. However, oxypurinol is not as potent an inhibitor of xanthine oxidase as allopurinol, but its half-life is much longer. Due to these properties, effective inhibition of xanthine oxidase activity is maintained for 24 hours after a single daily dose of allopurinol. In patients with normal renal function, plasma levels of oxypurinol slowly increase until equilibrium concentration is reached. After administration of allopurinol at a dose of 300 mg per day, plasma concentration of allopurinol is usually 5-10 mg/l. Other allopurinol metabolites include allopurinol-riboside and oxipurinol-7-riboside.
Approximately 20% of allopurinol taken peros is excreted unchanged through the intestine. About 10% of the daily dose is excreted by the glomerular apparatus of the kidney as unchanged allopurinol. Another 70% of the daily dose of allopurinol is excreted with urine in the form of oxipurinol. Oxipurinol is excreted unchanged by the kidneys, but due to tubular reabsorption, it has a long half-life. Allopurinol has a half-life of 1 to 2 hours, whereas oxipurinol has a half-life of 13 to 30 hours. These significant differences are likely due to differences in study patterns and/or creatinine clearance in patients.
Patients with impaired renal function
In patients with impaired renal function, excretion of allopurinol and oxipurinol may be significantly delayed, resulting in increased plasma concentrations of these compounds during long-term therapy. 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 plasma concentration of oxypurinol reached approximately 30 mg/l. This concentration of oxypurinol can be detected in patients with normal renal function against the background of allopurinol therapy at a dose of 600 mg per day. Therefore, when treating patients with impaired renal function the allopurinol dose should be reduced.
Elderly patients
In elderly patients significant changes in allopurinol pharmacokinetic properties are unlikely. The exception is patients with concomitant renal pathology (see section “Pharmacokinetics in patients with impaired renal function”).
Indications
Suppression of uric acid and its salts when there is a proven accumulation of these compounds (e.g., gout skin tofus nephrolithiasis) or a suspected clinical risk of accumulation (e.g., treatment of malignancies may be complicated by the development of acute urolithic nephropathy).
The main clinical conditions that may accompany the accumulation of uric acid and its salts include:
– idiopathic gout;
– urolithiasis (formation of uric acid concretions);
– acute uric acid nephropathy;
– tumor diseases and myeloproliferative syndrome with a high rate of cell population turnover when hyperuricemia occurs spontaneously or after cytotoxic therapy;
– Certain enzymatic disorders with hyperproduction of uric acid salts such as decreased hypo-xanthine guanine phosphoribosyltransferase activity (including Lesh-Nyhan syndrome) decreased glucose6-phosphatase (including glycogenoses) increased phosphoribosyl pyrophosphate synthetase activity increased phosphoribosyl pyrophosphate amido-transferase activity decreased adenine phosphoribosyltransferase activity.
The treatment of urolithiasis accompanied by the formation of 28-dihydroxyadenine (28-DHA) concrements due to decreased activity of adenine phosphoribosyltransferase.
The prevention and treatment of urolithiasis accompanied by the formation of mixed calcium-oxalate concrements on the background of hyperuricosuria when diet and increased fluid intake were unsuccessful.
Active ingredient
Composition
For 1 tablet of 100 mg:
The active ingredient: allopurinol – 100.0 mg.
Excipients: microcrystalline cellulose – 54.0 mg; corn starch – 25.0 mg; sodium carboxymethyl starch – 10.0 mg; povidone-K25 – 8.0 mg; colloidal silica – 1.0 mg; magnesium stearate – 2.0 mg.
How to take, the dosage
Ingestion. The drug should be taken once a day after meals with plenty of water. If the daily dose is more than 300 mg or if there are gastrointestinal symptoms of intolerance, the dose should be divided into several doses.
Adult patients
In order to reduce the risk of side effects, an initial dose of allopurinol of 100 mg once daily is recommended. If this dose is not sufficient to adequately reduce serum uric acid concentrations, the daily dose of the drug can be gradually increased until the desired effect is achieved. Particular caution should be exercised in cases of impaired renal function. If the dose of allopurinol is increased, serum uric acid concentration should be determined every 1 to 3 weeks.
The following dosing regimens are recommended when choosing a dose of the drug (100 mg or 300 mg tablets are recommended depending on the dosing regimen chosen).
The recommended dose of the drug is: 100-200 mg per day for mild disease; 300-600 mg per day for moderate disease; 700-900 mg per day for severe disease.
If we consider the patient’s body weight when we calculate the dose, the allopurinol dose should be 2 to 10 mg/kg/day.
Children and adolescents under 15 years of age
The recommended dose for children from 3 to 10 years of age is 5-10 mg/kg/day. For low doses, 100 mg tablets are used, which can be divided into two equal doses of 50 mg with a risk. The recommended dose for children 10 to 15 years of age is 10-20 mg/kg/day. The daily dose of the drug should not exceed 400 mg.
Allopurinol is rarely used for pediatric therapy. The exceptions are malignant cancers (especially leukemia) and some enzymatic disorders (e.g., Lesch-Nyhan syndrome).
Elderly patients
There is no specific data on the use of allopurinol in the elderly population. For the treatment of these patients the drug should be used in the lowest dose that provides a sufficient reduction of serum uric acid concentrations. Particular attention should be paid to the recommendations on selection of the drug dose for patients with impaired renal function (see section “Cautions”).
In impaired renal function
Because allopurinol and its metabolites are eliminated from the body by the kidneys, impaired renal function may lead to retention of the drug and its metabolites in the body with subsequent prolongation of the plasma elimination half-life of these compounds. In severe renal failure it is recommended to use allopurinol at a dose lower than 100 mg per day or to use single doses of 100 mg at intervals of more than one day.
If conditions allow plasma concentrations of oxypurinol to be monitored, the dose of allopurinol should be adjusted so that plasma levels of oxypurinol are below 100 µmol/L (152 mg/L).
Allopurinol and its derivatives are removed from the body by hemodialysis. If hemodialysis sessions are performed 2-3 times a week, it is reasonable to determine the need to switch to an alternative regimen of therapy – taking 300-400 mg of allopurinol immediately after hemodialysis session (between hemodialysis sessions the drug is not taken).
In patients with impaired renal function, allopurinol should be combined with thiazide diuretics with extreme caution. Allopurinol should be prescribed at the lowest effective dose with close monitoring of renal function (see section “Interaction with other drugs”).
Hepatic disorders
If liver function is impaired, the drug dose should be reduced. In the early phase of therapy, monitoring of laboratory indicators of liver function is recommended.
Conditions associated with increased uric acid salt metabolism (e.g., tumor diseases, Lesch-Nyhan syndrome)
Preceding therapy with cytotoxic medications, correction of existing hyperuricemia and/or hyperuricosuria with allopurinol is recommended. Adequate hydration is important to maintain optimal diuresis, as well as alkalinization of the urine, which increases the solubility of uric acid and its salts. The allopurinol dose should be close to the lower limit of the recommended dose range.
If the renal impairment is due to the development of acute urolithiasis or other renal pathology, treatment should continue as described in the renal impairment section.
The measures described can reduce the risk of xanthine and uric acid accumulation complicating the disease course.
Monitoring recommendations
The serum uric acid salt concentrations and urinary urate and urate levels should be assessed at optimal intervals to adjust the dose of the drug.
Interaction
6-mercaptopurine and azathioprine
Azathioprine is metabolized to form 6-mercaptopurine that is inactivated by the enzyme xanthine oxidase. If therapy with 6-mercaptopurine or azathioprine is combined with allopurinol, patients should receive only one-quarter of the usual dose of 6-mercaptopurine or azathioprine because the inhibition of xanthine oxidase activity increases the duration of action of these compounds.
Vidarabine (adenine arabinoside)
In the presence of allopurinol the half-life of vidarabine is prolonged. If these drugs are used concomitantly, special caution should be exercised with regard to the increased toxic effects of therapy.
Salicylates and uricosuric agents
The main active metabolite of allopurinol is oxypurinol, which is excreted by the kidneys as uric acid salts. Consequently, drugs with uricosuric activity such as probenecid or high doses of salicylates can enhance excretion of oxypurinol. In turn, enhanced excretion of oxypurinol is accompanied by a decrease in the therapeutic activity of allopurinol, but the significance of this type of interaction must be assessed on a case-by-case basis.
Chlorpropamide
The concomitant use of allopurinol and chlorpropamide in patients with impaired renal function increases the risk of prolonged hypoglycemia because allopurinol and chlorpropamide compete in the tubular excretion phase.
Coumarin derived anticoagulants
An increase in the effects of warfarin and other coumarin derived anticoagulants has been observed with allopurinol. Therefore, the condition of patients receiving concomitant therapy with these drugs should be closely monitored.
Phenytoin
Allopurinol can inhibit hepatic oxidation of phenytoin; however, the clinical significance of this interaction has not been established.
Theophylline
Allopurinol is known to inhibit the metabolism of theophylline. This interaction can be explained by the participation of xanthine oxidase in the biotransformation of theophylline in humans. Serum theophylline concentration should be monitored at the beginning of concomitant therapy with allopurinol as well as when increasing the dose of the latter.
Ampicillin and amoxicillin
Patients who received ampicillin or amoxicillin and allopurinol concomitantly had an increased incidence of skin reactions compared to patients who did not receive this concomitant therapy. The reason for this type of drug interaction has not been determined. However, patients receiving allopurinol are advised to prescribe other antibacterial agents instead of ampicillin and amoxicillin.
Cytotoxic drugs (cyclophosphamide doxorubicin bleomycin procarbazine mechlorethamine)
In patients with tumor diseases (except leukemia) receiving allopurinol increased suppression of bone marrow activity by cyclophosphamide and other cytotoxic drugs was observed. However, according to the results of controlled studies involving patients receiving cyclophosphamide doxorubicin bleomycin procarbazine and/or mechlorethamine (chlormethine hydrochloride) concomitant therapy with allopurinol did not increase the toxic effects of these cytotoxic drugs.
Cyclosporine
Some reports suggest that plasma concentrations of cyclosporine may increase with concomitant therapy with allopurinol. When concomitant use of these drugs it is necessary to consider the possibility of increasing toxicity of cyclosporine.
Didanosine
In healthy volunteers and HIV-infected patients receiving didanosine concomitantly with allopurinol therapy (300 mg per day) there was approximately a twofold increase in Cmax (maximum drug concentration in plasma) and AUC (area under the concentration-time curve) of didanosine. Half-life of didanosine did not change. As a rule, concomitant use of these drugs is not recommended. If concomitant therapy is unavoidable, reduction in the dose of didanosine and close monitoring of the patient’s condition may be required.
The concomitant use of ACE inhibitors
The concomitant use of ACEs with allopurinol is associated with an increased risk of leukopenia, so these drugs should be combined with caution.
The thiazide diuretics
The concomitant use of thiazide diuretics, including hydrochlorothiazide, may increase the risk of hypersensitivity side effects associated with allopurinol especially in patients with impaired renal function.
Special Instructions
Drug hypersensitivity syndrome SSD and TEN
Life-threatening skin reactions such as Stevens-Johnson syndrome and toxic epidermal necrolysis (SSD/TEN) have been reported with allopurinol. Patients should be informed about the symptoms of these reactions (progressive skin rash often with vesicles and mucosal lesions) and their development should be closely monitored. SSRIs/TEH develop most frequently during the first weeks of taking the drug. In the presence of signs and symptoms of SDS/TEN, Allopurinol should be immediately withdrawn and no longer prescribed. The manifestation of hypersensitivity reactions to allopurinol can range from maculopapular exanthema to drug hypersensitivity syndrome (DRESS) and SDS/TEN. These reactions are the clinical diagnosis and their clinical manifestations are the basis for appropriate decisions. Therapy with Allopurinol should be immediately discontinued if a skin rash or other manifestations of hypersensitivity reactions occur. Therapy should not be resumed in patients with hypersensitivity syndrome and SDS/TEH. Corticosteroids may be used to treat skin reactions in hypersensitivity.
Chronic renal impairment
Patients with chronic renal impairment have a greater risk of developing hypersensitivity reactions associated with allopurinol including SSD/TEN.
The HLA-B*5801 allele
The presence of the HLA-B*5801 allele has been found to be associated with the development of allopurinol hypersensitivity syndrome and SSD/TEN. The frequency of the presence of the HLA-B*5801 allele varies in different ethnic groups and can be as high as 20% in the Han Chinese population about 12% in Koreans and 1-2% in Japanese and Europeans. The use of genotyping for allopurinol therapy decisions has not been investigated. If a patient is known to be a carrier of the HLA-B*5801 allele, allopurinol should be prescribed only if the benefits of treatment outweigh the risks. The development of hypersensitivity syndrome and SSD/TEH should be monitored very closely. The patient should be informed of the need for immediate withdrawal of treatment at the first appearance of such symptoms.
Hepatic and renal impairment
The dose of allopurinol should be reduced when treating patients with impaired renal or hepatic function. Patients being treated for arterial hypertension or heart failure (e.g., those taking diuretics or ACE inhibitors) may have concomitant impairment of renal function, so allopurinol should be used with caution in this group of patients.
Asymptomatic hyperuricemia alone is not an indication for allopurinol use. In these cases, patients may improve with changes in diet and fluid intake along with addressing the underlying cause of the hyperuricemia.
An acute attack of gout
Allopurinol should not be used until the acute attack of gout has completely resolved, as this could provoke an additional exacerbation of the disease. Similar to allopurinol therapy, initiation of allopurinol therapy may provoke an acute attack of gout. To avoid this complication, prophylactic therapy with nonsteroidal anti-inflammatory drugs or colchicine for at least one month before allopurinol administration is recommended. Details of recommended dosage cautions and precautions can be found in the relevant literature.
If an acute attack of gout develops with allopurinol therapy, the drug should be continued at the same dose, and a suitable non-steroidal anti-inflammatory drug should be prescribed to treat the attack.
Xanthine deposits
In cases where uric acid production is significantly increased (e.g., malignant tumor disease and related antitumor therapy Lech-Nyhan syndrome), the absolute concentration of xanthine in urine may rarely increase significantly, contributing to xanthine deposition in urinary tract tissues. The likelihood of xanthine deposition in tissues can be minimized by adequate hydration, which ensures optimal dilution of the urine.
Uuric acid concretions implantation
Adequate allopurinol therapy may result in dissolution of large uric acid concretions in the renal pelvis, but the probability of implantation of these concretions into the ureters is low.
Hemochromatosis
The main effect of allopurinol in the treatment of gout is to inhibit 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 a population of patients with hemochromatosis. Allopurinol should be administered with caution in patients with hemochromatosis and their blood relatives.
An adverse reactions such as drowsiness dizziness (vertigo) and ataxia have been observed with allopurinol therapy. These adverse events may affect the ability to drive vehicles and operate machinery. Patients taking Allopurinol tablets should not drive vehicles and operate machinery until they are sure that Allopurinol has no adverse effect on their driving ability.
Contraindications
Hypersensitivity to allopurinol or any of the excipients in the drug.
Hepatic failure chronic renal failure (stage of azotemia) primary hemochromatosis asymptomatic hyperuricemia acute onset of gout children under 3 years of age (in solid dosage form)
Pregnancy Breast-feeding (see section “Administration during pregnancy and breast-feeding”).
Hepatic disorders hypothyroidism diabetes mellitus arterial hypertension simultaneous use of angiotensin-converting enzyme (ACE) inhibitors or diuretics childhood age (under 15 years old is indicated only during cytostatic therapy for leukemia and other malignant diseases and symptomatic treatment of enzyme disorders) advanced age.
Side effects
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 administered as monotherapy or in combination with other drugs. The side effect frequency classification is based on a rough estimate for most side effects there are no data to determine the frequency of side effects.
The classification of adverse reactions according to frequency of occurrence is as follows: very frequent (â¥1/10) frequent (â¥1/100 to < 1/10) infrequent (â¥1/1000 to < 1/100) rare (â¥1/10000 to < 1/1000) very rare (< 1/10000) frequency unknown (cannot be determined from available data).
Allopurinol therapy-related adverse reactions observed in the post-registration period are rare or very rare. In the general patient population the majority of cases are mild. The incidence of adverse events increases with renal and/or hepatic dysfunction.
Infections and parasitic diseases: very rare – furunculosis.
Disorders of the blood and lymphatic system: very rare – agranulocytosis aplastic anemia thrombocytopenia granulocytosis leukopenia leukocytosis eosinophilia and aplasia concerning erythrocytes only.
There have been very rare reports of thrombocytopenia agranulocytosis and aplastic anemia, particularly in persons with renal and/or hepatic impairment, which emphasizes the need for special caution in these patient groups.
Immune system disorders: infrequent – hypersensitivity reactions; rare – severe hypersensitivity reactions including skin reactions with epidermal detachment, fever, lymphadenopathy, arthralgia and/or eosinophilia (including Stevens-Johnson syndrome and toxic epidermal necrolysis) (see section “Skin and subcutaneous tissue disorders”). Associated vasculitis or tissue reactions may have various manifestations including hepatitis kidney damage acute cholangitis xanthine concrements and in very rare cases seizures. In addition, the development of anaphylactic shock has been observed very rarely. If severe adverse reactions develop, allopurinol therapy should be immediately discontinued and not resumed. In delayed multi-organ hypersensitivity (known as drug hypersensitivity syndrome /DRESS/) the following symptoms may develop in various combinations: fever skin rash vasculitis lymphadenopathy pseudolymphoma arthralgia leukopenia eosinophilia hepatosplenomegaly change in results of liver functional tests disappearing bile ducts syndrome (destruction or disappearance of intrahepatic bile ducts). If such reactions develop during any period of treatment Allopurinol should be immediately discontinued and never resumed. Generalized hypersensitivity reactions have developed in patients with impaired renal and/or hepatic function. Such cases have sometimes been fatal; angioimmunoblastic lymphadenopathy is very rare.
Angioimmunoblastic lymphadenopathy has very rarely been diagnosed after lymph node biopsy for generalized lymphadenopathy. Angioimmunoblastic lymphadenopathy is reversible and regresses after discontinuation of allopurinol therapy.
Metabolic and nutritional disorders: very rare – diabetes mellitus hyperlipidemia.
Mental disorders: very rare – depression.
Nervous system disorders: very rare – coma paralysis ataxia neuropathy paresthesia sleepiness headache perversion of sense of taste.
Visual system disorders: very rare – cataract visual impairment macular changes.
Hearing organ and labyrinth disorders: very rare – dizziness (vertigo).
Chronic disorders: very rare – angina bradycardia.
Vascular disorders: very rare – increase in blood pressure.
Gastrointestinal disorders: infrequent – vomiting nausea diarrhea.
In earlier clinical studies, nausea and vomiting were observed; however, more recent observations have confirmed that these reactions are not a clinically significant problem and can be avoided by prescribing allopurinol after meals; very rare – recurrent bloody vomiting steatorrhea stomatitis changes in defecation frequency; frequency unknown – abdominal pain.
Hepatic and biliary tract disorders: infrequent – asymptomatic increase in liver enzymes (increased serum levels of alkaline phosphatase and transaminases); rare – hepatitis (including necrotic and granulomatous forms). Liver disorders may develop without obvious signs of generalized hypersensitivity
Skin and subcutaneous tissue disorders: frequent – rash; rare – severe skin reactions: Stevens-Johnson syndrome (SSD) and toxic epidermal necrolysis (TEN); very rare – angioneurotic edema local medication rash alopecia hair discoloration.
In patients taking allopurinol, undesirable skin reactions are most common. During therapy with the drug, these reactions may develop at any time. Skin reactions may be manifested by itching maculopapular and scaly rashes. In other cases, purpura may develop. In rare cases, exfoliative skin lesions (SSD/TEN) are observed. If such reactions develop, therapy with allopurinol should be stopped immediately. If skin reactions are mild, allopurinol can be resumed at a lower dose (e.g. 50 mg per day) after these changes have disappeared. Subsequently the dose can be gradually increased. In case of recurrent skin reactions allopurinol therapy should be stopped and not resumed since further use of the drug may lead to more severe hypersensitivity reactions (see “Immune system disorders”).
Angioneurotic edema has been reported to occur with allopurinol therapy both alone and in combination with symptoms of generalized hypersensitivity reactions.
Muscular and connective tissue disorders: very rare – myalgia.
Renal and urinary tract disorders: very rare – hematuria renal failure uremia; frequency is unknown – urolithiasis.
Reproductive system and breast disorders: very rare – male infertility erectile dysfunction gynecomastia.
General disorders and disorders at the site of administration: very rare – edema general malaise general weakness fever.
In allopurinol therapy, fever has reportedly occurred both in isolation and in conjunction with symptoms of generalized hypersensitivity reactions (see Immune system disorders).
Reports of possible adverse reactions
If any adverse reactions occur, including those not mentioned in these instructions, the drug should be discontinued.
In the post-registration period any information about possible adverse reactions is important because these reports help keep track of the safety of the medication. Healthcare professionals have an obligation to report any suspected adverse reactions to their local pharmacovigilance agency.
Overdose
Symptoms
Nausea vomiting diarrhea and dizziness. Severe overdose of allopurinol can lead to significant inhibition of xanthine oxidase activity. This effect alone should not be accompanied by adverse reactions. The exception is the effect on concomitant therapy, especially treatment with 6-mercaptopurine and/or azathioprine.
Treatment
The specific antidote for allopurinol is unknown. Adequate hydration maintaining optimal diuresis promotes excretion of allopurinol and its derivatives with urine. Hemodialysis is performed if clinically indicated.
Pregnancy use
There are currently insufficient data on the safety of allopurinol therapy during pregnancy, although the drug has been widely used for many years without obvious adverse effects. Pregnant women should not take Allopurinol tablets unless there is no less dangerous alternative treatment and the disease poses a greater risk to the mother and fetus than taking the drug.
Allopurinol and oxypurinol have been reported to be excreted with breast milk. In women taking allopurinol at a dose of 300 mg/day, allopurinol and oxypurinol concentrations in breast milk reached 14 mg/L and 537 mg/L, respectively. However, there are no data on the effects of allopurinol and its metabolites in breastfed infants. Thus, Allopurinol tablets are not recommended during breastfeeding.
Similarities
Weight | 0.025 kg |
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Shelf life | 3 years. Do not use the drug after the expiration date. |
Conditions of storage | At a temperature not higher than 25 ° C. Keep out of reach of children. |
Manufacturer | Ozon, Russia |
Medication form | pills |
Brand | Ozon |
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