Instructions for Omez capsules 20 mg No. 30
Composition
active ingredient: omeprazole;
1 capsule contains omeprazole 20 mg;
excipients: mannitol (E 421); lactose monohydrate; sodium lauryl sulfate; disodium hydrogen phosphate; sucrose; hypromellose; methacrylate copolymer (type C); sodium hydroxide; macrogol; talc; titanium dioxide (E 171);
capsule composition: gelatin, methyl parahydroxybenzoate (E 218), propyl parahydroxybenzoate (E 216), carmoisine (E 122).
Dosage form
Capsules.
Main physicochemical properties: hard gelatin transparent capsules size 2, marked OMEZ, with a colorless body and a pink cap. The contents of the capsules are white or almost white pellets.
Pharmacotherapeutic group
Drugs for the treatment of peptic ulcer and gastroesophageal reflux disease. Proton pump inhibitors.
ATX code A02B C01.
Pharmacological properties
Pharmacodynamics.
Mechanism of action: Omeprazole, a racemic mixture of two enantiomers, reduces gastric acid secretion by a targeted mechanism of action. It is a specific inhibitor of the gastric proton pump in parietal cells. It acts rapidly and provides control of gastric acid suppression with once-daily dosing.
Omeprazole is a weak base that is concentrated and converted to the active form in the acidic environment of the intracellular tubules in parietal cells, where it inhibits the enzyme H+K+-ATPase - the acid pump. This effect on the final stage of the process of gastric acid formation is dose-dependent and provides highly effective inhibition of both basal and stimulated acid secretion, regardless of the nature of the stimulus.
Pharmacodynamic effects: All observed pharmacodynamic effects can be explained by the effect of omeprazole on acid secretion.
Effect on gastric acid secretion.
Oral administration of 20 mg omeprazole once daily causes rapid and effective inhibition of daytime and nighttime gastric acid secretion, with the maximum effect being achieved within 4 days of treatment. In patients with duodenal ulcer, a mean reduction in gastric acidity of approximately 80% occurs within 24 hours after taking 20 mg omeprazole, and a mean reduction in peak acid output after pentagastrin stimulation is approximately 70% 24 hours after taking omeprazole.
Oral administration of 20 mg omeprazole maintains an intragastric pH of ≥ 3 in patients with duodenal ulcer for a mean of 17 hours out of a 24-hour period. Omeprazole reduces/normalizes esophageal acid exposure in patients with gastroesophageal reflux disease in a dose-dependent manner by reducing acid secretion and intragastric acidity. The inhibition of acid secretion is associated with the area under the plasma concentration-time curve (AUC) of omeprazole and not with the actual plasma concentration at that time.
No tachyphylaxis was observed during treatment with omeprazole.
Effect on Helicobacter pylori (H. pylori).
Peptic ulcers are associated with H. pylori, including duodenal ulcers and gastric ulcers. H. pylori is considered a major determinant in the development of gastritis. H. pylori, together with gastric acid, are major factors in the development of peptic ulcer disease. H. pylori is a major factor in the development of atrophic gastritis, which is associated with an increased risk of gastric cancer.
Eradication of H. pylori with omeprazole and antimicrobials is associated with more rapid symptom relief, a high rate of mucosal healing, and long-term remission of peptic ulcer disease.
Other effects related to acid suppression.
A slightly increased incidence of gastric glandular cysts has been reported during long-term treatment. These changes are a physiological consequence of the existing inhibition of acid secretion, are benign and probably reversible.
Reducing stomach acid by any means, including proton pump inhibitors, increases the number of bacteria in the stomach that are normally present in the gastrointestinal tract. Treatment with acid-reducing drugs slightly increases the risk of gastrointestinal infections, such as those caused by Salmonella, Campylobacter, and Clostridium difficile in hospitalized patients.
Application in pediatrics.
In an uncontrolled study in children (aged 1 to 16 years) with severe erosive esophagitis, omeprazole at doses of 0.7–1.4 mg/kg improved the condition of patients with esophagitis in 90% of cases and significantly reduced reflux symptoms. In a blinded, non-comparative study in children aged 0 to 24 months with established gastroesophageal reflux disease treated with doses of 0.5 mg/kg, 1.0 mg/kg and 1.5 mg/kg of omeprazole, the frequency of vomiting/regurgitation episodes was reduced by 50% after 8 weeks of treatment regardless of dose.
A randomized, double-blind clinical trial (Héliot study) concluded that omeprazole in combination with two antibiotics (amoxicillin and clarithromycin) was safe and effective in the treatment of H. pylori infection in children aged 4 years and older with gastritis: H. pylori eradication rate: 74.2% (23/31 patients) in the omeprazole + amoxicillin + clarithromycin group, compared with 9.4% (3/32 patients) in the amoxicillin + clarithromycin group. However, no evidence of clinical benefit was demonstrated for dyspeptic symptoms. This study did not include children aged under 4 years.
Pharmacokinetics.
Absorption. Absorption of omeprazole is rapid, with peak plasma levels occurring approximately 1–2 hours after dosing. Absorption of omeprazole occurs in the small intestine and is usually complete within 3–6 hours. Concomitant food intake has no effect on bioavailability. The systemic availability (bioavailability) of omeprazole after a single oral dose of omeprazole is approximately 40%. After repeated once-daily administration, bioavailability increases to approximately 60%.
Distribution: The apparent volume of distribution in healthy subjects is approximately 0.3 l/kg body weight. The plasma protein binding of omeprazole is 97%.
Metabolism: Omeprazole is completely metabolised by the cytochrome P450 system. The majority of omeprazole metabolism is dependent on the expressed CYP2C19, responsible for the formation of hydroxyomeprazole, the major metabolite in plasma. The remainder is dependent on another specific isoform, CYP3A4, responsible for the formation of omeprazole sulfone. As a result of the high affinity of omeprazole for CYP2C19, there is a potential for competitive inhibition and metabolic interactions between drugs with other substrates for CYP2C19. However, due to its low affinity for CYP3A4, omeprazole has no potential to inhibit the metabolism of other CYP3A4 substrates. Furthermore, omeprazole has no inhibitory effect on major CYP enzymes.
Approximately 3% of the Caucasian population and 15–20% of Asian populations lack a functional CYP2C19 enzyme. In these individuals, the metabolism of omeprazole is likely to be primarily catalyzed by CYP3A4. After repeated once-daily administration of 20 mg omeprazole, the mean AUC was 5–10 times higher in poor metabolizers than in individuals with a functional CYP2C19 enzyme (extensive metabolizers). The mean peak plasma concentrations were also 3–5 times higher. These observations have no relevance to the dosing of omeprazole.
Elimination: The terminal half-life of omeprazole from plasma is generally less than 1 hour after both single and multiple once-daily oral administration. Omeprazole is completely eliminated from plasma between doses without a tendency for accumulation during once-daily administration. Approximately 80% of an oral dose of omeprazole is excreted as metabolites in the urine, the remainder in the faeces, mainly via biliary secretion.
With repeated administration, the AUC of omeprazole increases. This increase is dose-dependent and results in a non-linear relationship between dose and AUC after repeated administration. This time- and dose-dependence is associated with a decrease in presystemic metabolism and systemic clearance, possibly due to inhibition of the CYP2C19 enzyme by omeprazole and/or its metabolites (e.g. the sulfone).
The metabolite was not found to have any effect on gastric acid secretion.
Special populations.
Hepatic impairment: In patients with hepatic impairment, the metabolism of omeprazole is altered, leading to an increase in AUC. Omeprazole did not show any tendency for accumulation when administered once daily.
Renal impairment: The pharmacokinetics of omeprazole, including systemic bioavailability and elimination rate, are not altered in patients with reduced renal function.
Elderly patients: The metabolic rate of omeprazole is slightly reduced in elderly patients (75-79 years).
Children: When treated with recommended doses in children from 1 year of age, plasma concentrations were similar to those in adults. In children under 6 months of age, clearance of omeprazole is low due to a low capacity to metabolize omeprazole.
Clinical characteristics.
Indication
Adults:
- for the treatment and prevention of relapses of duodenal ulcers and benign gastric ulcers, including those associated with the use of non-steroidal anti-inflammatory drugs (NSAIDs);
- for the prevention of gastric and duodenal ulcers associated with the use of non-steroidal anti-inflammatory drugs (NSAIDs) in patients at risk;
- for eradication of Helicobacter pylori (H. pylori) in peptic ulcer disease - in combination with appropriate antibiotics;
- for the treatment of gastroesophageal reflux disease, including reflux esophagitis;
- for long-term treatment of patients with gastroesophageal reflux disease;
- for the treatment of Zollinger-Ellison syndrome.
Children:
children aged 1 year and over and weighing more than 10 kg:
- for the treatment of reflux esophagitis;
- for the symptomatic treatment of heartburn and acid regurgitation in gastroesophageal reflux disease;
children aged 4 and over:
- for the treatment of duodenal ulcers caused by H. pylori - in combination with antibiotics.
Contraindication
Hypersensitivity to omeprazole, substituted benzimidazoles or to any of the excipients. Omeprazole, like other proton pump inhibitors (PPIs), should not be used concomitantly with nelfinavir (see Interactions with other medicinal products and other forms of interaction).
Interaction with other medicinal products and other types of interactions
Effect of omeprazole on the pharmacokinetics of other drugs.
Drugs whose absorption depends on gastric pH
Inhibition of gastric secretion by omeprazole and other PPIs may reduce or increase the absorption of drugs whose absorption depends on gastric pH. As with other drugs that reduce gastric acidity, the absorption of drugs such as ketoconazole, itraconazole and erlotinib may be reduced, while the absorption of drugs such as digoxin may be increased by omeprazole. Concomitant administration of omeprazole (20 mg daily) and digoxin in healthy volunteers increased the bioavailability of digoxin by 10% (in two out of ten subjects – up to 30%).
Nelfinavir, atazanavir
Plasma levels of nelfinavir and atazanavir are decreased when co-administered with omeprazole.
Concomitant use of omeprazole and nelfinavir is contraindicated. Co-administration of omeprazole (40 mg once daily) decreased the mean exposure of nelfinavir by approximately 40% and the mean exposure of the pharmacologically active metabolite M8 decreased by approximately 75–90%. The interaction may also be due to inhibition of CYP2C19 activity.
Concomitant use of omeprazole with atazanavir is not recommended. Concomitant use of omeprazole (40 mg once daily) and atazanavir 300 mg/ritonavir 100 mg in healthy volunteers resulted in a 75% decrease in atazanavir exposure. Increasing the atazanavir dose to 400 mg did not compensate for the effect of omeprazole on atazanavir exposure. Concomitant use of omeprazole (20 mg once daily) with atazanavir 400 mg/ritonavir 100 mg in healthy volunteers resulted in an approximately 30% decrease in atazanavir exposure compared to atazanavir 300 mg/ritonavir 100 mg once daily.
Digoxin
Concomitant treatment with omeprazole (20 mg daily) and digoxin in healthy volunteers increased the bioavailability of digoxin by 10%. Rare cases of digoxin-induced toxicity have been reported. However, caution should be exercised when prescribing high doses of omeprazole to elderly patients. In case of concomitant use with digoxin, patients should be closely monitored by a physician.
Clopidogrel
A clinical study in healthy volunteers showed a pharmacokinetic/pharmacodynamic (PK/PD) interaction between clopidogrel (300 mg loading dose followed by 75 mg/day) and omeprazole (80 mg/day), resulting in a 46% decrease in exposure to the active metabolite of clopidogrel and a 16% decrease in maximal inhibition (ADP-induced) of platelet aggregation.
Conflicting data on the clinical consequences of PK/PD interactions with omeprazole in terms of major cardiovascular events have been obtained from both observational and clinical studies. Therefore, concomitant use of omeprazole and clopidogrel should be avoided.
Other medicines
The absorption of posaconazole, erlotinib, ketoconazole and itraconazole is significantly reduced and therefore clinical efficacy may be reduced. Concomitant use with posaconazole and erlotinib should be avoided.
Medicinal products metabolized by CYP2C19
Omeprazole is a moderate inhibitor of CYP2C19, the main enzyme that metabolizes omeprazole. Therefore, the metabolism of concomitant drugs that are also metabolized by CYP2C19 may be reduced and the systemic exposure of these drugs may be increased. Examples of such drugs are R-warfarin and other vitamin K antagonists, cilostazol, diazepam and phenytoin.
In healthy volunteers, a pharmacokinetic/pharmacodynamic interaction was observed between clopidogrel (loading dose 300 mg/daily maintenance dose 75 mg) and omeprazole (80 mg orally daily, i.e. a dose 4 times the standard daily dose), resulting in a mean 46% decrease in exposure to the active metabolite of clopidogrel and a mean 16% decrease in the maximum inhibitory effect (induced by ADP) on platelet aggregation. The clinical significance of this interaction remains unclear. As a precautionary measure, the concomitant use of omeprazole and clopidogrel should be avoided.
Cilostazol
In healthy volunteers, administration of omeprazole at a dose of 40 mg increased the Cmax and AUC of cilostazol by 18% and 26%, respectively, and of one of its active metabolites by 29% and 69%, respectively.
Phenytoin
Monitoring of phenytoin plasma concentrations is recommended during the first two weeks after starting treatment with omeprazole and, if phenytoin dose adjustment has been made, monitoring and further dose adjustment of the drug should be carried out after the end of treatment with omeprazole.
Unknown mechanism of interaction
Concomitant use of omeprazole with saquinavir/ritonavir resulted in an increase in plasma levels of saquinavir of approximately 70%, which was associated with good tolerability in HIV-infected patients.
Tacrolimus
Increased serum tacrolimus levels have been reported with concomitant use of omeprazole. Increased monitoring of tacrolimus concentrations and renal function (creatinine clearance) is required and, if necessary, tacrolimus dosage should be adjusted.
Methotrexate
Increased methotrexate levels have been reported in some patients when co-administered with proton pump inhibitors. If high doses of methotrexate are necessary, temporary withdrawal of omeprazole should be considered.
Effect of other drugs on the pharmacokinetics of omeprazole.
CYP2C19 and/or CYP3A4 inhibitors
Since omeprazole is metabolised by CYP2C19 and CYP3A4, drugs that inhibit CYP2C19 or CYP3A4 (such as clarithromycin and voriconazole) may increase omeprazole serum levels by decreasing its metabolic rate. Concomitant use of voriconazole resulted in a more than two-fold increase in omeprazole exposure. Since high doses of omeprazole were well tolerated, dose adjustment of omeprazole is generally not necessary. However, dose adjustment should be considered in patients with severe hepatic impairment and if long-term treatment is indicated.
Omeprazole is also partially metabolized by CYP3A4, but does not inhibit this enzyme. Thus, omeprazole does not affect the metabolism of drugs metabolized by CYP3A4, such as cyclosporine, lidocaine, quinidine, estradiol, erythromycin, and budesonide.
CYP2C19 and CYP3A4 inducers
Drugs that induce CYP2C19 or CYP3A4 activity (such as rifampicin and St. John's wort) may lead to decreased serum levels of omeprazole as a result of an increase in its metabolic rate.
Application features
In the presence of any alarming symptom (e.g. significant weight loss not due to diet; frequent vomiting; dysphagia; vomiting with blood or melena) and when gastric ulcer is diagnosed or suspected, malignant disease should be excluded, since taking the drug may mask its symptoms and delay the establishment of the correct diagnosis.
Concomitant use of atazanavir with proton pump inhibitors is not recommended. If the combination of atazanavir with a proton pump inhibitor cannot be avoided, close clinical monitoring (e.g. viral load) is recommended in conjunction with an increase in the dose of atazanavir to 400 mg per 100 mg of ritonavir; the dose of omeprazole should not exceed 20 mg.
Omeprazole, like all drugs that inhibit the secretion of hydrochloric acid in the stomach, may reduce the absorption of vitamin B12 (cyanocobalamin) due to hypo- or achlorhydria. This should be taken into account in patients with cachexia or risk factors for reduced absorption of vitamin B12 during long-term therapy.
Omeprazole is an inhibitor of CYP2C19. When initiating or ending treatment with omeprazole, the possibility of interactions with medicinal products metabolised by CYP2C19 should be considered. An interaction has been observed between clopidogrel and omeprazole (see section 4.5). The clinical significance of this interaction remains unclear. As a precautionary measure, concomitant use of omeprazole and clopidogrel should be avoided.
Patients taking proton pump inhibitors, including omeprazole, may develop severe hypomagnesemia for at least three months (in most cases of hypomagnesemia, patients have been taking the drug for about a year). Hypomagnesemia can be suspected by such serious manifestations as fatigue, muscle spasms, tetany, seizures, delirium, dizziness, ventricular arrhythmia. However, it should be borne in mind that in some cases the manifestations may be masked, which prevents timely recognition of such a complication. In most patients, the manifestations of hypomagnesemia disappear and the condition normalizes after the use of magnesium preparations and the withdrawal of proton pump inhibitors.
In patients on long-term treatment or taking PPIs with digoxin or drugs that can cause hypomagnesemia (e.g., diuretics), magnesium levels should be measured, if possible, before starting PPI treatment and periodically during treatment.
A prolonged decrease in gastric acidity can lead to an increase in the number of bacteria present in the gastrointestinal tract.
Treatment with proton pump inhibitors slightly increases the risk of gastrointestinal infections caused by Salmonella, Campylobacter, and Clostridium difficile in hospitalized patients.
The use of proton pump inhibitors, especially at high doses and in long-term treatment, may be associated with a small increased risk of fractures, predominantly in the elderly and in the presence of additional risk factors. Although a causal relationship between the use of omeprazole/esomeprazole and osteoporotic fractures has not been proven, appropriate clinical surveillance should be recommended in patients at risk of progressive osteoporosis or osteoporotic fracture, in accordance with current clinical guidelines.
Subacute cutaneous lupus erythematosus (SCL)
The use of proton pump inhibitors may be associated with very rare cases of PsA. If lesions occur, especially in sun-exposed areas of the skin, and if accompanied by arthralgia, the patient should seek medical advice immediately and the healthcare professional should consider discontinuing omeprazole. If PsA develops after previous treatment with a proton pump inhibitor, the risk of PsA increases with the use of other proton pump inhibitors.
Impact on research results
During treatment with antisecretory drugs, serum gastrin levels may increase in response to decreased hydrochloric acid secretion. Chromogranin A (CgA) levels may also increase due to decreased gastric acidity, which may affect the results of neuroendocrine tumor studies.
Available published data suggest that PPIs should be discontinued 5–14 days before CgA measurements. This prevents misinterpretation of CgA levels after PPI use and allows values to return to the reference range.
If chromogranin A and gastrin levels do not return to normal after initial determination, measurements should be repeated 14 days after completion of proton pump inhibitor treatment.
An increased number of enterochromaffin-like cells (ECL cells) may be associated with increased serum gastrin levels, which may be observed in some patients (both adults and children) during long-term treatment with omeprazole. These findings are not expected to be of clinical relevance.
For the treatment of chronic diseases, children should not use the drug for longer than recommended.
With long-term treatment, especially more than 1 year, the patient should be under medical supervision.
This medicinal product contains lactose and sucrose, therefore patients with rare hereditary forms of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take it. If you have been told by your doctor that you have an intolerance to some sugars, contact your doctor before taking this medicinal product.
The medicine contains methyl parahydroxybenzoate (E 218) and propyl parahydroxybenzoate (E 216), which may cause allergic reactions (possibly delayed).
The medicine contains carmoisine (E 122), which may cause allergic reactions.
Use during pregnancy or breastfeeding
The results of three prospective epidemiological studies (more than 1000 outcomes) indicate no adverse effects of omeprazole on pregnancy or on the health of the foetus/newborn child. Omeprazole can be used during pregnancy.
Omeprazole passes into breast milk, but when used in therapeutic doses, the likelihood of an effect on the child is negligible. If it is necessary to use omeprazole during breastfeeding, consult your doctor.
Ability to influence reaction speed when driving vehicles or other mechanisms
The drug is unlikely to affect the ability to drive or use machines. Undesirable effects such as dizziness and visual disturbances may occur (see section "Adverse reactions"). If such disorders are observed, patients should not drive or use machines.
Method of administration and doses
Dosage for adults.
Treatment and prevention of duodenal ulcers and benign gastric ulcers, including those associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs).
The recommended dose for patients with duodenal ulcer is 20 mg omeprazole once daily. In most patients, duodenal ulcer heals within 2 weeks. For patients who do not fully heal after the initial course, further treatment for 2 weeks is recommended. In severe or recurrent cases, 40 mg omeprazole per day is recommended, and healing is usually achieved within 4 weeks.
In the treatment of gastric ulcers, the recommended dose is 20 mg omeprazole once daily. In most patients, gastric ulcers heal within 4 weeks. In patients who do not fully heal after the initial course, further treatment for 4 weeks is recommended. In severe or recurrent cases, 40 mg omeprazole per day is recommended, and healing is usually achieved within 8 weeks.
For the prevention of relapse in patients with gastric ulcer and inadequate response to treatment, the recommended dose is 20 mg omeprazole once daily. If necessary, the dose may be increased to 40 mg once daily.
For the treatment of gastric and duodenal ulcers associated with the use of non-steroidal anti-inflammatory drugs, the recommended dose is 20 mg omeprazole once daily. In most patients, healing occurs within 4 weeks. In patients who do not fully heal after the initial course, further treatment for 4 weeks is recommended.
For the prevention of gastric and duodenal ulcers associated with the use of nonsteroidal anti-inflammatory drugs, in patients at increased risk (age > 60, history of gastric and duodenal ulcers, upper gastrointestinal bleeding), the recommended dose is 20 mg omeprazole once daily.
Eradication of H. pylori in peptic ulcer.
When choosing antibacterial drugs for H. Pylori eradication, individual drug tolerance, local characteristics, and treatment guidelines should be taken into account.
- Omeprazole 20 mg + clarithromycin 500 mg + amoxicillin 1000 mg 2 times a day for 1 week, or
- Omeprazole 20 mg + clarithromycin 250 mg (if necessary 500 mg) + metronidazole 400 mg (if necessary 500 mg or tinidazole 500 mg) 2 times a day for 1 week, or
- Omeprazole 40 mg once a day + amoxicillin 500 mg + metronidazole 400 mg (if necessary 500 mg or tinidazole 500 mg) 3 times a day for 1 week.
Treatment of gastroesophageal reflux disease, including reflux esophagitis.
The recommended dose is 20 mg omeprazole once daily. Most patients recover within 4 weeks. Patients who do not fully recover after the initial course are recommended to continue treatment for 4 weeks. For patients with severe esophagitis, 40 mg omeprazole daily is recommended, with recovery usually occurring within 8 weeks.
For long-term treatment of patients with gastroesophageal reflux disease, the recommended dose is 10 mg omeprazole once daily. If necessary, the dose may be increased to 20-40 mg omeprazole once daily.
In the treatment of symptoms of gastroesophageal reflux disease, the recommended dose is 20 mg omeprazole once daily. The patient may be satisfied with a dose of 10 mg, the dose should be adjusted individually. If the desired result is not achieved after 4 weeks of treatment with omeprazole at a dose of 20 mg per day, the patient should be further examined.
Treatment of Zollinger-Ellison syndrome.
For patients with Zollinger-Ellison syndrome, the dose should be selected individually. Treatment is continued until clinical symptoms disappear. The recommended initial dose is 60 mg omeprazole once daily. Observation of more than 90% of patients with severe disease and insufficient response to other treatments has shown the effectiveness of maintenance therapy in doses of 20–120 mg per day. Daily doses above 80 mg should be divided and administered in 2 doses.
Dosage for children
Children aged 1 year and over with a body weight ≥ 10 kg.
Treatment of reflux esophagitis.
Symptomatic treatment of heartburn and acid regurgitation in gastroesophageal reflux disease.
Dosage recommendations:
Age
Body weight
Dosage
≥ 1 year
10–20 kg
10 mg* once daily.
If necessary, the dose can be increased to 20 mg once a day.
≥ 2 years
Children weighing more than 20 kg
20 mg once a day.
If necessary, the dose can be increased to 40 mg once a day.
Treatment of reflux esophagitis: the duration of treatment is 4–8 weeks.
Symptomatic treatment of heartburn and acid regurgitation in gastroesophageal reflux disease: duration of treatment is 2–4 weeks. If the desired result is not achieved after 2–4 weeks, the patient should be further examined.
Children and adolescents aged 4 years and over.
Treatment of duodenal ulcers caused by H. pylori.
Combination therapy should be prescribed taking into account local bacterial resistance patterns. The duration of treatment (7 to 14 days) and the appropriate use of antibacterial drugs should also be taken into account. Treatment should be carried out under the supervision of a physician.
Dosage recommendations:
Body weight
Dosage
15–30 kg
Omeprazole 10 mg* + amoxicillin 25 mg/kg body weight + clarithromycin 7.5 mg/kg body weight. Take the drugs together 2 times a day for 1 week
31–40 kg
Omeprazole 20 mg + amoxicillin 750 mg + clarithromycin 7.5 mg/kg body weight. Take the drugs together 2 times a day for 1 week.
> 40 kg
Omeprazole 20 mg + amoxicillin 1000 mg + clarithromycin 500 mg. Take the drugs together 2 times a day for 1 week.
* If a dose of 10 mg is necessary, use the drug in the appropriate dosage.
Renal impairment: No dose adjustment is required for patients with renal impairment (see Pharmacokinetics).
Hepatic impairment: For patients with hepatic impairment, a daily dose of 10–20 mg is sufficient (see section 5.2).
Elderly patients (> 65 years): No dose adjustment is required for elderly patients (see section 5.2).
It is recommended to take the capsules in the morning, preferably before meals, without damaging the capsule (the capsules should not be chewed or broken) and with half a glass of water.
For patients with swallowing difficulties and for children who can drink or swallow semi-solid food. The capsules can be opened and the contents swallowed directly with half a glass of water, or mixed in a slightly acidic liquid, such as any fruit juice, applesauce or still water. This mixture should be drunk immediately after preparation within 30 minutes. The mixture should be shaken before taking and washed down with half a glass of water. Do not use milk or carbonated water. The contents of the capsules (enteric-coated granules) should not be chewed.
Children.
The drug should be used in children over 1 year of age with a body weight of more than 10 kg as prescribed by a doctor for reflux esophagitis and symptomatic treatment of heartburn and acid regurgitation in gastroesophageal reflux disease and in children over 4 years of age in combination with antibiotics for the treatment of duodenal ulcers caused by H. pylori, under the supervision of a doctor.
Overdose
Data on the effects of omeprazole overdose in humans are limited. Cases of overdose with omeprazole up to 560 mg have been described in the scientific literature, and there are also isolated reports of a single oral dose of 2400 mg omeprazole (120 times the usual recommended clinical dose). Nausea, vomiting, dizziness, abdominal pain, diarrhea and headache have been reported. Apathy, depression and confusion have also been reported in isolated cases.
The symptoms described were reversible. The elimination rate did not change (first-order kinetics) with increasing dose. Treatment, if necessary, is symptomatic.
Adverse reactions
The most common adverse reactions are headache, abdominal pain, constipation, diarrhea, bloating and nausea/vomiting. The following adverse drug reactions have been identified or suspected during clinical trials with omeprazole or during post-marketing use.
From the blood and lymphatic system: leukopenia, thrombocytopenia, agranulocytosis, pancytopenia.
Immune system disorders: hypersensitivity reactions, such as fever, angioedema and anaphylactic reaction/shock.
Metabolism and digestion: hyponatremia, hypomagnesemia, severe hypomagnesemia, which may lead to hypocalcemia. Hypomagnesemia may also be associated with hypokalemia.
On the part of the psyche: insomnia, agitation, confusion, depression, aggression, hallucinations.
From the nervous system: headache, dizziness, paresthesia, drowsiness, taste disturbance.
From the organs of vision: blurred vision.
From the organs of hearing and balance: tinnitus, vertigo.
Respiratory, thoracic and mediastinal disorders: bronchospasm.
Gastrointestinal: abdominal pain, constipation, diarrhea, bloating, nausea/vomiting, glandular polyps of the gastric fundus, dry mouth, stomatitis, gastrointestinal candidiasis, microscopic colitis.
Hepatobiliary disorders: increased liver enzymes, hepatitis with or without jaundice, hepatic failure, encephalopathy in patients with pre-existing liver disease.
Skin and subcutaneous tissue disorders: dermatitis, pruritus, rash, urticaria, alopecia, photosensitivity, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, subacute cutaneous lupus erythematosus (see section "Special warnings and precautions for use").
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