Omeprazole Ananta capsules 20 mg blister No. 100

Instructions for use Omeprazole Ananta capsules 20 mg blister No. 100

Composition

active ingredient: omeprazole;

1 capsule contains omeprazole (in the form of enteric-coated pellets) 20 mg;

excipients:

as part of enteric-coated omeprazole pellets: mannitol (E 421), calcium carbonate, sodium hydrogen phosphate dihydrate, sodium lauryl sulfate, sugar, povidone, sodium methylparaben (E 219), sodium propylparaben (E 217), hypromellose, methacrylate copolymer dispersion, sodium hydroxide, diethyl phthalate, talc, titanium dioxide (E 171), polysorbate 80, purified water;

Neutral pellets contain: corn starch, sugar, anhydrous lactose; gelatin.

Dosage form

Modified-release capsules.

Main physicochemical properties: hard gelatin capsules with a pink cap and a transparent body, containing white pellets.

Pharmacotherapeutic group

Drugs for the treatment of peptic ulcer and gastroesophageal reflux disease. Proton pump inhibitors. ATC code A02B C01.

Pharmacological properties

Pharmacodynamics.

Mechanism of action.

Omeprazole, a racemic mixture of two enantiomers, reduces gastric acid secretion through a targeted mechanism of action. It is a specific inhibitor of the parietal cell proton pump. It acts rapidly and controls the inhibition of gastric acid secretion when dosed once daily.

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, providing 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 an average of 17 hours out of a 24-hour period. Omeprazole reduces/normalizes esophageal acid exposure in patients with gastroesophageal reflux disease by dose-dependently 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, 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 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 reversible.

Reducing stomach acid by any means, including proton pump inhibitors, increases the number of bacteria normally present in the gastrointestinal tract. Treatment with acid-reducing drugs may lead to a slightly increased 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 to 9.4% (3/32 patients) in the amoxicillin+clarithromycin group. However, there was no evidence of clinical benefit on dyspeptic symptoms. This study does not provide information on 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 does not affect bioavailability. The systemic availability (bioavailability) of omeprazole after a single oral dose is approximately 40%. After repeated once-daily administration, bioavailability increases to approximately 60%.

Distribution.

The apparent volume of distribution in healthy volunteers is approximately 0.3 l/kg body weight. The binding of omeprazole to plasma proteins is 97%.

Metabolism.

Omeprazole is completely metabolised by the cytochrome P450 system. The majority of omeprazole metabolism is dependent on the expressed isoform 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 CYP2C19 substrates. 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 Caucasians and 15-20% of Asians 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 subjects 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.

Breeding.

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 with once-daily administration. Approximately 80% of an oral dose of omeprazole is excreted as metabolites in the urine, the remainder in the faeces, mainly in the bile.

With repeated dosing, the AUC of omeprazole increases. This increase is dose-dependent and results in a non-linear relationship between dose and AUC after repeated dosing. This time- and dose-dependence is associated with a decrease in pre-systemic metabolism and systemic clearance, possibly due to inhibition of the CYP2C19 enzyme by omeprazole and/or its metabolites (e.g. the sulfone).

No effect of the metabolite on gastric acid secretion was detected.

Special populations.

Liver dysfunction.

In patients with impaired hepatic function, the metabolism of omeprazole is altered, leading to an increase in AUC. Omeprazole did not show any tendency for accumulation when administered once daily.

Kidney dysfunction.

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 aged 1 year and above, plasma concentrations were similar to those in adults. In children aged less than 6 months, the clearance of omeprazole is reduced due to the low capacity to metabolise omeprazole.

Indication

In adults:

- treatment and prevention of relapses of duodenal ulcers and benign gastric ulcers, including those associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs);

- prevention of gastric and duodenal ulcers associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients at risk;

- eradication of Helicobacter pylori (H. pylori) in peptic ulcer in combination with appropriate antibiotics;

- treatment of gastroesophageal reflux disease, including reflux esophagitis;

- treatment of Zollinger-Ellison syndrome.

In children

Children aged 1 year and over, weighing more than 10 kg:

- treatment of reflux esophagitis;

- symptomatic treatment of heartburn and acid regurgitation in gastroesophageal reflux disease.

Children aged 4 and over:

- in combination with antibiotics for the treatment of duodenal ulcers caused by H. pylori.

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 section 4.5).

Interaction with other medicinal products and other types of interactions

Effect of omeprazole on the pharmacokinetics of other drugs.

Drugs whose absorption depends on the pH of the stomach.

Inhibition of gastric secretion during treatment with omeprazole and other PPIs may reduce or increase the absorption of drugs whose absorption depends on gastric pH. As with other drugs that reduce intragastric 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 during treatment with omeprazole. Concomitant use 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.

Digoxin.

Concomitant treatment with omeprazole (20 mg once 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 (induced by adenosine diphosphate (ADP)) of platelet aggregation.

Conflicting data on the clinical manifestations of this PK/PD interaction in terms of major cardiovascular diseases have been reported in 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.

Drugs 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/day orally, 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 (ADP-induced) on platelet aggregation. The clinical significance of this interaction remains unclear. As a precautionary measure, 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 initiation of omeprazole treatment and if phenytoin dose adjustment has been made. Monitoring and further dose adjustment of the drug should be carried out after discontinuation of omeprazole treatment.

The mechanism of interaction is unknown.

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 known to inhibit CYP2C19 or CYP3A4, or both (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/or CYP3A4 inducers.

Drugs known to induce the activity of CYP2C19 or CYP3A4, or both enzymes (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

If any alarming symptom is present (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, as taking the drug may mask its symptoms and delay the determination of the correct diagnosis.

Concomitant use of atazanavir with proton pump inhibitors is not recommended (see section 4.5). 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 significant 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, delirium, dizziness, ventricular arrhythmia. However, it should be borne in mind that sometimes the manifestations can 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 may cause hypomagnesemia (e.g., diuretics), magnesium levels should be measured, if possible, before starting PPI treatment and periodically during treatment.

Omeprazole can cause severe skin reactions. Symptoms may include redness of the skin, blistering and rash. If an allergic reaction occurs, treatment should be discontinued and medical attention should be sought.

Severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome, toxic epidermal necrolysis (TEN), drug reaction with eosinophilia and systemic symptoms (DRESS) and acute generalized exanthematous pustulosis (AGEP), which can be life-threatening or fatal, have been reported with omeprazole.

Treatment with proton pump inhibitors may lead to a slightly increased risk of developing gastrointestinal infections caused by Salmonella and Campylobacter and Clostridium difficile in hospitalized patients.

Proton pump inhibitor therapy, especially at high doses and in long-term courses (> 1 year), may be associated with a small increased risk of fractures of the spine, wrist, and hip, predominantly in the elderly and in the presence of additional risk factors. Observational studies have shown that PPIs increase the overall risk of fractures by 10–40%. Patients at risk of progressive osteoporosis or osteoporotic fracture should be advised to have appropriate clinical surveillance according to current clinical guidelines for this condition and to consume adequate amounts of vitamin D and calcium.

Kidney dysfunction

Acute tubulointerstitial nephritis (ATIN) has been reported in patients taking omeprazole and may occur at any time during omeprazole therapy (see section 4.8). Acute tubulointerstitial nephritis may progress to renal failure.

If GTIN is suspected, omeprazole should be discontinued and appropriate treatment should be initiated immediately.

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 due to decreased hydrochloric acid secretion. Decreased hydrochloric acid secretion leads to increased levels of chromogranin A (CgA). Increased CgA concentrations may interfere with the results of tests for the detection of neuroendocrine tumors.

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 CgA levels to return to the reference range. If chromogranin A and gastrin levels do not return to normal after initial measurement, measurements should be repeated 14 days after stopping proton pump inhibitor therapy.

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 sugar. If you have an intolerance to some sugars, contact your doctor before taking this medicinal product.

The medicine contains sodium methylparaben (E 219), sodium propylparaben (E 217), which may cause allergic reactions (possibly delayed).

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 is unlikely to affect the child if used in therapeutic doses. If necessary, use of omeprazole during breastfeeding should be consulted with a 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 4.8). If such disorders occur, 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).

For the prevention of recurrence of duodenal ulcers in patients with a negative test result for H. Pylori or in case of failure to eradicate H. Pylori, the recommended dose is 20 mg of omeprazole once daily. For some patients, a daily dose of 10 mg may be sufficient (use the drug in the appropriate dosage). In case of insufficient therapy, the dose can be increased to 40 mg.

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.

For the eradication of H. pylori, the choice of antibacterial drugs should take into account individual drug tolerance and follow national, regional, and local treatment guidelines.

- 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 (use the drug in the appropriate dosage) of omeprazole once daily. If necessary, the dose can be increased to 20-40 mg of omeprazole once daily.

In the treatment of symptoms of gastroesophageal reflux disease, the recommended dose is 20 mg of omeprazole once daily. The patient may be satisfied with a dose of 10 mg (use the drug in the appropriate dosage), 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 administered in 2 divided doses.

Dosage for children.

Children aged 1 year and over, weighing ≥10 kg.

Treatment of reflux esophagitis.

Symptomatic treatment of heartburn and acid regurgitation in gastroesophageal reflux disease.

Table 1

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 aged 4 and over.

Treatment of duodenal ulcers caused by H. pylori.

The selection of appropriate combination therapy should be based on official national, regional and local guidelines on bacterial resistance. The duration of treatment (7 to 14 days) and the appropriate use of antibacterial agents should also be considered. Treatment should be carried out under the supervision of a physician.

Table 2

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 or applesauce or unsalted water. This mixture should be drunk immediately after preparation or 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 pellets) should not be chewed.

Special patient groups.

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 a small amount of water.

Children.

The drug should be used in children over 1 year of age, whose body weight is 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 for the treatment of duodenal ulcers caused by the presence of H. pylori, under the supervision of a doctor.

Overdose

There is very limited data on the effects of omeprazole overdose in humans. Cases of overdose with omeprazole up to 560 mg have been described in the scientific literature and isolated reports of a single oral dose of 2400 mg omeprazole (120 times the usual recommended clinical dose) have been received. Nausea, vomiting, dizziness, abdominal pain, diarrhoea and headache have been reported. Apathy, depression and confusion have also been reported in isolated cases.

The described symptoms are transient in nature. The rate of elimination does not change (first-order kinetics) with increasing dose. If necessary, symptomatic treatment is required.

Adverse reactions

The most common adverse reactions (1–10% of patients) are headache, abdominal pain, constipation, diarrhea, bloating, and nausea/vomiting.

Severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome, toxic epidermal necrolysis (TEN), drug reaction with eosinophilia and systemic symptoms (DRESS) and acute generalised exanthematous pustulosis (AGEP), have been reported with omeprazole (see section 4.4).

The following adverse drug reactions have been identified or suspected during clinical trials with omeprazole or during post-marketing use. Adverse reactions are classified into groups according to their effect on organs or organ systems.

From the blood and lymphatic system: leukopenia, thrombocytopenia, agranulocytosis, pancytopenia.

Immune system disorders: Hypersensitivity reactions such as fever, angioedema and anaphylaxis