Aciloc 20 mg capsules are indicated in:
Adults
• Treatment of duodenal ulcers
• Prevention of relapse of duodenal ulcers
• Treatment of gastric ulcers
• Prevention of relapse of gastric ulcers
• In combination with appropriate antibiotics, Helicobacter pylori (H. pylori) eradication in peptic ulcer
disease

• Treatment of NSAID-associated gastric and duodenal ulcers
• Prevention of NSAID-associated gastric and duodenal ulcers in patients at risk
• Treatment of reflux oesophagitis
• Long-term management of patients with healed reflux oesophagitis
• Treatment of symptomatic gastro-oesophageal reflux disease
• Treatment of Zollinger-Ellison syndrome
Paediatric use
Children over 1 year of age and ≥ 10 kg
• Treatment of reflux oesophagitis

• Symptomatic treatment of heartburn and acid regurgitation in gastro-oesophageal reflux disease
Children and adolescents over 4 years of age
• In combination with antibiotics in treatment of duodenal ulcer caused by H. pylori

Posology
Adults
Treatment of duodenal ulcers
The recommended dose in patients with an active duodenal ulcer is Aciloc 20 mg once daily. In most
patients healing occurs within two weeks. For those patients who may not be fully healed after the initial
course, healing usually occurs during a further two weeks treatment period. In patients with poorly
responsive duodenal ulcer Aciloc 40 mg once daily is recommended and healing is usually achieved
within four weeks.

Prevention of relapse of duodenal ulcers
For the prevention of relapse of duodenal ulcer in H. pylori negative patients or when H.
pylori eradication is not possible the recommended dose is Aciloc 20 mg once daily. In some patients a
daily dose of 10 mg may be sufficient. In case of therapy failure, the dose can be increased to 40 mg.

Treatment of gastric ulcers
The recommended dose is Aciloc 20 mg once daily. In most patients healing occurs within four weeks.
For those patients who may not be fully healed after the initial course, healing usually occurs during a
further four weeks treatment period. In patients with poorly responsive gastric ulcer Aciloc 40 mg once
daily is recommended and healing is usually achieved within eight weeks.

Prevention of relapse of gastric ulcers

For the prevention of relapse in patients with poorly responsive gastric ulcer the recommended dose is
Aciloc 20 mg once daily. If needed the dose can be increased to Aciloc 40 mg once daily.

H. pylori eradication in peptic ulcer disease

For the eradication of H. pylori the selection of antibiotics should consider the individual patient's drug
tolerance, and should be undertaken in accordance with national, regional and local resistance patterns and
treatment guidelines.

• Aciloc 20 mg + clarithromycin 500 mg + amoxicillin 1,000 mg, each twice daily for one week, or
• Aciloc 20 mg + clarithromycin 250 mg (alternatively 500 mg) + metronidazole 400 mg (or 500 mg or
tinidazole 500 mg), each twice daily for one week or
• Aciloc 40 mg once daily with amoxicillin 500 mg and metronidazole 400 mg (or 500 mg or tinidazole
500 mg), both three times a day for one week.

In each regimen, if the patient is still H. pylori positive, therapy may be repeated.

Treatment of NSAID-associated gastric and duodenal ulcers

For the treatment of NSAID-associated gastric and duodenal ulcers, the recommended dose is Aciloc 20
mg once daily. In most patients healing occurs within four weeks. For those patients who may not be fully
healed after the initial course, healing usually occurs during a further four weeks treatment period.

Prevention of NSAID-associated gastric and duodenal ulcers in patients at risk

For the prevention of NSAID-associated gastric ulcers or duodenal ulcers in patients at risk (age> 60,
previous history of gastric and duodenal ulcers, previous history of upper GI bleeding) the recommended
dose is Aciloc 20 mg once daily.

Treatment of reflux oesophagitis
The recommended dose is Aciloc 20 mg once daily. In most patients healing occurs within four weeks.
For those patients who may not be fully healed after the initial course, healing usually occurs during a
further four weeks treatment period.

In patients with severe oesophagitis Aciloc 40 mg once daily is recommended and healing is usually
achieved within eight weeks.

Long-term management of patients with healed reflux oesophagitis

For the long-term management of patients with healed reflux oesophagitis the recommended dose is
Aciloc 10 mg once daily. If needed, the dose can be increased to Aciloc 20-40 mg once daily.

Treatment of symptomatic gastro-oesophageal reflux disease

The recommended dose is Aciloc 20 mg daily. Patients may respond adequately to 10 mg daily, and
therefore individual dose adjustment should be considered.

If symptom control has not been achieved after four weeks treatment with Aciloc 20 mg daily, further
investigation is recommended.

Treatment of Zollinger-Ellison syndrome

In patients with Zollinger-Ellison syndrome the dose should be individually adjusted and treatment
continued as long as clinically indicated. The recommended initial dose is Aciloc 60 mg daily. All
patients with severe disease and inadequate response to other therapies have been effectively controlled
and more than 90% of the patients maintained on doses of Aciloc 20-120 mg daily. When dose exceed
Aciloc 80 mg daily, the dose should be divided and given twice daily.

Paediatric population

Children over 1 year of age and ≥ 10 kg

Treatment of reflux oesophagitis

Symptomatic treatment of heartburn and acid regurgitation in gastro-oesophageal reflux disease

The posology recommendations are as follows:

Age Weight Posology

Reflux oesophagitis: The treatment time is 4-8 weeks.

Symptomatic treatment of heartburn and acid regurgitation in gastro-oesophageal reflux disease: The
treatment time is 2–4 weeks. If symptom control has not been achieved after 2–4 weeks the patient should
be investigated further.

Children and adolescents over 4 years of age

Treatment of duodenal ulcer caused by H. pylori

When selecting appropriate combination therapy, consideration should be given to official national,
regional and local guidance regarding bacterial resistance, duration of treatment (most commonly 7 days
but sometimes up to 14 days), and appropriate use of antibacterial agents.

The treatment should be supervised by a specialist.

The posology recommendations are as follows:

Special populations
Renal impairment
Dose adjustment is not needed in patients with impaired renal function (see section 5.2).
Hepatic impairment
In patients with impaired hepatic function a daily dose of 10–20 mg may be sufficient (see section 5.2).
Elderly
Dose adjustment is not needed in the elderly (see section 5.2).

In the presence of any alarm symptom (e.g. significant unintentional weight loss, recurrent vomiting,
dysphagia, haematemesis or melena) and when gastric ulcer is suspected or present, malignancy
should be excluded, as treatment may alleviate symptoms and delay diagnosis.

Co-administration of atazanavir with proton pump inhibitors is not recommended (see section 4.5). If
the combination of atazanavir with a proton pump inhibitor is judged unavoidable, close clinical
monitoring (e.g virus load) is recommended in combination with an increase in the dose of atazanavir
to 400 mg with 100 mg of ritonavir; omeprazole 20 mg should not be exceeded.

Omeprazole, as all acid-blocking medicines, may reduce the absorption of vitamin
B12 (cyanocobalamin) due to hypo- or achlorhydria. This should be considered in patients with
reduced body stores or risk factors for reduced vitamin B12absorption on long-term therapy.

Omeprazole is a CYP2C19 inhibitor. When starting or ending treatment with omeprazole, the potential
for interactions with drugs metabolised through CYP2C19 should be considered. An interaction is
observed between clopidogrel and omeprazole (see section 4.5). The clinical relevance of this
interaction is uncertain. As a precaution, concomitant use of omeprazole and clopidogrel should be
discouraged.

Severe hypomagnesaemia has been reported in patients treated with proton pump inhibitors (PPIs) like
omeprazole for at least three months, and in most cases for a year. Serious manifestations of
hypomagnesaemia such as fatigue, tetany, delirium, convulsions, dizziness and ventricular arrhythmia
can occur but they may begin insidiously and be overlooked. In most affected patients,
hypomagnesaemia improved after magnesium replacement and discontinuation of the PPI.

For patients expected to be on prolonged treatment or who take PPIs with digoxin or drugs that may
cause hypomagnesaemia (e.g. diuretics), healthcare professionals should consider measuring
magnesium levels before starting PPI treatment and periodically during treatment.

Proton pump inhibitors, especially if used in high doses and over long durations (>1 year), may
modestly increase the risk of hip, wrist and spine fracture, predominantly in the elderly or in presence
of other recognised risk factors. Observational studies suggest that proton pump inhibitors may
increase the overall risk of fracture by 10-40%. Some of this increase may be due to other risk factors.
Patients at risk of osteoporosis should receive care according to current clinical guidelines and they
should have an adequate intake of vitamin D and calcium.

Subacute cutaneous lupus erythematosus (SCLE)

Proton pump inhibitors are associated with very infrequent cases of SCLE. If lesions occur, especially
in sun-exposed areas of the skin, and if accompanied by arthralgia, the patient should seek medical
help promptly and the health care professional should consider stopping Aciloc . SCLE after previous
treatment with a proton pump inhibitor may increase the risk of SCLE with other proton pump
inhibitors.

Interference with laboratory tests

Increased Chromogranin A (CgA) level may interfere with investigations for neuroendocrine tumours.
To avoid this interference, omeprazole treatment should be stopped for at least 5 days before CgA
measurements (see section 5.1). If CgA and gastrin levels have not returned to reference range after
initial measurement, measurements should be repeated 14 days after cessation of proton pump
inhibitor treatment.

Some children with chronic illnesses may require long-term treatment although it is not recommended.

Aciloc contains lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp
lactase deficiency or glucose-galactose malabsorption should not take this medicine.

Treatment with proton pump inhibitors may lead to slightly increased risk of gastrointestinal infections
such as Salmonellaand Campylobacter and, in hospitalised patients, possibly also Clostridium
difficile (see section 5.1).

As in all long-term treatments, especially when exceeding a treatment period of 1 year, patients should
be kept under regular surveillance.

Effects of omeprazole on the pharmacokinetics of other active substances
Active substances with pH dependent absorption

The decreased intragastric acidity during treatment with omeprazole might increase or decrease the
absorption of active substances with a gastric pH dependent absorption.

Nelfinavir, atazanavir
The plasma levels of nelfinavir and atazanavir are decreased in case of co-administration with
omeprazole.

Concomitant administration of omeprazole with nelfinavir is contraindicated (see section 4.3). Coadministration
of omeprazole (40 mg once daily) reduced mean nelfinavir exposure by ca. 40% and the
mean exposure of the pharmacologically active metabolite M8 was reduced by ca. 75 –90%. The
interaction may also involve CYP2C19 inhibition.

Concomitant administration of omeprazole with atazanavir is not recommended (see section 4.4).
Concomitant administration of omeprazole (40 mg once daily) and atazanavir 300 mg/ritonavir 100 mg to
healthy volunteers resulted in a 75% decrease of the atazanavir exposure. Increasing the atazanavir dose to
400 mg did not compensate for the impact of omeprazole on atazanavir exposure. The co-administration
of omeprazole (20 mg once daily) with atazanavir 400 mg/ritonavir 100 mg to healthy volunteers resulted
in a decrease of approximately 30% in the atazanavir exposure as compared to atazanavir 300
mg/ritonavir 100 mg once daily.

Digoxin
Concomitant treatment with omeprazole (20 mg daily) and digoxin in healthy subjects increased the
bioavailability of digoxin by 10%. Digoxin toxicity has been rarely reported. However caution should be
exercised when omeprazole is given at high doses in elderly patients. Therapeutic drug monitoring of
digoxin should be then be reinforced.

Clopidogrel
Results from studies in healthy subjects have shown a pharmacokinetic (PK)/pharmacodynamic (PD)
interaction between clopidogrel (300 mg loading dose/75 mg daily maintenance dose) and omeprazole (80
mg p.o. daily) resulting in a decreased exposure to the active metabolite of clopidogrel by an average of
46% and a decreased maximum inhibition of (ADP induced) platelet aggregation by an average of 16%.
Inconsistent data on the clinical implications of a PK/PD interaction of omeprazole in terms of major
cardiovascular events have been reported from both observational and clinical studies. As a precaution,
concomitant use of omeprazole and clopidogrel should be discouraged (see section 4.4).

Other active substances
The absorption of posaconazole, erlotinib, ketoconazole and itraconazole is significantly reduced and thus
clinical efficacy may be impaired. For posaconazole and erlotinib concomitant use should be avoided.
Active substances metabolised by CYP2C19

Omeprazole is a moderate inhibitor of CYP2C19, the major omeprazole metabolising enzyme. Thus, the
metabolism of concomitant active substances also metabolised by CYP2C19, may be decreased and the
systemic exposure to these substances increased. Examples of such drugs are R-warfarin and other
vitamin K antagonists, cilostazol, diazepam and phenytoin.

Cilostazol
Omeprazole, given in doses of 40 mg to healthy subjects in a cross-over study, increased Cmax and AUC
for cilostazol by 18% and 26% respectively, and one of its active metabolites by 29% and 69%
respectively.

Phenytoin
Monitoring phenytoin plasma concentration is recommended during the first two weeks after initiating
omeprazole treatment and, if a phenytoin dose adjustment is made, monitoring and a further dose
adjustment should occur upon ending omeprazole treatment.

Unknown mechanism

Saquinavir
Concomitant administration of omeprazole with saquinavir/ritonavir resulted in increased plasma levels
up to approximately 70% for saquinavir associated with good tolerability in HIV-infected patients.

Tacrolimus
Concomitant administration of omeprazole has been reported to increase the serum levels of tacrolimus. A
reinforced monitoring of tacrolimus concentrations as well as renal function (creatinine clearance) should
be performed, and dosage of tacrolimus adjusted if needed.

Methotrexate
When given together with proton-pump inhibitors, methotrexate levels have been reported to increase in
some patients. In high-dose methotrexate administration a temporary withdrawal of omeprazole may need
to be considered.

Effects of other active substances on the pharmacokinetics of omeprazole
Inhibitors of CYP2C19 and/or CYP3A4

Since omeprazole is metabolised by CYP2C19 and CYP3A4, active substances known to inhibit
CYP2C19 or CYP3A4 (such as clarithromycin and voriconazole) may lead to increased omeprazole
serum levels by decreasing omeprazole's rate of metabolism. Concomitant voriconazole treatment resulted
in more than doubling of the omeprazole exposure. As high doses of omeprazole have been well-tolerated
adjustment of the omeprazole dose is not generally required. However, dose adjustment should be
considered in patients with severe hepatic impairment and if long-term treatment is indicated.

Inducers of CYP2C19 and/or CYP3A4
Active substances known to induce CYP2C19 or CYP3A4 or both (such as rifampicin and St John's wort)
may lead to decreased omeprazole serum levels by increasing omeprazole's rate of metabolism.

Pregnancy
Results from three prospective epidemiological studies (more than 1000 exposed outcomes) indicate no
adverse effects of omeprazole on pregnancy or on the health of the foetus/newborn child. Omeprazole can
be used during pregnancy.

Breast-feeding
Omeprazole is excreted in breast milk but is not likely to influence the child when therapeutic doses are used.

Fertility
Animal studies with the racemic mixture omeprazole, given by oral administration do not indicate effects
with respect to fertility.

Aciloc is not likely to affect the ability to drive or use machines. Adverse drug reactions such as dizziness
and visual disturbances may occur (see section 4.8). If affected, patients should not drive or operate
machinery.

Summary of the safety profile
The most common side effects (1-10% of patients) are headache, abdominal pain, constipation, diarrhoea,
flatulence and nausea/vomiting.
Tabulated list of adverse reactions
The following adverse drug reactions have been identified or suspected in the clinical trials programme
for omeprazole and post-marketing. None was found to be dose-related. Adverse reactions listed below
are classified according to frequency and System Organ Class (SOC). Frequency categories are defined
according to the following convention: Very common (≥ 1/10), Common (≥ 1/100 to < 1/10), Uncommon
(≥ 1/1,000 to < 1/100), Rare (≥ 1/10,000 to < 1/1,000), Very rare (< 1/10,000), Not known (cannot be
estimated from the available data).

Paediatric population
The safety of omeprazole has been assessed in a total of 310 children aged 0 to 16 years with acid-related
disease. There are limited long-term safety data from 46 children who received maintenance therapy of
omeprazole during a clinical study for severe erosive oesophagitis for up to 749 days. The adverse event

profile was generally the same as for adults in short- as well as in long-term treatment. There are no longterm
data regarding the effects of omeprazole treatment on puberty and growth.
 

There is limited information available on the effects of overdoses of omeprazole in humans. In the
literature, doses of up to 560 mg have been described, and occasional reports have been received when
single oral doses have reached up to 2,400 mg omeprazole (120 times the usual recommended clinical
dose). Nausea, vomiting, dizziness, abdominal pain, diarrhoea and headache have been reported. Also
apathy, depression and confusion have been described in single cases.

The symptoms described have been transient, and no serious outcome has been reported. The rate of
elimination was unchanged (first order kinetics) with increased doses. Treatment, if needed, is
symptomatic.

Pharmacotherapeutic group: Drugs for acid-related disorders, proton pump inhibitors, ATC code:
A02BC01

Mechanism of action
Omeprazole, a racemic mixture of two enantiomers reduces gastric acid secretion through a highly
targeted mechanism of action. It is a specific inhibitor of the acid pump in the parietal cell. It is rapidly
acting and provides control through reversible inhibition of gastric acid secretion with once daily dosing.

Omeprazole is a weak base and is concentrated and converted to the active form in the highly acidic
environment of the intracellular canaliculi within the parietal cell, where it inhibits the enzyme H+ K+-
ATPase - the acid pump. This effect on the final step of the gastric acid formation process is dosedependent
and provides for highly effective inhibition of both basal acid secretion and stimulated acid
secretion, irrespective of stimulus.

Pharmacodynamic effects
All pharmacodynamic effects observed can be explained by the effect of omeprazole on acid secretion.
Effect on gastric acid secretion

Oral dosing with omeprazole once daily provides for rapid and effective inhibition of daytime and nighttime
gastric acid secretion with maximum effect being achieved within 4 days of treatment. With
omeprazole 20 mg, a mean decrease of at least 80% in 24-hour intragastric acidity is then maintained in
duodenal ulcer patients, with the mean decrease in peak acid output after pentagastrin stimulation being
about 70% 24 hours after dosing.

Oral dosing with omeprazole 20 mg maintains an intragastric pH of ≥ 3 for a mean time of 17 hours of the
24-hour period in duodenal ulcer patients.

As a consequence of reduced acid secretion and intragastric acidity, omeprazole dose-dependently
reduces/normalizes acid exposure of the oesophagus in patients with gastro-oesophageal reflux disease.

The inhibition of acid secretion is related to the area under the plasma concentration-time curve (AUC) of
omeprazole and not to the actual plasma concentration at a given time.

No tachyphylaxis has been observed during treatment with omeprazole.

Effect on H. pylori
H. pylori is associated with peptic ulcer disease, including duodenal and gastric ulcer disease. H. pylori is
a major factor 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 developing gastric cancer.

Eradication of H. pylori with omeprazole and antimicrobials is associated with, high rates of healing and
long-term remission of peptic ulcers.

Dual therapies have been tested and found to be less effective than triple therapies. They could, however,
be considered in cases where known hypersensitivity precludes use of any triple combination.

Other effects related to acid inhibition

During long-term treatment gastric glandular cysts have been reported in a somewhat increased frequency.
These changes are a physiological consequence of pronounced inhibition of acid secretion, are benign and
appear to be reversible.

Decreased gastric acidity due to any means including proton pump inhibitors, increases gastric counts of
bacteria normally present in the gastrointestinal tract. Treatment with acid-reducing drugs may lead to
slightly increased risk of gastrointestinal infections such as Salmonella and Campylobacter and, in
hospitalised patients, possibly also Clostridium difficile.

During treatment with antisecretory medicinal products, serum gastrin increases in response to the
decreased acid secretion. Also CgA increases due to decreased gastric acidity. The increased CgA level
may interfere with investigations for neuroendocrine tumours. Available published evidence suggests that
proton pump inhibitors should be discontinued between 5 days and 2 weeks prior to CgA measurements.
This is to allow CgA levels that might be spuriously elevated following PPI treatment to return to
reference range.

An increased number of ECL cells possibly related to the increased serum gastrin levels, have been
observed in some patients (both children and adults) during long term treatment with omeprazole. The
findings are considered to be of no clinical significance.

Paediatric population
In a non-controlled study in children (1 to 16 years of age) with severe reflux oesophagitis, omeprazole at
doses of 0.7 to 1.4 mg/kg improved oesophagitis level in 90% of the cases and significantly reduced reflux
symptoms. In a single-blind study, children aged 0–24 months with clinically diagnosed gastrooesophageal
reflux disease were treated with 0.5, 1.0 or 1.5 mg omeprazole/kg. The frequency of
vomiting/regurgitation episodes decreased by 50% after 8 weeks of treatment irrespective of the dose.

Eradication of H. pylori in children
A randomised, double blind clinical study (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 age 4 years old and above with gastritis: H. pylori eradication rate: 74.2%
(23/31 patients) with omeprazole + amoxicillin + clarithromycin versus 9.4% (3/32 patients) with
amoxicillin + clarithromycin. However, there was no evidence of any clinical benefit with respect to
dyspeptic symptoms. This study does not support any information for children aged less than 4

Absorption
Omeprazole and omeprazole magnesium are acid labile and are therefore administered orally as
enteric-coated granules in capsules or tablets. Absorption of omeprazole is rapid, with peak plasma
levels occurring approximately 1-2 hours after dose. Absorption of omeprazole takes place in the
small intestine and is usually completed within 3-6 hours. Concomitant intake of food has no influence
on the bioavailability. The systemic availability (bioavailability) from a single oral dose of omeprazole
is approximately 40%. After repeated once-daily administration, the bioavailability increases to about 60%.

Distribution
The apparent volume of distribution in healthy subjects is approximately 0.3 l/kg body weight.
Omeprazole is 97% plasma protein bound.

Biotransformation
Omeprazole is completely metabolised by the cytochrome P450 system (CYP). The major part of its
metabolism is dependent on the polymorphically expressed CYP2C19, responsible for the formation
of hydroxyomeprazole, the major metabolite in plasma. The remaining part is dependent on another
specific isoform, CYP3A4, responsible for the formation of omeprazole sulfone. As a consequence of
high affinity of omeprazole to CYP2C19, there is a potential for competitive inhibition and metabolic
drug-drug interactions with other substrates for CYP2C19. However, due to low affinity to CYP3A4,
omeprazole has no potential to inhibit the metabolism of other CYP3A4 substrates. In addition,
omeprazole lacks an inhibitory effect on the main CYP enzymes.

Approximately 3% of the Caucasian population and 15-20% of Asian populations lack a functional
CYP2C19 enzyme and are called poor metabolisers. In such individuals the metabolism of omeprazole
is probably mainly catalysed by CYP3A4. After repeated once-daily administration of 20 mg
omeprazole, the mean AUC was 5 to 10 times higher in poor metabolisers than in subjects having a
functional CYP2C19 enzyme (extensive metabolisers). Mean peak plasma concentrations were also
higher, by 3 to 5 times. These findings have no implications for the posology of omeprazole.

Elimination
The plasma elimination half-life of omeprazole is usually shorter than one hour both after single and
repeated oral once-daily dosing. Omeprazole is completely eliminated from plasma between doses
with no tendency for accumulation during once-daily administration. Almost 80% of an oral dose of
omeprazole is excreted as metabolites in the urine, the remainder in the faeces, primarily originating
from bile secretion.

Linearity/non-linearity
The AUC of omeprazole increases with repeated administration. This increase is dose-dependent and
results in a non-linear dose-AUC relationship after repeated administration. This time- and dosedependency
is due to a decrease of first pass metabolism and systemic clearance probably caused by
an inhibition of the CYP2C19 enzyme by omeprazole and/or its metabolites (e.g. the sulfone).

No metabolite has been found to have any effect on gastric acid secretion.
Special populations

Hepatic impairment
The metabolism of omeprazole in patients with liver dysfunction is impaired, resulting in an increased
AUC. Omeprazole has not shown any tendency to accumulate with once daily dosing.

Renal impairment
The pharmacokinetics of omeprazole, including systemic bioavailability and elimination rate, are
unchanged in patients with reduced renal function.

Elderly
The metabolism rate of omeprazole is somewhat reduced in elderly subjects (75-79 years of age).

Paediatric population
During treatment with the recommended doses to children from the age of 1 year, similar plasma
concentrations were obtained as compared to adults. In children younger than 6 months, clearance
of omeprazole is low due to low capacity to metabolize omeprazole.

Gastric ECL-cell hyperplasia and carcinoids, have been observed in life-long studies in rats treated with
omeprazole. These changes are the result of sustained hypergastrinaemia secondary to acid inhibition.
Similar findings have been made after treatment with H2-receptor antagonists, proton pump inhibitors and
after partial fundectomy. Thus, these changes are not from a direct effect of any individual active
substance.

Mannitol

Disodium Hydrogen orthosphosphate

Sodium Lauryl Sulphate

HPMC phthalate HP55

HPMC E5

Cetyl Alcohol

Sucrose

Calcium Carbonate

TiO2

Not applicable.

Do not store above 30°C
Protect from light. Keep out of reach of children

Primary :
Immediate container: Alu-Alu printed blister strip.
Secondary:
Outer individual carton
PIL

No special requirements