Medically reviewed by Kovalenko Svetlana Olegovna, PharmD. Last updated on 2020-03-13
Attention! Information on this page is intended only for medical professionals! Information is collected in open sources and may contain significant errors! Be careful and double-check all the information on this page!
Top 20 medicines with the same components:
- Treatment of duodenal and gastric ulcer
- Treatment of reflux oesophagitis
- Prophylaxis of reflux oesophagitis
- Eradication of Helicobacter pylori (H. pylori) concurrently given with appropriate antibiotic therapy for treatment of H.pylori-associated ulcers
- Treatment of NSAID-associated benign gastric and duodenal ulcers in patients requiring continued NSAID treatment
- Prophylaxis of NSAID-associated gastric ulcers and duodenal ulcers in patients at risk requiring continued therapy
- Symptomatic gastroesophageal reflux disease
- Zollinger-Ellison syndrome.
Treatment of duodenal ulcer:
The recommended dose is 30 mg once daily for 2 weeks. In patients not fully healed within this time, the medication is continued at the same dose for another two weeks.
Treatment of gastric ulcer:
The recommended dose is 30 mg once daily for 4 weeks. The ulcer usually heals within 4 weeks, but in patients not fully healed within this time, the medication may be continued at the same dose for another 4 weeks.
The recommended dose is 30 mg once daily for 4 weeks. In patients not fully healed within this time, the treatment may be continued at the same dose for another 4 weeks.
Prophylaxis of reflux oesophagitis:
15 mg once daily. The dose may be increased up to 30 mg daily as necessary.
Eradication of Helicobacter pylori:
When selecting appropriate combination therapy consideration should be given to official 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 recommended dose is 30 mg of Lansoprazole OD Chemiphar FasTab twice daily for 7 days in combination with one of the following:
clarithromycin 250-500 mg twice daily + amoxicillin 1 g twice daily
clarithromycin 250 mg twice daily + metronidazole 400-500 mg twice daily
H. pylori eradication rates of up to 90% are obtained when clarithromycin is combined with Lansoprazole OD Chemiphar FasTab and amoxicillin or metronidazole.
Six months after successful eradication treatment, the risk of re infection is low and relapse is therefore unlikely.
Use of a regimen including lansoprazole 30 mg twice daily, amoxicillin 1 g twice daily and metronidazole 400-500 mg twice daily has also been examined. Lower eradication rates were seen using this combination than in regimens involving clarithromycin. It may be suitable for those who are unable to take clarithromycin as part of an eradication therapy, when local resistance rates to metronidazole are low.
Treatment of NSAID associated benign gastric and duodenal ulcers in patients requiring continued NSAID treatment:
30 mg once daily for four weeks. In patients not fully healed the treatment may be continued for another four weeks. For patients at risk or with ulcers that are difficult to heal, a longer course of treatment and/or a higher dose should probably be used.
Prophylaxis of NSAID associated gastric and duodenal ulcers in patients at risk (such as age > 65 or history of gastric or duodenal ulcer) requiring prolonged NSAID treatment:
15 mg once daily. If the treatment fails the dose 30 mg once daily should be used.
Symptomatic gastro-oesophageal reflux disease:
The recommended dose is 15 mg or 30 mg daily. Relief of symptoms is obtained rapidly. Individual adjustment of dosage should be considered. If the symptoms are not relieved within 4 weeks with a daily dose of 30 mg, further examinations are recommended.
The recommended initial dose is 60 mg once daily. The dose should be individually adjusted and the treatment should be continued for as long as necessary. Daily doses of up to 180 mg have been used. If the required daily dose exceeds 120 mg, it should be given in two divided doses.
There is no need for a dose adjustment in patients with impaired renal function.
Patients with moderate or severe liver disease should be kept under regular supervision and a 50% reduction of the daily dose is recommended.
Due to reduced clearance of lansoprazole in the elderly an adjustment of dose may be necessary based on individual requirements. A daily dose of 30 mg should not be exceeded in the elderly unless there are compelling clinical indications.
Paediatric population:Treatment of small children below one year of age should be avoided as available data have not shown beneficial effects in the treatment of gastro-oesophageal reflux disease.
Method of administration
For optimal effect, Lansoprazole OD Chemiphar FasTab should be taken once daily in the morning, except when used for H. pylori eradication when treatment should be twice a day, once in the morning and once in the evening. Lansoprazole OD Chemiphar FasTab should be taken at least 30 minutes before food. Lansoprazole OD Chemiphar FasTab is strawberry flavoured and should be placed on the tongue and gently sucked. The tablet rapidly disperses in the mouth, releasing gastro-resistant microgranules which are swallowed with the patient's saliva. Alternatively, the tablet can be swallowed whole with a drink of water.
The orodispersible tablets can be dispersed in a small amount of water and administered via a naso-gastric tube or oral syringe.
In common with other anti-ulcer therapies, the possibility of malignant gastric tumour should be excluded when treating a gastric ulcer with lansoprazole because lansoprazole can mask the symptoms and delay the diagnosis.
Lansoprazole, like all proton pump inhibitors (PPIs), might increase the counts of bacteria normally present in the gastrointestinal tract. This may increase the risk of gastrointestinal infections caused by bacteria such as Salmonella, Campylobacter and, especially in hospitalized patients, Clostridium difficile.
Co-administration of lansoprazole is not recommended with HIV protease inhibitors for which absorption is dependent on acidic intragastric pH, such as atazanavir and nelfinavir, due to significant reduction in their bioavailability. If co-administration of lansoprazole with HIV protease inhibitors is unavoidable, close clinical monitoring is recommended.
Severe hypomagnesaemia has been reported in patients treated with PPIs like lansoprazole 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 medicinal products that may cause hypomagnesaemia (e.g., diuretics), health care professionals should consider measuring magnesium levels before starting PPI treatment and periodically during treatment.
Increased Chromogranin A (CgA) level may interfere with investigations for neuroendocrine tumours. To avoid this interference, Lansoprazole OD Chemiphar FasTab treatment should be stopped for at least 5 days before CgA measurements. 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.
Daily treatment with any acid-suppressing medications over a prolonged period of time (several years) may lead to malabsorption of cyanocobalamin (vitamin B12) caused by hypo- or achlorhydria. Cyanocobalamin deficiency should be considered in patients with Zollinger-Ellison syndrome and other pathological hypersecretory conditions requiring long-term treatment, individuals with reduced body stores or risk factors for reduced vitamin B12 absorption (such as the elderly) on long-term therapy or if relevant clinical symptoms are observed.
Lansoprazole should be used with caution in patients with moderate and severe hepatic dysfunction.
Decreased gastric acidity due to lansoprazole might be expected to increase gastric counts of bacteria normally present in the gastrointestinal tract. Treatment with lansoprazole may lead to a slightly increased risk of gastrointestinal infections such as Salmonella and Campylobacter.
In patients suffering from gastro-duodenal ulcers, the possibility of H. pylori infection as an etiological factor should be considered.
If lansoprazole is used in combination with antibiotics for eradication therapy of H.pylori, then the instructions for the use of these antibiotics should also be followed.
Because of limited safety data for patients on maintenance treatment for longer than 1 year, regular review of the treatment and a thorough risk/benefit assessment should regularly be performed in these patients.
Very rarely cases of colitis have been reported in patients taking lansoprazole. Therefore, in the case of severe and/or persistent diarrhoea, discontinuation of therapy should be considered.
With the exception of patients treated for the eradication of H. pylori infection, if diarrhoea persists, administration of lansoprazole should be discontinued, due to the possibility of microscopic colitis with thickening of the collagen bundle or infiltration of inflammatory cells noted in the large intestine submucosa. In majority of cases, symptoms of microscopic colitis resolve on discontinuation of lansoprazole.
The treatment for the prevention of peptic ulceration of patients in need of continuous NSAID treatment should be restricted to high risk patients (e.g. previous gastrointestinal bleeding, perforation or ulcer, advanced age, concomitant use of medication known to increase the likelihood of upper GI adverse events [e.g. corticosteroids or anticoagulants], the presence of a serious co-morbidity factor or the prolonged use of NSAID maximum recommended doses).
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 the 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 Lansoprazole OD Chemiphar FasTab. SCLE after previous treatment with a proton pump inhibitor may increase the risk of SCLE with other proton pump inhibitors.
As Lansoprazole OD Chemiphar FasTab contains lactose, patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
Adverse drug reactions such as dizziness, vertigo, visual disturbances and somnolence may occur. Under these conditions the ability to react may be decreased.
Frequencies are defined as common (> 1/100, < 1/10); uncommon (> 1/1,000, < 1/100); rare (> 1/10,000, <1/1,000); very rare (<1/10,000).
Blood and lymphatic system disorders
leucopenia, thrombocytopenia, eosinophilia
pancytopenia , agranulocytosis
Immune system disorders
Metabolism and nutritional disorders
hallucination, insomnia, confusion
Nervous system disorders
paresthesia, vertigo, restlessness, somnolence, tremor
vomiting, nausea, diarrhoea, stomach ache, constipation, flatulence, dry mouth or throat, fundic gland polyps (benign)
pancreatitis, candidiasis of the oesophagus, glossitis, taste disturbances
increase in liver enzyme levels
Skin and subcutaneous tissue disorders
urticaria, itching, rash
petechiae, purpura, erythema multiforme, photosensitivity, hair loss,
Stevens-Johnson syndrome, toxic epidermal necrolysis
subacute cutaneous lupus erythematosus
Musculoskeletal and connective tissue disorders
fracture of the hip, wrist or spine , arthralgia, myalgia,
Renal and urinary disorders
Reproductive system and breast disorders
General disorders and administration site conditions
angioedema, fever, hyperhidrosis,
increase in cholesterol and triglyceride levels, hyponatremia
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at www.mhra.gov.uk/yellowcard.
The effects of overdose on lansoprazole in humans are not known (although the acute toxicity is likely to be low) and, consequently, instruction for treatment cannot be given. However, daily doses of up to 180 mg of lansoprazole orally and up to 90 mg of lansoprazole intravenously have been administered in trials without significant undesirable effects.
In the case of suspected overdose the patient should be monitored. Lansoprazole is not significantly eliminated by haemodialysis. If necessary, gastric emptying, charcoal and symptomatic therapy is recommended.
Pharmacotherapeutic group: Proton pump inhibitors, ATC code: A02BC03
Lansoprazole is a gastric proton pump inhibitor. It inhibits the final stage of gastric acid formation by inhibiting the activity of H+/K+ ATPase of the parietal cells in the stomach. The inhibition is dose-dependent and reversible, and the effect applies to both basal and stimulated secretion of gastric acid. Lansoprazole is concentrated in the parietal cells and becomes active in their acidic environment, whereupon it reacts with the sulphydryl group of H+/K+ATPase causing inhibition of the enzyme activity.
Effect on gastric acid secretion:
Lansoprazole is a specific inhibitor of the parietal cell proton pump. A single oral 30 mg dose of lansoprazole inhibits pentagastrin-stimulated gastric acid secretion by about 80%. After repeated daily administration for seven days, about 90% inhibition of gastric acid secretion is achieved. It has a corresponding effect on the basal secretion of gastric acid. A single oral dose of 30 mg reduces basal secretion by about 70%, and the patients' symptoms are consequently relieved starting from the very first dose. After eight days of repeated administration the reduction is about 85%. A rapid relief of symptoms is obtained by one oro-dispersible tablet (30 mg) daily, and most patients with duodenal ulcer recover within 2 weeks, patients with gastric ulcer and reflux oesophagitis within 4 weeks. By reducing gastric acidity, lansoprazole creates an environment in which appropriate antibiotics can be effective against H. pylori.
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.
Lansoprazole is a racemate of two active enantiomers that are biotransformed into the active form in the acidic environment of the parietal cells. As lansoprazole is rapidly inactivated by gastric acid, it is administered orally in enteric-coated form(s) for systemic absorption.
Absorption and distribution
Lansoprazole exhibits high (80-90%) bioavailability with a single dose. Peak plasma levels occur within 1.5 to 2.0 hours. Intake of food slows the absorption rate of lansoprazole and reduces the bioavailabilty by about 50%. The plasma protein binding is 97%.
Studies have shown that oro-dispersible tablets dispersed in a small amount of water and given via syringe directly into the mouth or administered via naso-gastric tube result in equivalent AUC compared to the usual mode of administration.
Biotransformation and elimination
Lansoprazole is extensively metabolised by the liver and the metabolites are excreted by both the renal and biliary route. The metabolism of lansoprazole is mainly catalysed by the enzyme CYP2C19. The enzyme CYP3A4 also contributes to the metabolism. The plasma elimination half-life ranges from 1 to 2 hours following single or multiple doses in healthy subjects. There is no evidence of accumulation following multiple doses in healthy subjects. Sulphone, sulphide and 5-hydroxyl derivatives of lansoprazole have been identified in plasma. These metabolites have very little or no antisecretory activity.
A study with 14C labelled lansoprazole indicated that approximately one-third of the administered radiation was excreted in the urine and two-thirds was recovered in the faeces.
Pharmacokinetics in elderly patients
The clearance of lansoprazole is decreased in the elderly, with elimination half-life increased approximately 50% to 100%. Peak plasma levels were not increased in the elderly.
Pharmacokinetics in paediatric patients
The evaluation of the pharmacokinetics in children aged 1 -17 years of age showed a similar exposure as compared to adults with doses of 15 mg for those below 30 kg of weight and 30 mg for those above. The investigation of a dose of 17 mg/m2 body surface or 1 mg/kg body weight also resulted in comparable exposure of lansoprazole in children aged 2-3 months up to one year of age compared to adults.
Higher exposure to lansoprazole in comparison to adults has been seen in infants below the age of 2-3 months with doses of both 1.0 mg/kg and 0.5 mg/kg body weight given as a single dose
Pharmacokinetics in hepatic insufficiency
The exposure of lansoprazole is doubled in patients with mild hepatic impairment and much more increased in patients with moderate and severe hepatic impairment.
CYP2C19 poor metabolisers
CYP2C19 is subject to genetic polymorphism and 2-6 % of the population, called poor metabolisers (PMs), are homozygote for a mutant CYP2C19 allele and therefore lacks a functional CYP2C19 enzyme. The exposure of lansoprazole is several-fold higher in PMs than in extensive metabolisers (EMs).
Non-clinical data reveal no special hazards for humans based on conventional studies of safety pharmacology, repeated dose toxicity, toxicity to reproduction or genotoxicity.
In two rat carcinogenicity studies, lansoprazole produced dose-related gastric ECL cell hyperplasia and ECL cell carcinoids associated with hypergastrinaemia due to inhibition of acid secretion. Intestinal metaplasia was also observed, as were Leydig cell hyperplasia and benign Leydig cell tumours. After 18 months of treatment retinal atrophy was observed. This was not seen in monkeys, dogs or mice.
In mouse carcinogenicity studies dose-related gastric ECL cell hyperplasia developed as well as liver tumours and adenoma of rete testis.
The clinical relevance of these findings is unknown.
No special requirements.
Any unused medicinal product or waste material should be disposed of in accordance with local requirements.