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Pantoprazole sodium sesquihydrate 22.6mg eq. to pantoprazole 20mg
Each delayed –release tablet contain:
Pantoprazole sodium sesquihydrate 22.6mg eq. to pantoprazole 20mg
Sodium Carbonate, Mannitol, Crospovidone, Povidone K90, Magnesium stearate, Hydroxy Methyl Cellulose, Povidone K25, Titanium Dioxide, Iron Oxide Yellow, Propylene Glycol, Methacrylic acid copolymer, Triethyl Citrate.
Delayed -release tablet
Adults and adolescents 12 years of age and above
Symptomatic gastro-oesophageal reflux disease.
For long-term management and prevention of relapse in reflux oesophagitis.
Adults
Prevention of gatroduodenal ulcers induced by non-selective non-steroidal anti-inflammatory drugs (NSAIDs) in patients at risk with a need for continuous NSAID treatment
Tablets should not be chewed or crushed, and should be swallowed whole 1 hour before a meal with some water.
Recommended dose:
Adults and adolescents 12 years of age and above
Symptomatic gastro-oesophageal reflux disease
The recommended oral dosage is one delayed releasetabletPantotrazolin 20 mg per day. Symptom relief is generally accomplished within 2-4 weeks. If this is not sufficient, symptom relief will normally be achieved within a further 4 weeks. When symptom relief has been achieved, reoccurring symptoms can be controlled using an on-demand regimen of 20 mg once daily, when required. A switch to continuous therapy may be considered in case satisfactory symptom control cannot be maintained with on-demand treatment.
Long-term management and prevention of relapse in reflux oesophagitis
For long-term management, a maintenance dose of one delayed releasetabletPantotrazolin 20 mg per day is recommended, increasing to 40 mg pantotrazolin per day if a relapse occurs. Pantotrazolin 40 mg is available for this case. After healing of the relapse the dose can be reduced again to 20 mg pantotrazolin.
Adults:
Prevention of gastroduodenal ulcers induced by non-selective non-steroidal anti-inflammatory drugs (NSAIDs) in patients at risk with a need for continuous NSAID treatment.
The recommended oral dose is one delayed releasetabletPantotrazolin 20 mg per day.
Special populations
Children below 12 years of age:
Pantotrazolin is not recommended for use in children below 12 years of age due to limited data on safety and efficacy in this age group
Hepatic impairment
A daily dose of 20 mg pantotrazolin should not be exceeded in patients with severe aver impairment.
Renal impairment
No dose adjustment is necessary in patients with impaired renal function.
Elderly
No dose adjustment is necessary in elderly patients
Pharmacotherapeutic group: Proton Pump Inhibitors., ATC code: A02BC02.
Mechanism of action
Pantoprazole is a substituted benzimidazole, which inhibits the secretion of hydrochloric acid in the stomach by specific blockade of the proton pumps of the parietal cells.
Pantoprazole is converted to its active form in the acidic environment in the parietal cells where it inhibits the H+, K+-ATPase enzyme, i.e. the final stage in the production of hydrochloric acid in the stomach. The inhibition is dose-dependent and affects both basal and stimulated acid secretion. In most patients, freedom from symptoms is achieved within two weeks. As with other proton pump inhibitors and H2 receptor inhibitors, treatment with pantoprazole reduces acidity in the stomach and thereby increases gastrin in proportion to the reduction in acidity. The increase in gastrin is reversible. Since pantoprazole binds to the enzyme distal to the cell receptor level, it can inhibit hydrochloric acid secretion independently of the stimulation by other substances (acetylcholine, histamine, gastrin).
Pantoprazole has the same effect whether administered orally or intravenously.
The fasting gastrin values increase under pantoprazole. On short-term use, in most cases they do not exceed the upper limit of normal. During long-term treatment, gastrin levels double in most cases. An excessive increase, however, occurs only in isolated cases. As a result, a mild to moderate increase in the number of specific endocrine (ECL) cells in the stomach is observed in a minority of cases during long term treatment (simple to adenomatoid hyperplasia). However, according to thestudiesconducted so far, the formation of carcinoid precursors (atypical hyperplasia) or gastric carcinoids as were found in animal experiments (see Section 5.3) have not been observed in humans.
An influence of a long term treatment with pantoprazole exceeding one year cannot be completely ruled out on endocrine parameters of the thyroid according to results in animal studies
Absorption:
Pantoprazole is rapidly absorbed and the maximal plasma concentration is achieved even after one single 20 mg oral dose. On average at about 2.0 h - 2.5 h p.a. the maximum serum concentrations of about 1-1.5 µg/ml are achieved and these values remain constant after multiple administration. Pharmacokinetics do not vary after single or repeated administration. In the dose range of 10 to 80 mg, the plasma kinetics of pantoprazole are linear after both oral and intravenous administration.
The absolute bioavailability from the tablet was found to be about 77 %. Concomitant intake of food had no influence on AUC, maximum serum concentration and thus bioavailability. Only the variability of the lag-time will be increased by concomitant food intake.
Distribution:
Pantoprazole's serum protein binding is about 98%. Volume of distribution is about 0.15 1/kg.
Elimination:
The substance is almost exclusively metabolized in the liver. The main metabolic pathway is demethylation by CYP2C19 with subsequent sulphateconjugation, other metabolic pathways include oxidation by CYP3A4. Terminal half-life is about 1 hour and clearance is about 0.1 l/h/kg. There were a few cases of subjects with delayed elimination. Because of the specific binding of pantoprazole to the proton pumps of the parietal cell the elimination half-life does not correlate with the much longer duration of action (inhibition of acid secretion).
Renal elimination represents the major route of excretion (about 80%) for the metabolites of pantoprazole, the rest is excreted with the faeces. The main metabolite in both the serum and urine is desmethylpantoprazole which is conjugated with sulphate. The half-Life of the main metabolite (about 1.5 hours) is not much longer than that of pantoprazole.
Characteristics in patients/special groups of subjects
Approximately 3 % of the European population lacks a functional CYP2C19 enzyme and are called poor metabolisers. In these individuals the metabolism of pantoprazole is probably mainly catalysed by CYP3A4. After a single-dose administration of 40 mg pantoprazole, the mean area under the plasma concentration-time curve was approximately 6 times higher in poor metabolisers than in subjects having a functional CYP2C19 enzyme (extensive metabolisers). Mean peak plasma concentrations were increased by about 60%. These findings have no implications for the posology of pantoprazole.
No dose reduction is requested when pantoprazole is administered to patients with impaired kidney function (including dialysis patients). As with healthy subjects, pantoprazole's half-life is short. Only very small amounts of pantoprazole can be dialyzed. Although the main metabolite has a moderately delayed half-life (2 - 3h), excretion is still rapid and thus accumulation does not occur.
Although for patients with liver cirrhosis (classes A and B according to Child) the half-life values increased to between 3 and 6 h and the AUC values increased by a factor of 3 - 5, the maximum serum concentration only increased slightly by a factor of 1.3 compared with healthy subjects.
A slight increase in AUC and Cmax in elderly volunteers compared with younger counterparts is also not clinically relevant.
Children
Following administration of single oral doses of 20 or 40 mg pantoprazole to children aged 5 – 16 years AUC and Cmax were in the range of corresponding values in adults.
Following administration of single i.v. doses of 0.8 or 1.6 mg/kg pantoprazole to children aged 2-16 years there was no significant association between pantoprazole clearance and age or weight. AUC and volume of distribution were in accordance with data from adults.
Several published observational studies suggest that proton pump inhibitor (PPI) therapy may be associated with an increased risk for osteoporosis-related fractures of the hip,wrist,or spine. The risk of fracture wase increased in patients who received high-dose, defined as multiple daily doses, and long-term PPI therapy (a year or longer). Patients should use the lowest dose and shortest duration of PPI therapy appropriate to the condition being treated. Patients at risk for osteoporosis-related fractures should be managed according to the established treatment guidelines
• Prescription proton pump inhibitor (PPI) drugs may cause low serum magnesium levels (hypomagnesemia) if taken for prolonged periods of time (in most cases, longer than one year), magnesium supplementation alone did not improve low serum magnesium levels and the PPI had to be discontinued.
• Low serum magnesium levels can result in serious adverse events including muscle spasm (tetany), irregular heartbeat (arrhythmias), and convulsions (seizures); however, patients do not always have these symptoms. Treatment of hypomagnesemia generally requires magnesium supplements. Treatment in patients taking a PPI and who have hypomagnesemia may also require stopping the PPI
If there is some problem in tolerate some kind of sugar please ask doctor firstbefore taking these drug
Hepatic impairment
In patients with severe liver impairment the liver enzymes should be monitored regularly during treatment with pantotrazolin, particularly on long-term use. In the case of a rise of the liver enzymes the treatment should be discontinued.
Co-administration with NSAIDs
The use of Pantotrazolin 20 mg as a preventive of gastroduodenal ulcers induced by non-selective non-steroidal anti-inflammatory drugs (NSAIDs) should be restricted to patients who require continued NSAID treatment and have an increased risk to develop gastrointestinal complications. The increased risk should be assessed according to individual risk factors, e.g. high age >65 years), history of gastric or duodenal ulcer or upper gastrointestinal bleeding.
In presence of alarm symptoms
In the presence of any alarm symptom (e. g. significant unintentional weight loss, recurrent vomiting, dysphagia, haematemesis, anaemia or melaena) and when gastric ulcer is suspected or present, malignancy should be excluded, as treatment with pantotrazolin may alleviate symptoms and delay diagnosis.
Further investigation is to be considered if symptoms persist despiteadequatetreatment.
Co-administration with atazanavir
Co-administration of atazanavir with proton pump inhibitors is not recommended. 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. A pantotrazolin dose of 20 mg per day should not be exceeded.
Influence on vitamin B12 absorption
Pantotrazolin, 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 B12 absorption on long-term therapy or if respective clinical symptoms are observed.
Long term treatment
In long-term treatment, especially when exceeding a treatment period of 1 year, patients should be kept under regular surveillance.
Gastro-intestinal infections caused by bacteria
Pantototrazolin, like all proton pump inhibitors (PPIs), might be expected to increase the counts of bacteria normally present in the upper gastrointestinal tract. Treatment with Pantotrazolin may lead to a slightly increased risk of gastrointes caused by bacteria such as Salmonella and Campylobacter.
Hypomagnesameia:
For patients expected to be on prolonged treatment or who take PPIs with digoxin or drugs that may cause hypomagnesaemia (e.g. diuretics), health care professionals should consider measuring magnesium levels before starting PPI treatment and periodically during treatment.
Bone fractures
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
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