DSM-PANPRA Tablet

The short-term treatment of duodenal ulcer, gastric ulcer and reflux oesophagitis. If the duodenal ulcer has been demonstrated to be associated with Helicobacter pylori infection, DSM-PANPRA used in combination with appropriate antibiotics may be useful.

Dosage and directions for use:

The recommended once daily dose of DSM-PANPRA should be taken in the morning.

DSM-PANPRA should be swallowed whole with a little water either before or during breakfast.

Duodenal ulcer

The recommended oral dose is 40mgonced daily. The total treatment with pantoprazole should be 2-4 weeks or as directed by the Physician.

If the duodenal ulcer has been demonstrated to be associated with Helicobacter pylori infection, 40mg of DSM-PANPRA used in combination with appropriate antibiotics may be useful.

Gastric ulcer

The recommended oral dose is 40mg once daily for 4-8 weeks or as directed by the Physician. In the case of a suspected gastric ulcer, malignancy of the gastric ulcer should be excluded, as treatment could conceal the symptoms and may delay diagnosis.

Hypersensitivity to pantoprazole, or to any of the ingredients of DSM-PANPRA.

Safety and efficacy in children has not been established.

Blood and lymphatic system.

Less frequent: Leukopenia, thrombocytopenia.

Gastro-intestinal disorders

Frequent: Gastro-intestinal complaints such as upper abdominal pain, diarrhoea, constipation or flatulence.

Less frequent: Nausea, vomiting.

Concomitant intake of food has no influence on the bioavailability.

DSM-PANPRA may reduce or increase the absorption of medicines whose absorption is pH-dependent, e.g. ketoconazole.

Atazanavir: It has been shown that o-administration of atazanavir/ritonavir with omeprazole or atazanavir with lansoprazole resulted in a substantial reduction in the bioavailability of atazanavir. The absorption of atazanavir is pH-dependent. Therefore, pantoprazole must not be co-administered with atazanavir.

In patients with severe liver impairment the liver enzymes should be monitored regularly during treatment with DSM-OANPRA, particularly on long-term use. In the case of a rise of the liver enzymes DSM-PANPRA should be discontinued. DSM-PANPRA is not indicated for milk gastro-intestinal complaints such as nervous dyspepsia. Prior to treatment the possibility of malignancy of gastric ulcer or a malignant disease of the oesophagus should be excluded, as the treatment with DSM-PANPRA may alleviate the symptoms of malignant ulcers and can thus delay diagnosis. Diagnosis of reflux oesophagitis should be confirmed by endoscopy. Daily treatment with any acid-blocking medicines over a long period of time (e.g. longer than 3 years) may lead to malabsorption of cyanocobalamin caused by hypo- or achlorhydria. Rare cases of cyanocobalamin deficiency under acid-blocking therapy have been reported in the literature. This should be considered when respective clinical symptoms are observed.

Pantoprazole is a proton pump inhibitor, i.e. it inhibits specifically and dose-proportionally H+,K+-ATPase, the enzyme, which is responsible for gastric acid secretion in the parietal cells of the stomach. Pantoprazole is a substituted benzimidazole, which accumulates in the acidic compartment of the parietal cells after absorption. In the parietal cell it is protonated and chemically re-arranged to the active inhibitor, a cyclic sulphonamide, which binds to the H+K+-ATPase, thus inhibiting the proton pump and causing suppression of stimulated and basal gastric acid secretion after single and multiple intravenous and oral pantoprazole dosing. Because pantoprazole acts distal to the receptor level, it can influence gastric acid secretion irrespective of the nature of the stimulus. Pantoprazole exerts is full effect in a strongly acidic environment (pH<3) and remains mostly inactive at higher pH values, which explains its selectivity for the acid secreting parietal cells. By means of a feedback mechanism this effect is diminished at the same rate as acid secretion is inhibited.

Effect on gastric acid secretion

Following oral administration, pantoprazole inhibits the pentagastrin-stimulated gastric acid secretion. The mean acid inhibition was 85%, 2 1/2- 3 1/2 hours after dosing with 40mg/day for 7 days. Pantoprazole maintains the physiological pH-rhythm. The values, however, are shifted to higher levels. During the night, periods of pH values approximating placebo have been found to occur.

Although pantoprazole has a half-life of approximately 1 hour, the antisecretory effect increases during repeated once daily administration, demonstrating that the duration of action markedly exceeds the serum elimination half-life.