PANTO-DENK-20 20MG GASTRO-RESISTANT TABLETS

Indications

• Gastroesophageal reflux disease (GERD)
• Peptic ulcers
• Zollinger-Ellison syndrome
• Erosive esophagitis caused by acid reflux

Dosage

Adults: The usual adult oral dose for gastroesophageal reflux disease is 20 mg once daily for up to 4 weeks. For Zoll

Mechanism of action

Pantoprazole accumulates in the acidic environment of the canaliculi of parietal cells, where it is converted to an active sulfenamide form. This active form binds to the sulfhydryl group of the H+, K+-ATPase enzyme, inhibiting its function and leading to a significant reduction in gastric acid secretion. This inhibition is more potent and longer-lasting than that achieved by H2 receptor antagonists.

Pharmacodynamics

Pantoprazole effectively decreases gastric acid secretion, leading to reduced acidity in the stomach. It alleviates symptoms associated with acid reflux, promotes healing of esophagitis, and enhances the quality of life for patients. The drug is noted for its excellent safety profile and low incidence of drug interactions, making it suitable for use in high-risk populations such as the elderly or those with renal or hepatic impairment. Long-term use may lead to adverse effects, including increased risk of gastrointestinal infections, malabsorption of nutrients, and potential metabolic bone disease.

Pharmacokinetics

Pantoprazole is well absorbed after oral administration, with peak plasma concentrations occurring within 2 to 4 hours. It undergoes extensive hepatic metabolism, primarily via cytochrome P450 enzymes, with a half-life of approximately 1 hour. The drug is excreted mainly in the urine as metabolites. The bioavailability of pantoprazole is not significantly altered by food, which allows for flexible dosing. It is important to note that the pharmacokinetics may vary in individuals with hepatic impairment.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Constipation
• Abdominal pain
• Flatulence
• Headache
• Dizziness
• Rash
• Increased risk of gastrointestinal infections
• Reduced absorption of vitamin B12
• Hypomagnesemia
• Hypocalcemia

Interactions

• pantoprazole+alpelisib: Unknown (increases exposure)

Precautions

• Use with caution in patients with liver disease
• Consider potential for increased risk of gastrointestinal infections
• Monitor for signs of magnesium deficiency with long-term use

Pregnancy

Pantoprazole should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus. Consult healthcare provider for guidance.

Breast-feeding

Pantoprazole is excreted in breast milk, but the effects on a nursing infant are unknown. Use caution and consult a healthcare provider.

Storage

Store below 30 degrees Celsius, protected from light. Keep out of reach of children.

Formulations

• Tablets
• Injection

Mechanism of action

Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump, expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid). Proton pump inhibitors such as pantoprazole are substituted _benzimidazole_ derivatives, weak bases, which accumulate in the acidic space of the parietal cell before being converted in the _canaliculi_ (small canal) of the gastric parietal cell, an acidic environment, to active _sulfenamide_ derivatives. This active form then makes disulfide bonds with important cysteines on the gastric acid pump, inhibiting its function. Specifically, pantoprazole binds to the _sulfhydryl group_ of H+, K+-ATPase, which is an enzyme implicated in accelerating the final step in the acid secretion pathway. The enzyme is inactivated, inhibiting gastric acid secretion. The inhibition of gastric acid secretion is stronger with proton pump inhibitors such as pantoprazole and lasts longer than with the H(2) antagonists. Pantoprazole is a proton pump inhibitor. It accumulates in the acidic compartment of parietal cells and is converted to the active form, a sulfanilamide, which binds to hydrogen-potassium-ATP-ase at the secretory surface of gastric parietal cells. Inhibition of hydrogen-potassium-ATPase blocks the final step of gastric acid production, leading to inhibition of both basal and stimulated acid secretion. The duration of inhibition of acid secretion does not correlate with the much shorter elimination half-life of pantoprazole. /Pantoprazole sodium/

Pharmacodynamics

This drug acts to decrease gastric acid secretion, which reduces stomach acidity. Pantoprazole administration leads to long-lasting inhibition of gastric acid secretion. **General Effects** Pantoprazole has been shown to reduce acid reflux-related symptoms, heal inflammation of the esophagus, and improve patient quality of life more effectively than histamine-2 receptor antagonists (H2 blockers). This drug has an excellent safety profile and a low incidence of drug interactions. It can be used safely in various high-risk patient populations, including the elderly and those with renal failure or moderate hepatic dysfunction. Due to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as pantoprazole have been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal _C. difficile_), reduced absorption of micronutrients including iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life. PPIs such as pantoprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginie (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes. **A note on laboratory testing abnormalities** During treatment with antisecretory medicinal products such as pantoprazole, serum gastrin (a peptide hormone that stimulates secretion of gastric acid) increases in response to the decreased acid secretion caused by proton pump inhibition. The increased gastrin level may interfere with investigations for neuroendocrine tumors. Published evidence suggests that proton pump inhibitors should be stopped 14 days before chromogranin A (CgA) measurements. This permits chromogranin A levels, that might be falsely elevated after proton pump inhibitor treatment, to return to the normal reference range. Reports have been made of false-positive results in urine screening tests for tetrahydrocannabinol (THC) in patients receiving the majority of proton pump inhibitors, including pantoprazole. A confirmatory method should be used.