What is Asterias Rubens used for?

Hypersensitivity to the active substance, benzimidazole derivatives, or to any excipient of the product.

What is the active ingredient in Asterias Rubens?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Asterias Rubens available in?

Asterias Rubens: Granulki; granulki w pojemniku jednodawkowym; krople doustne, roztwór 4CH, 5CH, 7CH, 9CH, 12CH, 15CH, 30CH, 200CH, 6K, 12K, 30K, 200K, 1MK, 10MK, 100MK (podanie doustne)

Is Asterias Rubens OTC or prescription only?

Asterias Rubens is available over-the-counter (OTC) — no prescription required.

What are the side effects of Asterias Rubens?

Adverse reactions were observed in approximately 5% of patients. Adverse effects are classified by frequency of occurrence according to the following categories: 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 (frequency cannot be estimated from available data). Blood and lymphatic system disorders. Rare: agranulocytosis. Very rare: leukopenia, thrombocytopenia, pancytopenia. Immune system disord

Does Asterias Rubens interact with other medications?

Medicinal products with pH-dependent absorption. Due to the complete and prolonged inhibition of hydrochloric acid secretion, pantoprazole may affect the absorption of drugs for which gastric pH is an important factor in their bioavailability (e.g., certain antifungal agents such as ketoconazole, itraconazole, posaconazole, or other drugs such as erlotinib). HIV protease inhibitors. Coadministration of pantoprazole with HIV protease inhibitors (such as atazanavir), the absorption of which is dep

Can Asterias Rubens be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxicity or fetal/neonatal toxicity. Reproductive toxicity was observed in animal studies. As a precautionary measure, the use of Nolpaza® should be avoided during pregnancy. Breastfeeding. Animal studies have shown excretion of pantoprazole in breast milk. There are insufficient data regarding the excretion of pantoprazole in human breast milk, although such excretion has been reported. A risk to the newborn/in

Asterias Rubens

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This information is for educational purposes only. It is not intended as medical advice. Always consult a qualified healthcare professional.

Pharmacodynamics. Mechanism of action. Pantoprazole is a substituted benzimidazole that inhibits the secretion of hydrochloric acid in the stomach by specifically blocking the proton pumps of parietal cells. Pantoprazole is converted to its active form in the acidic environment of parietal cells, where it inhibits the H+/K+-ATPase enzyme, thereby blocking the final step of hydrochloric acid production in the stomach. The inhibition is dose-dependent and affects both basal and stimulated acid secretion. Most patients become symptom-free within 2 weeks. Administration of pantoprazole, as with other proton pump inhibitors (PPIs) and H2-receptor antagonists, reduces gastric acidity and consequently increases gastrin secretion proportionally to the decrease in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds to the enzyme at a site distal to the cellular receptor, it can inhibit hydrochloric acid secretion regardless of stimulation by other substances (acetylcholine, histamine, gastrin). The effect is the same whether the drug is administered orally or intravenously. Fasting gastrin levels increase during treatment with pantoprazole. During short-term use, they generally do not exceed the upper limit of normal. During long-term treatment, gastrin levels double in most cases. Excessive increases occur only in isolated cases. As a consequence, a mild to moderate increase in specific endocrine (ECL) cells in the stomach (similar to adenomatoid hyperplasia) is observed in a small number of cases during long-term treatment. However, according to studies conducted to date, formation of neuroendocrine tumor precursor cells (atypical hyperplasia) or gastric neuroendocrine tumors, which were observed in animal studies, have not been found in humans. Based on results from animal studies, the influence of long-term (more than one year) treatment with pantoprazole on endocrine parameters of the thyroid gland cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to decreased acid secretion. In addition, chromogranin A (CgA) levels increase due to decreased gastric acidity. Elevated CgA levels may interfere with diagnostic investigations for neuroendocrine tumors. Available published data suggest that proton pump inhibitor therapy should be discontinued between 5 days and 2 weeks prior to CgA measurements. This allows CgA levels to return to the normal reference range, which may be falsely elevated following PPI therapy. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and maximum plasma concentrations are achieved after a single oral dose of 40 mg. The maximum serum concentration of approximately 2–3 μg/mL is reached on average 2.5 hours after administration; this concentration remains constant after repeated dosing. Pharmacokinetic properties do not change after single or repeated administration. In the dose range of 10 to 80 mg, plasma pharmacokinetics of pantoprazole remain linear for both oral and intravenous administration. The absolute bioavailability of the tablets has been established at approximately 77%. Concomitant food intake does not affect AUC (area under the concentration-time curve) or maximum serum concentration, and therefore does not affect bioavailability. Only the variability of the lag time increases with concomitant food intake. Distribution. Serum protein binding of pantoprazole is approximately 98%. The volume of distribution is approximately 0.15 L/kg. Biotransformation. The substance is metabolized almost exclusively in the liver. The main metabolic pathway is demethylation by CYP2C19 with subsequent sulfate conjugation; other metabolic pathways include oxidation by CYP3A4. Elimination. The terminal elimination half-life is approximately 1 hour, and clearance is 0.1 L/hr/kg. A few cases of delayed elimination have been noted. Due to specific binding of pantoprazole to the proton pumps of parietal cells, the elimination half-life does not correlate with the much longer duration of action (inhibition of acid secretion). The majority of pantoprazole metabolites are excreted renally (approximately 80%), with the remainder excreted in feces. The main metabolite in both serum and urine is desmethylpantoprazole conjugated with sulfate. The half-life of the main metabolite (approximately 1.5 hours) is not much longer than that of pantoprazole. Special patient populations. Poor metabolizers. Approximately 3% of the European population lack functional CYP2C19 enzyme activity; these individuals are referred to as poor metabolizers. In these individuals, pantoprazole metabolism is likely catalyzed primarily by CYP3A4. After a single dose of 40 mg pantoprazole, the mean area under the plasma concentration-time curve was approximately 6-fold greater in poor metabolizers than in subjects with functionally active CYP2C19 enzyme (extensive metabolizers). The mean peak plasma concentration was increased by approximately 60%. These findings do not affect the dosing recommendations for pantoprazole. Renal impairment. No dose reduction is recommended when administering pantoprazole to patients with impaired renal function (including patients on dialysis). As in healthy subjects, the half-life of pantoprazole is short. Only very small amounts of pantoprazole are dialyzed. Although the main metabolite has a moderately longer half-life (2–3 hours), elimination is still rapid and accumulation does not occur. Hepatic impairment. Although in patients with hepatic cirrhosis (Child-Pugh class A and B) the half-life increases to 7–9 hours and the AUC increases 5- to 7-fold, the maximum serum concentration increases only slightly — approximately 1.5-fold compared to healthy volunteers. Elderly patients. A slight increase in AUC and Cmax in elderly volunteers compared to younger volunteers is also not clinically significant.

⚠️ Warnings

Hepatic impairment. Patients with severe hepatic impairment should have their hepatic enzyme levels monitored regularly, particularly during long-term treatment. Treatment with the medicinal product should be discontinued if hepatic enzyme levels increase. Combination therapy. During combination therapy, the instructions for medical use of the respective medicinal products must be followed. Gastric malignancy. Symptomatic response to pantoprazole treatment may mask the symptoms of gastric malignancy and delay its diagnosis. In the presence of alarm symptoms (e.g., significant weight loss, recurrent vomiting, dysphagia, hematemesis, anemia, melena) and when gastric ulcer is suspected or confirmed, malignancy should be excluded. If symptoms persist despite adequate treatment, further investigation should be considered. HIV protease inhibitors. Coadministration of pantoprazole with HIV protease inhibitors (such as atazanavir), the absorption of which is dependent on intragastric pH, is not recommended due to a significant reduction in their bioavailability (see section "Interactions with other medicinal products and other forms of interaction"). Effect on vitamin B12 absorption. Pantoprazole may reduce the absorption of vitamin B12 (cyanocobalamin) due to hypo- or achlorhydria. This should be taken into account in patients with reduced body weight or in the presence of risk factors for decreased absorption of vitamin B12 (cyanocobalamin), particularly during long-term treatment or in the presence of corresponding clinical symptoms. Long-term treatment. During long-term treatment, especially exceeding 1 year, patients should be kept under regular medical supervision. Gastrointestinal infections caused by bacteria. Treatment with the medicinal product may slightly increase the risk of gastrointestinal infections caused by bacteria such as Salmonella, Campylobacter, or C. difficile. Hypomagnesemia. Rare cases of severe hypomagnesemia have been reported in patients receiving PPIs such as pantoprazole for at least 3 months, and in most cases for 1 year. The following serious clinical manifestations of hypomagnesemia may occur and develop insidiously: fatigue, tetany, delirium, seizures, dizziness, and ventricular arrhythmia. Hypomagnesemia may lead to hypocalcemia and/or hypokalemia (see section "Special warnings and precautions for use"). In cases of hypomagnesemia (and associated hypocalcemia and/or hypokalemia), most patients improved after magnesium replacement therapy and discontinuation of the PPI. Patients requiring long-term therapy, or those taking PPIs concurrently with digoxin or drugs that may cause hypomagnesemia (e.g., diuretics), should have their magnesium levels measured prior to initiating PPI treatment and periodically during treatment. Bone fractures. Long-term (more than 1 year) treatment with high-dose proton pump inhibitors may moderately increase the risk of hip, wrist, and spine fractures, predominantly in elderly patients or in the presence of other risk factors. Observational studies indicate that PPI use may increase the overall risk of fractures by 10–40%. Some of these fractures may be attributable to other risk factors. Patients at risk of osteoporosis should receive treatment in accordance with current clinical guidelines and should ensure adequate intake of vitamin D and calcium. Severe cutaneous adverse reactions (SCARs). Severe cutaneous adverse reactions have been reported with the use of pantoprazole, including erythema multiforme, cases of Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS syndrome), which may be life-threatening or fatal. The frequency of these reactions is not known (see section "Adverse reactions"). When prescribing pantoprazole, patients should be informed about the signs and symptoms and should be closely monitored for cutaneous reactions. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole should be discontinued immediately and alternative treatments should be considered. Subacute cutaneous lupus erythematosus. The use of proton pump inhibitors has been associated with very rare cases of subacute cutaneous lupus erythematosus. If lesions develop, particularly in sun-exposed areas, accompanied by arthralgia, the patient should seek prompt medical attention, and the physician should consider whether discontinuation of Nolpaza® is necessary. The occurrence of subacute cutaneous lupus erythematosus during previous PPI therapy may increase the risk of its development with other proton pump inhibitors. Effect on laboratory test results. Elevated chromogranin A (CgA) levels may interfere with diagnostic investigations for neuroendocrine tumors. To avoid such interference, Nolpaza® treatment should be temporarily discontinued at least 5 days before CgA level assessment (see section "Pharmacodynamics"). If CgA and gastrin levels have not returned to normal after the initial measurement, repeat measurements should be performed 14 days after discontinuation of proton pump inhibitor therapy. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not use this medicinal product.

Asterias Rubens

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