What is Calcium Polfarmex used for?

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

What is the active ingredient in Calcium Polfarmex?

Calcii glubionas + Calcii lactobionas (Calcii glubionas, Calcii lactobionas)

What pharmaceutical form is Calcium Polfarmex available in?

Calcium Polfarmex: Syrop 115 mg Ca 2+/5 ml (doustna)

Is Calcium Polfarmex OTC or prescription only?

Calcium Polfarmex is available over-the-counter (OTC) — no prescription required.

What are the side effects of Calcium Polfarmex?

Adverse reactions were observed in approximately 5% of patients. Adverse effects are classified by frequency of occurrence as follows: 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 (cannot be estimated from the available data). Blood and lymphatic system disorders. Rare: agranulocytosis. Very rare: leucopenia, thrombocytopenia, pancytopenia. Immune system disorders. Rare: hypersensitivity react

Does Calcium Polfarmex interact with other medications?

Medicinal products with pH-dependent absorption. Due to the profound and prolonged inhibition of hydrochloric acid secretion, pantoprazole may affect the absorption of medicinal products for which gastric pH is an important determinant of bioavailability (e.g. certain antifungal agents such as ketoconazole, itraconazole, posaconazole, or other agents such as erlotinib). HIV protease inhibitors. Concomitant use of pantoprazole with HIV protease inhibitors (such as atazanavir), t

Can Calcium Polfarmex be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxicity or foetal/neonatal toxicity of the medicinal product. Reproductive toxicity has been observed in animal studies. As a precautionary measure, the use of Nolpaza® should be avoided during pregnancy. Breast-feeding. Animal studies have demonstrated excretion of pantoprazole in breast milk. There are insufficient data on the excretion of pantoprazole in human breast milk, although such exc

What ATC class does Calcium Polfarmex belong to?

Calcium Polfarmex: ATC A12AA20. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Calcium Polfarmex

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

Calcium Polfarmex — Description, Dosage, Side Effects | PillsCard

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 the parietal cells. Pantoprazole is converted to its active form in the acidic environment of the 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. Treatment with pantoprazole, as with other proton pump inhibitors (PPIs) and H₂-receptor antagonists, reduces gastric acidity and thus increases gastrin secretion proportionally to the reduction in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds to the enzyme distal to the cell 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 treatment, these levels do not exceed the upper limit of normal in most cases. 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, the formation of neuroendocrine tumour precursor cells (atypical hyperplasia) or gastric neuroendocrine tumours, which have been observed in animal studies, has not been observed in humans. Based on the results of animal studies, an effect 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 reduced acid secretion. In addition, chromogranin A (CgA) levels increase due to reduced gastric acidity. Elevated CgA levels may interfere with diagnostic investigations for neuroendocrine tumours. Available published data suggest that PPI therapy should be discontinued within 5 days to 2 weeks before CgA measurements. This allows CgA levels to return to the normal range, which may be falsely elevated after PPI treatment. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and peak plasma concentrations are achieved after a single oral dose of 40 mg. Peak serum concentrations of approximately 2–3 µg/mL are reached on average 2.5 hours after administration; concentrations remain at a constant level after repeated dosing. Pharmacokinetic properties do not change after single or repeated administration. Within the dose range of 10 to 80 mg, plasma pharmacokinetics of pantoprazole are linear after both oral and intravenous administration. The absolute bioavailability of the tablets is approximately 77%. Concomitant food intake does not affect AUC (area under the concentration-time curve) or peak serum concentration, and therefore bioavailability. Only the variability of the lag time is increased with concomitant food intake. Distribution. Pantoprazole serum protein binding is approximately 98%. The volume of distribution is approximately 0.15 L/kg. Biotransformation. The substance is metabolised almost exclusively in the liver. The main metabolic pathway is demethylation by CYP2C19 with subsequent sulphate conjugation; other metabolic pathways include oxidation by CYP3A4. Elimination. The terminal elimination half-life is approximately 1 hour, and clearance is 0.1 L/h/kg. A few cases of delayed elimination have been noted. Due to the specific binding of pantoprazole to the proton pumps of the 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%); the remainder is excreted in the faeces. The main metabolite in both serum and urine is desmethylpantoprazole conjugated with sulphate. The half-life of the main metabolite (approximately 1.5 hours) is not much longer than that of pantoprazole. Special patient populations. Poor metabolisers. Approximately 3% of the European population lacks functional CYP2C19 enzyme activity; these individuals are referred to as poor metabolisers. In these individuals, pantoprazole metabolism is probably catalysed primarily by CYP3A4. After administration of a single 40 mg dose of pantoprazole, the mean area under the plasma concentration-time curve was approximately 6-fold higher in poor metabolisers compared with subjects with functionally active CYP2C19 (extensive metabolisers). The mean peak plasma concentration was increased by approximately 60%. These findings do not affect the dosage recommendations for pantoprazole. Renal impairment. No dose reduction is recommended when pantoprazole is administered 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 dialysed. Although the main metabolite has a moderately prolonged half-life (2–3 hours), elimination is still rapid and therefore accumulation does not occur. Hepatic impairment. Although in patients with hepatic cirrhosis (Child-Pugh classes A and B) the half-life increases to 7–9 hours and the AUC increases 5- to 7-fold, peak serum concentration increases only slightly — 1.5-fold compared with healthy volunteers. Elderly patients. A slight increase in AUC and Cmax in elderly volunteers compared with younger volunteers is also not clinically relevant.

⚠️ Warnings

Hepatic impairment.‍‍‍‍‍‍‍ Patients with severe hepatic impairment should have their liver enzymes monitored regularly, particularly during long-term treatment. If liver enzyme levels are elevated, treatment with the medicinal product should be discontinued. Combination therapy. During combination therapy, the instructions for use of the respective medicinal products must be followed. Gastric malignancy. Symptomatic response to pantoprazole 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, haematemesis, anaemia, melaena), and when gastric ulcer is suspected or present, malignancy must be excluded. If symptoms persist despite adequate treatment, further investigation should be considered. HIV protease inhibitors. Concomitant use 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 "Interaction 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 considered in patients with reduced body weight or risk factors for decreased vitamin B₁₂ (cyanocobalamin) absorption, especially during long-term treatment or in the presence of relevant clinical symptoms. Long-term treatment. During long-term treatment, particularly for more than 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 and Campylobacter or C. difficile. Hypomagnesaemia. Rare cases of severe hypomagnesaemia have been reported in patients treated with PPIs such as pantoprazole for at least 3 months, and in most cases for a year. Serious clinical manifestations of hypomagnesaemia may occur and progress insidiously, including fatigue, tetany, delirium, seizures, dizziness, and ventricular arrhythmia. Hypomagnesaemia may lead to hypocalcaemia and/or hypokalaemia (see section "Special warnings and precautions for use"). In most cases of hypomagnesaemia (and associated hypocalcaemia and/or hypokalaemia), patients improved after magnesium replacement therapy and discontinuation of PPI treatment. For patients expected to be on prolonged treatment or who take PPIs concomitantly with digoxin or medicinal products that may cause hypomagnesaemia (e.g. diuretics), magnesium levels should be measured before initiating PPI therapy and periodically during treatment. Bone fractures. Long-term treatment (more than 1 year) with high doses of proton pump inhibitors may moderately increase the risk of hip, wrist, and spine fractures, predominantly in the elderly or in the presence of other risk factors. Observational studies suggest that proton pump inhibitors may increase the overall risk of fractures by 10–40%. Some of these may be due to other risk factors. Patients at risk of osteoporosis should receive treatment in accordance with current clinical guidelines and should have an adequate intake of vitamin D and calcium. Severe cutaneous adverse reactions (SCARs). Severe cutaneous adverse reactions have been reported with pantoprazole, including erythema multiforme, 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 advised of the signs and symptoms and monitored closely for cutaneous reactions. If symptoms suggesting these severe cutaneous reactions appear, pantoprazole should be discontinued immediately and alternative treatment should be considered. Subacute cutaneous lupus erythematosus. The use of proton pump inhibitors is associated with very rare cases of subacute cutaneous lupus erythematosus. If lesions occur, especially in sun-exposed areas of the skin, and are accompanied by arthralgia, the patient should seek medical advice promptly, and the physician should consider whether discontinuation of Nolpaza® is necessary. The occurrence of subacute cutaneous lupus erythematosus with 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 tumours. To avoid such interference, treatment with Nolpaza® should be temporarily discontinued at least 5 days before CgA measurements (see section "Pharmacodynamics"). If CgA and gastrin levels have not returned to the normal range after the initial measurement, repeat measurements should be performed 14 days after discontinuation of PPI treatment. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not take this medicinal product.

Calcium Polfarmex

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