What is Calcium Sandoz + Vitamin C used for?

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

What is the active ingredient in Calcium Sandoz + Vitamin C?

Calcii lactogluconas + Calcii carbonas + Acidum ascorbicum (Acidum ascorbicum, Calcii carbonas praecipitatus, Calcii glubionas)

What pharmaceutical form is Calcium Sandoz + Vitamin C available in?

Calcium Sandoz + Vitamin C: Tabletki musujące 260 mg Ca2+ + 1000 mg (doustna)

Is Calcium Sandoz + Vitamin C OTC or prescription only?

Calcium Sandoz + Vitamin C is available over-the-counter (OTC) — no prescription required.

What are the side effects of Calcium Sandoz + Vitamin C?

Adverse reactions were observed in approximately 5% of patients. Adverse effects are classified by frequency of occurrence into 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 disorders. Rar

Does Calcium Sandoz + Vitamin C interact with other medications?

Medicinal products with pH-dependent absorption. Due to 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. Co-administration of pantoprazole with HIV protease inhibitors (such as atazanavir), the absorption of which depends o

Can Calcium Sandoz + Vitamin C be used during pregnancy?

Pregnancy. Available data regarding 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, use of Nolpaza® should be avoided during pregnancy. Breastfeeding. Animal studies have shown excretion of pantoprazole into breast milk. There are insufficient data on the excretion of pantoprazole into human breast milk, although such excretion has been reported. A risk to the newborn/in

What ATC class does Calcium Sandoz + Vitamin C belong to?

Calcium Sandoz + Vitamin C: ATC A11GB01. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Calcium Sandoz + Vitamin C

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 gastric hydrochloric acid secretion by specifically blocking proton pumps in 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. Inhibition is dose-dependent and affects both basal and stimulated acid secretion. Most patients become symptom-free within 2 weeks. As with other proton pump inhibitors (PPIs) and H₂-receptor antagonists, pantoprazole reduces gastric acidity and thereby 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 cellular receptor, it can inhibit hydrochloric acid secretion independently 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 pantoprazole treatment. With short-term use, they 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 result, in a small number of cases during long-term treatment, a mild to moderate increase in specific endocrine (ECL) cells in the stomach is observed (similar to adenomatoid hyperplasia). However, according to studies conducted to date, the formation of carcinoid precursor cells (atypical hyperplasia) or gastric neuroendocrine tumors, which were observed in animal studies, has not been seen in humans. Based on the results of animal studies, the effect of long-term (more than one year) pantoprazole treatment on endocrine parameters of the thyroid gland cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels rise in response to decreased acid secretion. In addition, chromogranin A (CgA) levels increase due to reduced gastric acidity. Elevated CgA levels may interfere with diagnostic investigations for neuroendocrine tumors. Available published data suggest that PPI therapy should be discontinued between 5 days and 2 weeks prior to 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 concentration of approximately 2–3 µg/mL is reached on average 2.5 hours after administration; concentrations remain at a steady level after repeated dosing. Pharmacokinetic properties do not change after single or repeated administration. In the dose range of 10 to 80 mg, pantoprazole plasma pharmacokinetics remain 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 consequently does not affect bioavailability. Only the variability of the lag time increases 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 metabolized almost exclusively in the liver. The main metabolic pathway is demethylation by CYP2C19 followed by 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/h/kg. A few cases of delayed elimination have been noted. Due to the specific binding of pantoprazole to the proton pumps of parietal cells, the half-life does not correlate with the much longer duration of action (inhibition of acid secretion). The majority of pantoprazole metabolites are excreted in urine (approximately 80%); the remainder is 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 the half-life of pantoprazole. Special patient populations. Slow metabolizers. Approximately 3% of Europeans lack functional CYP2C19 enzyme activity; they are referred to as poor metabolizers. In these individuals, pantoprazole metabolism is probably catalyzed mainly by CYP3A4. After a single dose of 40 mg pantoprazole, the mean area under the plasma concentration-time curve was approximately 6 times greater in poor metabolizers than in subjects with functionally active CYP2C19 (extensive metabolizers). Mean peak plasma concentration was increased by approximately 60%. These findings do not affect the dosing of pantoprazole. Renal impairment. No dose reduction is recommended when prescribing pantoprazole to patients with impaired renal function (including patients on dialysis). As in healthy individuals, the half-life of pantoprazole is short. Only very small amounts of pantoprazole are dialyzed. Although the main metabolite has a moderately prolonged half-life (2–3 hours), elimination is still rapid; therefore, accumulation does not occur. Hepatic impairment. Although the half-life increases to 7–9 hours and AUC increases 5- to 7-fold in patients with hepatic cirrhosis (Child-Pugh classes A and B), peak serum concentration increases only slightly — approximately 1.5 times compared with that in healthy volunteers. Elderly patients. The slight increase in AUC and Cmax in elderly volunteers compared with younger volunteers is also not clinically significant.

⚠️ Warnings

Hepatic impairment. Patients with severe hepatic impairment should have liver enzyme levels monitored regularly, particularly during long-term treatment. Treatment should be discontinued if liver enzyme levels increase. Combination therapy. During combination therapy, the prescribing information for the respective medicinal products should be followed. Gastric malignancy. Symptomatic response to pantoprazole may mask the symptoms of gastric malignancy and delay their diagnosis. In the presence of alarm symptoms (e.g., significant weight loss, recurrent vomiting, dysphagia, hematemesis, anemia, melena), and when a gastric ulcer is suspected or present, malignancy should be excluded. If symptoms persist despite adequate treatment, further investigations should be considered. HIV protease inhibitors. Co-administration of pantoprazole with HIV protease inhibitors (such as atazanavir), the absorption of which depends 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 risk factors for decreased vitamin B12 (cyanocobalamin) absorption, particularly during long-term treatment or in the presence of relevant 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 may slightly increase the risk of gastrointestinal infections caused by bacteria such as Salmonella and Campylobacter or C. difficile. Hypomagnesemia. Rare cases of severe hypomagnesemia have been reported in patients treated with 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 PPI treatment. Patients requiring long-term therapy or those taking PPIs concomitantly with digoxin or medications that may cause hypomagnesemia (e.g., diuretics) should have magnesium levels measured before initiating PPI therapy and periodically during treatment. Bone fractures. Long-term treatment (more than 1 year) 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 may be attributable to other risk factors. Patients at risk of osteoporosis should receive treatment in accordance with current clinical guidelines and should have 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, 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 cutaneous reactions should be carefully monitored. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole should be discontinued immediately and alternative treatments 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 occur, especially in sun-exposed areas of the skin, accompanied by arthralgia, the patient should seek immediate medical attention, and the physician should consider whether to discontinue Nolpaza®. The occurrence of subacute cutaneous lupus erythematosus with a 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 prior to CgA level assessment (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 use this product.

Calcium Sandoz + Vitamin C

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