What is Calcium Hasco used for?

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

What is the active ingredient in Calcium Hasco?

Calcii glubionas anhydricus + Calcii lactobionas dihydricus (Calcii glubionas, Calcii lactobionas)

What pharmaceutical form is Calcium Hasco available in?

Calcium Hasco: Syrop 115,6 mg Ca 2+/5 ml (doustna)

Is Calcium Hasco OTC or prescription only?

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

What are the side effects of Calcium Hasco?

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

Does Calcium Hasco interact with other medications?

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

Can Calcium Hasco be used during pregnancy?

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

Who manufactures Calcium Hasco?

Przedsiębiorstwo Produkcji Farmaceutycznej HASCO-LEK S.A. (Polska)

What ATC class does Calcium Hasco belong to?

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

Calcium Hasco

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 hydrochloric acid secretion in the stomach by specifically blocking the proton pumps of 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. Administration of pantoprazole, as with other proton pump inhibitors (PPIs) and H2-receptor antagonists, reduces gastric acidity and thereby increases gastrin secretion proportionally to the decrease 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 regardless of stimulation by other substances (acetylcholine, histamine, gastrin). The effect is the same following oral and intravenous administration. During pantoprazole therapy, fasting gastrin levels increase. 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 of specific endocrine (ECL) cells in the stomach is observed (similar to adenomatoid hyperplasia). However, according to studies conducted to date, the formation of neuroendocrine tumour precursor cells (atypical hyperplasia) or gastric neuroendocrine tumours, which were found in animal studies, has not been observed in humans. Based on results from animal studies, an effect of long-term (more than one year) pantoprazole treatment on thyroid endocrine parameters cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to the decrease in acid secretion. Additionally, due to decreased gastric acidity, chromogranin A (CgA) levels increase. Elevated CgA levels may interfere with investigations for neuroendocrine tumours. Available published data suggest that proton pump inhibitor treatment should be discontinued within a period of 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 maximum plasma concentrations are achieved after a single oral dose of 40 mg. Maximum serum concentrations of approximately 2–3 µg/mL are reached on average 2.5 hours after administration; concentrations remain constant after multiple 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 following 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 maximum serum concentration, and therefore 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 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 half-life is approximately 1 hour, and clearance is 0.1 L/h/kg. A few cases of delayed elimination were 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 major portion of pantoprazole metabolites is excreted renally (approximately 80%); the remainder is excreted in 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. Slow metabolisers. Approximately 3% of Europeans lack functional CYP2C19 enzyme activity and are referred to as slow metabolisers. In these individuals, pantoprazole metabolism is likely catalysed mainly by CYP3A4. After a single 40 mg dose of pantoprazole, the mean area under the plasma concentration-time curve was approximately 6 times greater in slow metabolisers than in subjects with functionally active CYP2C19 (extensive metabolisers). The 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 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 longer half-life (2–3 hours), elimination is still rapid, so 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, the maximum serum concentration increases only slightly—by 1.5-fold compared to 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 their liver enzyme levels monitored regularly, especially during long-term treatment. If liver enzyme levels increase, treatment with the medicinal product should be discontinued. Combination therapy. When used as part of combination therapy, the prescribing information for each respective medicinal product should be followed. Gastric malignancy. Symptomatic response to pantoprazole may mask symptoms of gastric malignancy and delay its diagnosis. In the presence of alarm symptoms (e.g. significant unintentional weight loss, recurrent vomiting, dysphagia, haematemesis, anaemia, melaena), as well as when a gastric ulcer is suspected or present, malignancy should 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) whose absorption is pH-dependent 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 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, especially exceeding 1 year, patients should remain 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. 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 1 year. The following serious clinical manifestations of hypomagnesaemia may occur and develop insidiously: fatigue, tetany, delirium, convulsions, dizziness, and ventricular arrhythmia. Hypomagnesaemia may lead to hypocalcaemia and/or hypokalaemia (see section "Special warnings and precautions for use"). In cases of hypomagnesaemia (and associated hypocalcaemia and/or hypokalaemia), most patients improved following magnesium replacement therapy and discontinuation of PPI treatment. Patients requiring long-term therapy, or those taking PPIs concomitantly with digoxin or medicinal products that may cause hypomagnesaemia (e.g. diuretics), should have magnesium levels measured before initiating PPI treatment 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 the elderly or in the presence of other risk factors. Observational studies suggest that PPIs 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 closely monitored for cutaneous reactions. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole should be discontinued immediately and alternative treatment 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, and are accompanied by arthralgia, the patient should seek medical attention promptly and the physician should consider whether discontinuation of Nolpaza® is necessary. The occurrence of subacute cutaneous lupus erythematosus during prior 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 investigations for neuroendocrine tumours. To avoid such interference, Nolpaza® treatment should be temporarily discontinued at least 5 days before CgA measurement (see section "Pharmacodynamics"). If CgA and gastrin levels have not returned to the normal range after 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 medicinal product.

Calcium Hasco

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