What is Argentum Metallicum used for?

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

What is the active ingredient in Argentum Metallicum?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Argentum Metallicum available in?

Argentum Metallicum: 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 Argentum Metallicum OTC or prescription only?

Argentum Metallicum is available over-the-counter (OTC) — no prescription required.

What are the side effects of Argentum Metallicum?

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 available data). Blood and lymphatic system disorders. Rare: agranulocytosis. Very rare: leukopenia, thrombocytopenia, pancytopenia. Immune system disorders. Rare: hypersensitivity reactions (in

Does Argentum Metallicum interact with other medications?

Medicinal products whose absorption is pH-dependent. Due to the profound and long-lasting inhibition of hydrochloric acid secretion, pantoprazole may affect the absorption of medicinal products for which intragastric 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. Co-administration of pantoprazole with HIV protease inhibitors (such as ataza

Can Argentum Metallicum 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 precaution, the use of Nolpaza® should be avoided during pregnancy. Breastfeeding. Animal studies have shown excretion of pantoprazole into breast milk. There are insufficient data regarding the excretion of pantoprazole into human breast milk, although such excretion has been reported. A risk to the newborn/infant c

Argentum Metallicum

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

Argentum Metallicum — Description, Dosage, Side Effects | PillsCard

Pharmacodynamics. Mechanism of action. Pantoprazole is a substituted benzimidazole that inhibits gastric hydrochloric acid secretion through specific blockade of the proton pumps of parietal cells. Pantoprazole is converted to its active form in the acidic environment within parietal cells, where it inhibits the H⁺/K⁺-ATPase enzyme, thereby blocking the final step of hydrochloric acid production in the stomach. This inhibition is dose-dependent and affects both basal and stimulated acid secretion. Most patients achieve symptom relief 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 in proportion to the reduction in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds the enzyme at a site 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. During pantoprazole therapy, fasting gastrin levels increase. With short-term use, they generally do not exceed the upper limit of normal. During long-term treatment, gastrin levels typically double. Excessive increases occur only in isolated cases. As a consequence, a slight 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 were observed in animal studies, has not been seen in humans. Based on results from animal studies, the effect of long-term (more than one year) pantoprazole treatment on thyroid gland endocrine parameters cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to the decrease in 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 between 5 days and 2 weeks prior to CgA measurements. This allows CgA levels to return to the normal range, as they may be falsely elevated following PPI treatment. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and peak plasma concentrations are achieved after a single oral dose of 40 mg. The mean peak serum concentration of approximately 2–3 µg/mL is reached approximately 2.5 hours after administration; concentrations remain constant 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 for both oral and intravenous administration. The absolute bioavailability of the tablets is approximately 77%. Concomitant food intake does not affect the AUC (area under the concentration-time curve) or peak serum concentration, and therefore does not affect bioavailability. Only the variability of 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 followed by sulfate 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 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 renally (approximately 80%); the remainder is excreted in faeces. 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 itself. Special patient populations. Poor metabolisers. Approximately 3% of Europeans have a functional deficiency of the CYP2C19 enzyme; they are referred to as poor metabolisers. In these individuals, pantoprazole metabolism is likely primarily catalysed 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 poor 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 prescribing 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 dialysable. Although the main metabolite has a moderately prolonged half-life (2–3 hours), elimination is still rapid, and therefore no accumulation occurs. 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 peak serum concentration is only slightly increased — by a factor of 1.5 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. If hepatic enzyme levels are elevated, treatment with the medicinal product should be discontinued. Combination therapy. During combination therapy, the prescribing information of the respective co-administered medicinal products should be followed. Gastric malignancy. The symptomatic response to pantoprazole therapy may mask the 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) and when gastric ulcer is suspected or present, the possibility of malignancy should be excluded. If symptoms persist despite adequate treatment, further investigation should be considered. HIV protease inhibitors. Co-administration 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 risk factors for decreased vitamin B₁₂ (cyanocobalamin) absorption, particularly during long-term treatment or in the presence of corresponding clinical symptoms. Long-term treatment. During long-term treatment, particularly 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 and Campylobacter or C. difficile. Hypomagnesaemia. Rare cases of severe hypomagnesaemia have been reported in patients receiving PPIs such as pantoprazole for at least 3 months, and in most cases for a year. Serious clinical manifestations of hypomagnesaemia may develop insidiously and include 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 the majority of cases of hypomagnesaemia (and associated hypocalcaemia and/or hypokalaemia), patients improved following magnesium replacement therapy and discontinuation of the PPI. Patients requiring long-term therapy or those taking PPIs concomitantly with digoxin or medicinal products that may cause hypomagnesaemia (e.g. diuretics) should have their magnesium levels measured prior to 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 elderly patients 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 fractures may be attributable to other risk factors. Patients at risk of osteoporosis should receive treatment according to current clinical guidelines and 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, 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 skin reactions should be closely monitored. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole should be discontinued immediately and alternative treatments should be considered. Subacute cutaneous lupus erythematosus. Proton pump inhibitor use has been associated with very rare cases of subacute cutaneous lupus erythematosus. If lesions occur, especially on sun-exposed skin areas, accompanied by arthralgia, the patient should seek prompt medical attention, and the physician should consider discontinuing Nolpaza®. 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 diagnostic investigations for neuroendocrine tumours. To avoid such interference, Nolpaza® therapy should be temporarily discontinued at least 5 days before 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 proton pump inhibitor therapy. Information on excipients Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not take this medicinal product.

Argentum Metallicum

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