What is Anagallis Arvensis used for?

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

What is the active ingredient in Anagallis Arvensis?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Anagallis Arvensis available in?

Anagallis Arvensis: Granulki; granulki w pojemniku jednodawkowym; krople doustne, roztwór 2CH, 4CH, 5CH, 7CH, 9CH, 12CH, 15CH, 30CH, 200CH, 6K, 12K, 30K, 200K, 1MK, 10MK, 100MK (podanie doustne)

Is Anagallis Arvensis OTC or prescription only?

Anagallis Arvensis is available over-the-counter (OTC) — no prescription required.

What are the side effects of Anagallis Arvensis?

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 (frequency cannot be estimated from available data). Blood and lymphatic system disorders. Rare: agranulocytosis. Very rare: leucopenia, thrombocytopenia, pancytopenia. Immune system disorders. Rare: hypersensitivity

Does Anagallis Arvensis interact with other medications?

Medicinal products whose absorption is pH-dependent. As a result of 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 medicinal products such as erlotinib). HIV protease inhibitors. Concomitant use of pantoprazole with HIV protease inhibitors (such as atazanavir),

Can Anagallis Arvensis be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxic or foeto/neonatal toxicity. Reproductive toxicity has been 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 into breast milk. There are insufficient data regarding excretion of pantoprazole into human breast milk; however, such excretion has been reported. A risk to the newborn/

Anagallis Arvensis

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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 through specific blockade of the proton pumps of parietal cells. Pantoprazole is converted to its active form in the acidic environment of parietal cells, where it inhibits the enzyme H⁺/K⁺-ATPase, 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 achieve symptom relief within 2 weeks. Treatment with pantoprazole, as with other proton pump inhibitors (PPIs) and H2-receptor antagonists, reduces gastric acidity and thereby increases gastrin secretion in proportion 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 with oral and intravenous administration. Fasting gastrin levels increase during treatment with pantoprazole. During short-term use, they usually 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 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 neuroendocrine tumour precursor cells (atypical hyperplasia) or neuroendocrine tumours of the stomach, which were observed in animal studies, has not been found 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 reduced acid secretion. Additionally, due to decreased gastric acidity, chromogranin A (CgA) levels increase. 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 following PPI treatment. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and maximum plasma concentrations are reached 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; the concentration remains constant after repeated dosing. Pharmacokinetic properties do not change after single or repeated dosing. In the dose range of 10 to 80 mg, the plasma pharmacokinetics of pantoprazole are linear following 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 the maximum 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 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 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 elimination half-life does not correlate with the much longer duration of action (acid secretion inhibition). The main fraction of pantoprazole metabolites is excreted renally (approximately 80%); the remainder is excreted in faeces. The major metabolite in both serum and urine is desmethylpantoprazole conjugated with sulfate. The half-life of the major metabolite (approximately 1.5 hours) is not much longer than that of pantoprazole. Special patient populations. Slow metabolisers. Approximately 3% of Europeans have a functional deficiency of the CYP2C19 enzyme; they are referred to as slow metabolisers. In these individuals, the metabolism of pantoprazole is likely catalysed mainly by CYP3A4. After a single dose of 40 mg of pantoprazole, the mean area under the plasma concentration-time curve was approximately 6 times greater in slow metabolisers than in individuals with a functionally active CYP2C19 enzyme (extensive metabolisers). 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 pantoprazole is administered 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 dialysed. Although the major metabolite has a moderately prolonged half-life (2–3 hours), elimination remains rapid, and therefore accumulation does not occur. Hepatic impairment. Although in patients with liver cirrhosis (Child-Pugh classes A and B) the half-life increases to 7–9 hours and the AUC increases 5–7-fold, the maximum serum concentration increases only slightly — by 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 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 become elevated, treatment with the medicinal product should be discontinued. Combination therapy. During combination therapy, the instructions for medical use of the respective medicinal products should be followed. Gastric malignancy. The symptomatic response to pantoprazole may mask the symptoms of gastric malignancy and delay diagnosis. In the presence of alarm symptoms (e.g. significant weight loss, recurrent vomiting, dysphagia, haematemesis, anaemia, melaena), and when a gastric ulcer is suspected or confirmed, 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), the absorption of which depends 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, 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 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. 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 therapy. Patients expected to require prolonged treatment, or those taking PPIs concomitantly with digoxin or other medicinal products that may cause hypomagnesaemia (e.g. diuretics), should have their magnesium levels measured before initiation of PPI therapy and periodically during treatment. Bone fractures. Long-term treatment (longer 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 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, 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 monitored closely for cutaneous reactions. If symptoms suggestive of these severe cutaneous reactions occur, 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, particularly on sun-exposed areas of the skin accompanied by arthralgia, the patient should seek medical attention promptly and the physician should consider discontinuing treatment with 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® 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 therapy. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not use this medicinal product.

Anagallis Arvensis

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