What is Avena Sativa used for?

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

What is the active ingredient in Avena Sativa?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Avena Sativa available in?

Avena Sativa: 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 Avena Sativa OTC or prescription only?

Avena Sativa is available over-the-counter (OTC) — no prescription required.

What are the side effects of Avena Sativa?

Adverse reactions were observed in approximately 5% of patients. Adverse effects are classified by frequency of occurrence according to 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 the available data). Blood and lymphatic system disorders. Rare: agranulocytosis. Very rare: leucopenia, thrombocytopenia, pancytopenia. Immune system di

Does Avena Sativa interact with other medications?

Medicinal products whose absorption is pH-dependent. 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 medicinal products such as erlotinib). HIV protease inhibitors. Co-administration of pantoprazole with HIV protease inhibitors (such as atazanavir), t

Can Avena Sativa be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxicity or foeto/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 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/infant ca

Avena Sativa

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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 by specifically blocking the proton pumps of the parietal cells. Pantoprazole is converted to its active form in the acidic environment within 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 in proportion to the reduction in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds the enzyme distal to the cell receptor level, 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 treatment with pantoprazole. 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, a small number of patients on long-term treatment develop a mild to moderate increase in specific endocrine (ECL) cells in the stomach (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 the results of animal studies, an effect of long-term pantoprazole treatment (exceeding one year) 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 investigations for neuroendocrine tumours. Available published data suggest that proton pump inhibitor 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 following PPI treatment. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed and maximum plasma concentrations are achieved even after a single oral dose of 40 mg. On average, the maximum serum concentration of approximately 2–3 µg/mL is reached about 2.5 hours after administration; the concentration remains constant after repeated dosing. Pharmacokinetic properties do not change after single or repeated administration. In 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 maximum serum concentration and, consequently, bioavailability. Only the variability of the lag time increases with concomitant food intake. Distribution. Serum protein binding of pantoprazole 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 the clearance is 0.1 L/h/kg. A few cases of delayed elimination have been observed. 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 (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 Europeans have a functional deficiency of the CYP2C19 enzyme and are referred to as poor metabolisers. In these individuals, the metabolism of pantoprazole is probably mainly 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 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 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 no accumulation occurs. Hepatic impairment. Although in patients with hepatic cirrhosis (Child-Pugh classes A and B) the half-life increases to 7–9 hours and AUC increases 5- to 7-fold, the maximum serum concentration increases only slightly — approximately 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 enzyme levels 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 prescribing information of the respective co-administered medicinal products should be followed. Gastric malignancy. Symptomatic response to pantoprazole therapy may mask the symptoms of gastric malignancy and may delay its diagnosis. If alarm symptoms are present (e.g. significant unintentional weight loss, recurrent vomiting, dysphagia, haematemesis, anaemia, melaena), as well as when gastric ulcer is suspected or present, 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 significant reduction in their bioavailability (see section "Interaction with other medicinal products and other forms of interaction"). Effect on absorption of vitamin B₁₂ Pantoprazole may reduce the absorption of vitamin B₁₂ (cyanocobalamin) due to hypo- or achlorhydria. This should be taken into consideration in patients with reduced body weight or relevant risk factors for reduced vitamin B₁₂ (cyanocobalamin) absorption, especially during long-term treatment or in the presence of corresponding 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 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), the condition of most patients improved after magnesium replacement therapy and discontinuation of the PPI. In 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 (exceeding 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 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 should have an 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, cases of 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 of the signs and symptoms and closely monitored for cutaneous reactions. If symptoms suggestive of these severe cutaneous reactions develop, pantoprazole should be discontinued immediately and alternative treatment should be considered. Subacute cutaneous lupus erythematosus. 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, accompanied by arthralgia, the patient should seek prompt medical attention and the physician should consider whether discontinuation of Nolpaza® is necessary. The occurrence of subacute cutaneous lupus erythematosus during previous proton pump inhibitor therapy may increase the risk of its development with other proton pump inhibitors. Effects 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 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 proton pump inhibitor therapy. Information regarding excipients Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not take this medicinal product.

Avena Sativa

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