What is Achillea Millefolium used for?

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

What is the active ingredient in Achillea Millefolium?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Achillea Millefolium available in?

Achillea Millefolium: 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 Achillea Millefolium OTC or prescription only?

Achillea Millefolium is available over-the-counter (OTC) — no prescription required.

What are the side effects of Achillea Millefolium?

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: leucopenia, thrombocytopenia, pancytopenia. Immune system disorders. Rare: hypersensitivity reactions (in

Does Achillea Millefolium interact with other medications?

Medicinal products with pH-dependent absorption. Due to profound and sustained inhibition of gastric 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 atazanavi

Can Achillea Millefolium be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryonic or foetal/neonatal toxicity. Reproductive toxicity has been observed in animal studies. As a precautionary measure, the use of Nolpaza® during pregnancy should be avoided. Breast-feeding. 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

Achillea Millefolium

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

Achillea Millefolium — Description, Dosage, Side Effects | PillsCard

Pharmacodynamics. Mechanism of action.‍‍‍‍‍‍‍‍‍‍‍‍‍ Pantoprazole is a substituted benzimidazole that inhibits gastric hydrochloric acid secretion by specifically blocking the proton pumps of 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. 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 thus 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 cellular receptor, it can inhibit hydrochloric acid secretion regardless 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. Consequently, 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 observed in humans. Based on the results of animal studies, an 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 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 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, which may be falsely elevated following PPI treatment. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and peak 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; levels remain 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 therefore 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 half-life is approximately 1 hour and the 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 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. 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 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 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 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 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 a factor of 1.5 compared with 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.‍‍‍‍‍‍‍‍‍‍‍‍‍ Hepatic enzyme levels should be monitored regularly in patients with severe hepatic impairment, particularly during long-term treatment. Treatment should be discontinued if hepatic enzyme levels are elevated. Combination therapy. When combination therapy is prescribed, the prescribing information for the co-administered medicinal products should be followed. Gastric malignancy. The symptomatic response to pantoprazole 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, 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) whose absorption is dependent 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, especially during long-term treatment or in the presence of relevant clinical symptoms. Long-term treatment. Patients on long-term treatment, especially exceeding 1 year, 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, 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. Serious clinical manifestations of hypomagnesaemia, which may develop insidiously, include 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 patients with hypomagnesaemia (and associated hypocalcaemia and/or hypokalaemia), improvement was observed in most cases following magnesium replacement therapy and discontinuation of the PPI. In patients expected to require prolonged therapy, or in those taking PPIs concomitantly with digoxin or other medicinal products that may cause hypomagnesaemia (e.g. diuretics), magnesium levels should be determined before initiating PPI therapy and periodically during treatment. Bone fractures. Long-term treatment (exceeding 1 year) with high-dose PPIs 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 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 according to 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 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"). Patients should be advised of the signs and symptoms when prescribing pantoprazole, and should be closely monitored for cutaneous reactions. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole should be discontinued immediately and alternative treatment should be considered. Subacute cutaneous lupus erythematosus. PPI use 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 promptly seek medical attention, and the prescriber should consider whether Nolpaza® should be discontinued. The occurrence of subacute cutaneous lupus erythematosus during previous PPI therapy may increase the risk of its development with other PPIs. 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 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 therapy. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not take this medicinal product.

Achillea Millefolium

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