What is Clematis Erecta used for?

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

What is the active ingredient in Clematis Erecta?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Clematis Erecta available in?

Clematis Erecta: 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 Clematis Erecta OTC or prescription only?

Clematis Erecta is available over-the-counter (OTC) — no prescription required.

What are the side effects of Clematis Erecta?

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: leukopenia, thrombocytopenia, pancytopenia. Immune system disorders. Rare: hypersensitivity reactions

Does Clematis Erecta interact with other medications?

Medicinal products whose absorption is pH-dependent. Due to the complete and sustained 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. Co-administration of pantoprazole with HIV protease inhibitors (such as atazanavir),

Can Clematis Erecta be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxicity or fetal/neonatal toxicity. Reproductive toxicity has been 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 newborns/infants

Clematis Erecta

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

Clematis Erecta — Description, Dosage, Side Effects | PillsCard

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 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 experience symptom relief within 2 weeks. Administration of pantoprazole, as with other proton pump inhibitors (PPIs) and H₂-receptor inhibitors, 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 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. During treatment with pantoprazole, fasting gastrin levels increase. With short-term use, levels do not exceed the upper limit of normal in most cases. With 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 tumor precursor cells (atypical hyperplasia) or neuroendocrine tumors of the stomach, which were found in animal studies, has not been observed in humans. Based on the results of animal studies, the 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 rise in response to decreased acid secretion. Additionally, due to reduced gastric acidity, chromogranin A (CgA) levels increase. Elevated CgA levels may interfere with the diagnostic investigation of neuroendocrine tumors. 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 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; 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, the plasma pharmacokinetics of pantoprazole 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 the peak serum concentration, and therefore does not affect 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 metabolized almost exclusively in the liver. The main metabolic pathway is demethylation via CYP2C19 with subsequent sulfate conjugation; other metabolic pathways include oxidation via 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 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 in the urine (approximately 80%); the remainder is excreted in the feces. 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. Slow metabolizers. Approximately 3% of the European population lack functional CYP2C19 enzyme activity and are referred to as poor metabolizers. In these individuals, pantoprazole metabolism is probably mainly catalyzed 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 metabolizers than in subjects with functionally active CYP2C19 (extensive metabolizers). The mean peak plasma concentration was increased by approximately 60%. These findings do not affect pantoprazole dosing. 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 dialyzed. Although the main metabolite has a moderately longer half-life (2–3 hours), elimination is still rapid and accumulation does not occur. Hepatic impairment. Although the half-life increases to 7–9 hours and AUC increases 5- to 7-fold in patients with hepatic cirrhosis (Child-Pugh classes A and B), the peak serum concentration increases only slightly — by 1.5-fold compared to that in 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 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 for the respective medicinal products must be followed. Gastric malignancy. The symptomatic response to pantoprazole may mask the symptoms of gastric malignancy and delay their diagnosis. In the presence of alarm symptoms (e.g., significant unintentional weight loss, recurrent vomiting, dysphagia, hematemesis, anemia, melena), and 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. 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 "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 when relevant clinical symptoms are present. 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. Hypomagnesemia. Rare cases of severe hypomagnesemia have been reported in patients treated with PPIs such as pantoprazole for at least 3 months, and in most cases for one year. Serious clinical manifestations of hypomagnesemia may occur and develop insidiously, including fatigue, tetany, delirium, seizures, dizziness, and ventricular arrhythmia. Hypomagnesemia may lead to hypocalcemia and/or hypokalemia (see section "Special warnings and precautions for use"). In patients with hypomagnesemia (and associated hypocalcemia and/or hypokalemia), the condition improved in most cases after magnesium replacement therapy and discontinuation of PPI treatment. For patients who are expected to require prolonged treatment or who take PPIs concomitantly with digoxin or medicinal products that may cause hypomagnesemia (e.g., diuretics), magnesium levels should be measured before initiating PPI therapy 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 those with other risk factors. Observational studies suggest that PPI use may increase the overall risk of fractures by 10–40%. Some of this increase 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 pantoprazole use, 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 skin 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. 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, 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 previous 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 the diagnostic investigation of neuroendocrine tumors. To avoid this 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 the 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.

Clematis Erecta

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