What is Calendula Officinalis used for?

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

What is the active ingredient in Calendula Officinalis?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Calendula Officinalis available in?

Calendula Officinalis: 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 Calendula Officinalis OTC or prescription only?

Calendula Officinalis is available over-the-counter (OTC) — no prescription required.

What are the side effects of Calendula Officinalis?

Adverse reactions were observed in approximately 5% of patients. Adverse effects are classified by frequency of occurrence into 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: leukopenia, thrombocytopenia, pancytopenia. Immune system disorders.

Does Calendula Officinalis 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 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 atazanavi

Can Calendula Officinalis be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryonic or feto/neonatal toxicity of the medicinal product. Reproductive toxicity has been observed in animals. As a precautionary measure, the use of Nolpaza® should be avoided in pregnant women. Breastfeeding. Animal studies have demonstrated excretion of pantoprazole into breast milk. There is insufficient information on the excretion of pantoprazole into human breast milk, although such excretion has been report

Calendula Officinalis

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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 hydrochloric acid secretion in the stomach 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 become symptom-free 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 proportionally to the decrease in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds to the enzyme distally 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 pantoprazole treatment, fasting gastrin levels increase. 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, 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 observed in animal studies, has not been observed 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 decreased acid secretion. Additionally, due to decreased gastric acidity, chromogranin A (CgA) levels increase. Elevated CgA levels may interfere with diagnostic investigations for neuroendocrine tumors. Available published data suggest that proton pump inhibitor treatment should be discontinued within a period of 5 days to 2 weeks before CgA measurements. This allows CgA levels to return to the normal range, which may be falsely elevated after PPI treatment. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and maximum plasma concentrations are achieved 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 at a constant level after repeated dosing. Pharmacokinetic properties do not change after single or repeated administration. In the dose range of 10 to 80 mg, pantoprazole pharmacokinetics in plasma remain linear for 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 maximum serum concentration, and accordingly 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 metabolized almost exclusively in the liver. The main metabolic pathway is demethylation by CYP2C19 with subsequent 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 (inhibition of acid secretion). 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 Europeans have a functional deficiency of the CYP2C19 enzyme; they are called slow metabolizers. In these individuals, pantoprazole metabolism is probably mainly catalyzed by the CYP3A4 enzyme. After a single dose of 40 mg pantoprazole, the mean area under the plasma concentration-time curve was approximately 6 times greater in slow metabolizers than in individuals with functionally active CYP2C19 enzyme (extensive metabolizers). The mean peak plasma concentration 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 individuals, the half-life of pantoprazole is short in these patients. Only very small amounts of pantoprazole are dialyzed. 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 liver cirrhosis (Child-Pugh class A and B) the half-life increases to 7–9 hours and AUC increases 5–7 fold, the maximum 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 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 unintentional weight loss, recurrent vomiting, dysphagia, hematemesis, anemia, melena), 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), 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 considered in patients with reduced body mass or with risk factors for decreased vitamin B12 (cyanocobalamin) absorption, especially 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 this 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. The following serious clinical manifestations of hypomagnesemia may occur and develop insidiously: fatigue, tetany, delirium, convulsions, dizziness, and ventricular arrhythmia. Hypomagnesemia may lead to hypocalcemia and/or hypokalemia (see section "Special warnings and precautions for use"). In most cases of hypomagnesemia (and hypocalcemia and/or hypokalemia associated with hypomagnesemia), patients improved after magnesium replacement therapy and discontinuation of PPI treatment. In patients expected to be on 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 initiation of 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 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 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 about the signs and symptoms, and skin reactions should be closely monitored. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole should be immediately discontinued, and alternative treatment should be considered. Subacute cutaneous lupus erythematosus. The 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, and are 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 prior therapy with a proton pump inhibitor 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 tumors. To avoid such interference, treatment with Nolpaza® 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 initial measurement, repeat measurements should be performed 14 days after discontinuation of proton pump inhibitor treatment. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary problems of fructose intolerance should not use this medicinal product.

Calendula Officinalis

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