What is the active ingredient in Advantage 80 mg roztwór do nakrapiania dla kotów?

Imidaclopridum (Imidaclopridum)

What pharmaceutical form is Advantage 80 mg roztwór do nakrapiania dla kotów available in?

Advantage 80 mg roztwór do nakrapiania dla kotów: Roztwór do nakrapiania 100 mg/ml (przez nakrapianie)

Is Advantage 80 mg roztwór do nakrapiania dla kotów OTC or prescription only?

Advantage 80 mg roztwór do nakrapiania dla kotów is available over-the-counter (OTC) — no prescription required.

What are the side effects of Advantage 80 mg roztwór do nakrapiania dla kotów?

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

Does Advantage 80 mg roztwór do nakrapiania dla kotów 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 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)

Can Advantage 80 mg roztwór do nakrapiania dla kotów be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryonic or feto/neonatal toxicity. Reproductive toxicity was 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 on excretion of pantoprazole into human breast milk, although such excretion has been reported. A risk to the newborn/infant cannot b

Who manufactures Advantage 80 mg roztwór do nakrapiania dla kotów?

Elanco Animal Health GmbH (Niemcy)

What ATC class does Advantage 80 mg roztwór do nakrapiania dla kotów belong to?

Advantage 80 mg roztwór do nakrapiania dla kotów: ATC QP53A. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Advantage 80 mg roztwór do nakrapiania dla kotów

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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 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 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. 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 reduction in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds the enzyme distal to the cell 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 treatment with pantoprazole. During short-term treatment, they generally do not exceed the upper limit of normal. During long-term treatment, gastrin levels double in most cases. An excessive increase occurs 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 found in animal studies, has not been observed in humans. Based on the results of animal studies, the effect of long-term treatment (more than one year) with pantoprazole on thyroid endocrine parameters cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to the decrease in acid secretion. In addition, chromogranin A (CgA) levels increase due to decreased 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 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 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 thus bioavailability. Only the variability of the lag time is increased 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 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 renally (approximately 80%), the remainder is excreted in 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 lack functional CYP2C19 enzyme activity; they are termed poor metabolisers. In these individuals, pantoprazole metabolism is probably catalysed mainly 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 individuals with functional CYP2C19 enzyme activity (extensive metabolisers). 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 dialysis patients). 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 remains 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 — by a factor of 1.5 compared to healthy volunteers. Elderly patients. A slight increase in AUC and Cmax in elderly volunteers compared with younger volunteers is also of no clinical significance.

⚠️ Warnings

Hepatic impairment. Patients with severe hepatic impairment should have their liver enzyme levels monitored regularly, particularly during long-term treatment. Treatment with the medicinal product must be discontinued if liver enzyme levels are elevated. Combination therapy. During combination therapy, the instructions for use of the corresponding medicinal products must be observed. Gastric malignancy. Symptomatic response to pantoprazole may mask symptoms of gastric malignancy and delay diagnosis. In the presence of alarm symptoms (e.g. significant unintentional weight loss, recurrent vomiting, dysphagia, haematemesis, anaemia, melaena), and when a gastric ulcer is suspected or present, the presence of a malignant process 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 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, especially during long-term treatment or in the presence of relevant clinical symptoms. Long-term treatment. During long-term treatment, particularly exceeding 1 year, patients should remain under regular medical supervision. Gastrointestinal infections caused by bacteria Treatment with the product 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. 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 the majority of cases of hypomagnesaemia (and associated hypocalcaemia and/or hypokalaemia), patients improved following replacement magnesium therapy and discontinuation of the PPI. Patients requiring long-term therapy or those taking PPIs concomitantly with digoxin or medicinal products that may cause hypomagnesaemia (e.g. diuretics) should have their magnesium levels 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 spinal fractures, predominantly in elderly patients or those with other risk factors. Observational studies suggest that proton pump inhibitor therapy 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 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, 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 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, particularly in sun-exposed areas of the skin, and are accompanied by arthralgia, the patient should seek medical attention promptly, and the physician should consider discontinuation of 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 for at least 5 days before measuring CgA levels (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.

Advantage 80 mg roztwór do nakrapiania dla kotów

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