What is Cholinex used for?

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

What is the active ingredient in Cholinex?

Cholini salicylas (Cholini salicylas)

What pharmaceutical form is Cholinex available in?

Cholinex: Pastylki twarde 150 mg (doustna)

Is Cholinex OTC or prescription only?

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

What are the side effects of Cholinex?

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 Cholinex interact with other medications?

Medicinal products with pH-dependent absorption. Due to profound and sustained inhibition of hydrochloric acid secretion, pantoprazole may affect the absorption of drugs for which the gastric juice pH is an important determinant of bioavailability (e.g., certain antifungal agents such as ketoconazole, itraconazole, posaconazole, or other agents such as erlotinib). HIV protease inhibitors. Concomitant use of pantoprazole with HIV protease inhibitors (such as atazanavir), whose absorption is depen

Can Cholinex be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryonic or fetal/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 in breast milk. There are insufficient data regarding excretion of pantoprazole in human breast milk, although such excretion has been reported. A risk to the newborn/infant cann

What ATC class does Cholinex belong to?

Cholinex: ATC N02BA03. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Cholinex

Preparing your business dashboard

Almost ready…

Loading the latest data0%

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 through specific blockade of proton pumps in parietal cells. Pantoprazole is converted to its active form in the acidic environment of parietal cells, where it inhibits the enzyme H⁺/K⁺-ATPase, thereby blocking the final step of hydrochloric acid production in the stomach. This inhibition is dose-dependent and affects both basal and stimulated acid secretion. Most patients achieve symptom relief within 2 weeks. The use of pantoprazole, as with other proton pump inhibitors (PPIs) and H2-receptor antagonists, reduces gastric acidity and consequently increases gastrin secretion in proportion to the reduction in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds to the enzyme at a site distal to the cell receptor, it can inhibit hydrochloric acid secretion irrespective 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, 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 found in humans. Based on the results of animal studies, an effect of long-term (more than one year) treatment with pantoprazole on thyroid endocrine parameters cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to decreased acid secretion. In addition, 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 PPI therapy should be discontinued within a period of 5 days to 2 weeks prior to CgA measurements. This allows CgA levels to return to the normal range, as they 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 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, the plasma pharmacokinetics of pantoprazole are 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 the AUC (area under the concentration–time curve) or the 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 metabolized 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 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 parietal cell proton pumps, 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 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 itself. Special patient populations. Slow metabolizers. Approximately 3% of the European population lacks functional CYP2C19 enzyme activity; these individuals are referred to as poor metabolizers. In these individuals, pantoprazole metabolism is probably mainly catalyzed by CYP3A4. After a single dose of 40 mg pantoprazole, the mean area under the plasma concentration–time curve was approximately 6 times higher 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 recommendations. 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 dialyzed. Although the main metabolite has a moderately longer half-life (2–3 hours), excretion is still rapid, and therefore accumulation does not occur. Hepatic impairment. Although in patients with liver 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 to that in healthy volunteers. Elderly patients. The 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 their hepatic enzyme levels monitored regularly, especially during long-term treatment. If hepatic enzyme levels increase, treatment with the product should be discontinued. Combination therapy. During combination therapy, the instructions for medical use of the respective medicinal products should be followed. Gastric malignancy. A symptomatic response to pantoprazole may mask the symptoms of gastric malignancy and delay its diagnosis. In the presence of alarm symptoms (e.g., significant weight loss, recurrent vomiting, dysphagia, hematemesis, anemia, melena), and when gastric ulcer is suspected or confirmed, malignancy should be excluded. If symptoms persist despite adequate treatment, further investigation should be considered. HIV protease inhibitors. Concomitant use 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 weight or in those 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 for more than 1 year, patients should be kept under regular medical supervision. Gastrointestinal bacterial infections. Treatment with the 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 1 year. The following serious clinical manifestations of hypomagnesemia may occur and develop insidiously: 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 the majority of cases of hypomagnesemia (and associated hypocalcemia and/or hypokalemia), patient condition improved following magnesium replacement therapy and discontinuation of PPI treatment. For patients expected to be on prolonged treatment, or for patients taking PPIs concomitantly with digoxin or drugs that may cause hypomagnesemia (e.g., diuretics), magnesium levels should be measured before initiation of PPI therapy and periodically during treatment. Bone fractures. Long-term (more than 1 year) treatment 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 inhibitor use 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 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, 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 they should be 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, 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 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 tumors. To avoid such interference, Nolpaza® therapy should be temporarily discontinued at least 5 days prior to 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 therapy. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not use this product.

Cholinex

User Reviews