What is Avenalax used for?

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

What is the active ingredient in Avenalax?

Glyceroli suppositoria (Glycerolum 86 %)

What pharmaceutical form is Avenalax available in?

Avenalax: Czopki 2 g (doodbytnicza)

Is Avenalax OTC or prescription only?

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

What are the side effects of Avenalax?

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 available data). Blood and lymphatic system disorders. Rare: agranulocytosis. Very rare: leucopenia, thrombocytopenia, pancytopenia. Immune system disorders. Rare: hypersensitivity reactions (including an

Does Avenalax 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 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 ata

Can Avenalax be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxic or foetal/neonatal toxicity. Reproductive toxicity has been observed in animal studies. As a precautionary measure, the use of Nolpaza® should be avoided during pregnancy. Breast-feeding. Animal studies have demonstrated excretion of pantoprazole in breast milk. There are insufficient data on the excretion of pantoprazole in human breast milk, although such excretion has been reported. A

What ATC class does Avenalax belong to?

Avenalax: ATC A06AG04. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Avenalax

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 the proton pumps of 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. 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 consequently 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 level, it can inhibit hydrochloric acid secretion independently of stimulation by other substances (acetylcholine, histamine, gastrin). The effect is the same following both oral and intravenous administration. Fasting gastrin levels increase during treatment with pantoprazole. During 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, a mild to moderate increase in specific endocrine (ECL) cells in the stomach is observed in a small number of cases during long-term treatment (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 have been observed in animal studies, have not been found in humans. Based on the results of animal studies, an effect of long-term pantoprazole treatment (exceeding one year) on thyroid endocrine parameters cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to decreased acid secretion. Additionally, chromogranin A (CgA) levels increase due to decreased gastric acidity. Elevated CgA levels may interfere with 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 following 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; this 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 has no influence on AUC (area under the concentration-time curve) or maximum serum concentration, and consequently on 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/hr/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 major portion of pantoprazole metabolites is 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. Slow metabolisers. Approximately 3% of Europeans have a functional deficiency of the CYP2C19 enzyme and are referred to as poor metabolisers. In these individuals, pantoprazole metabolism is likely primarily 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 a functionally active CYP2C19 enzyme (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 administering pantoprazole 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 dialysed. 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 the half-life increases to 7–9 hours and the AUC increases 5- to 7-fold in patients with hepatic cirrhosis (Child-Pugh classes A and B), the maximum serum concentration increases only slightly — by a factor of 1.5 compared to healthy volunteers. Elderly patients. The slight increase in AUC and Cmax in elderly volunteers compared with younger volunteers is also not clinically relevant.

⚠️ Warnings

Hepatic impairment.‍‍‍‍‍‍‍ Patients with severe hepatic impairment should have their 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. When using combination therapy, the instructions for use of the respective medicinal products should be followed. Gastric malignancy. Symptomatic response to pantoprazole treatment 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, haematemesis, anaemia, melaena), as well as when gastric ulcer is suspected or present, malignancy should be excluded. If symptoms persist despite adequate treatment, further investigations 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 with risk factors for decreased vitamin B12 (cyanocobalamin) absorption, particularly 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 the product may slightly increase the risk of gastrointestinal infections caused by bacteria such as Salmonella and 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 a 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 case of hypomagnesaemia (and hypocalcaemia and/or hypokalaemia associated with hypomagnesaemia), the condition of most patients improved after magnesium replacement therapy and discontinuation of the PPI. For patients expected to be on prolonged treatment, or who take PPIs with digoxin or medicinal products that may cause hypomagnesaemia (e.g. diuretics), magnesium levels should be measured before initiation of PPI therapy and periodically during treatment. Bone fractures. Long-term treatment (exceeding 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 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 of 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, and are accompanied by arthralgia, the patient should seek medical attention promptly, and the prescriber 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 investigations for neuroendocrine tumours. To avoid such interference, Nolpaza® treatment should be temporarily discontinued for 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 treatment. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not take this medicinal product.

Avenalax

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