What is Cina used for?

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

What is the active ingredient in Cina?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Cina available in?

Cina: 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 Cina OTC or prescription only?

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

What are the side effects of Cina?

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

Does Cina interact with other medications?

Medicinal products with pH-dependent absorption. Due to the profound and prolonged 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 agents such as erlotinib). HIV protease inhibitors. Co-administration of pantoprazole with HIV protease inhibitors (such as atazanavir) whose absorption i

Can Cina be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxic or foeto/neonatal toxicity. Reproductive toxicity was observed in animal studies. As a precautionary measure, the use of Nolpaza® during pregnancy should be avoided. Breastfeeding. Animal studies have shown excretion of pantoprazole in breast milk. Data on the excretion of pantoprazole in human breast milk are insufficient, although such excretion has been reported. A risk to newborns/infants cannot be exc

Cina — Description, Dosage, Side Effects

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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 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 of the 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. Administration of pantoprazole, as with other proton pump inhibitors (PPIs) and H2-receptor antagonists, 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. Fasting gastrin levels increase during pantoprazole treatment. 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 tumour precursor cells (atypical hyperplasia) or gastric neuroendocrine tumours, 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) pantoprazole treatment on endocrine parameters of the thyroid gland cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to decreased 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 prior to 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 maximum serum concentration of approximately 2–3 µg/mL is reached on average 2.5 hours after administration; concentrations remain 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 plasma pharmacokinetics remain linear for both oral administration and intravenous injection. The absolute bioavailability of tablets has been found to be approximately 77%. Concomitant food intake does not affect AUC (area under the concentration–time curve) or maximum serum concentration, and therefore does not affect bioavailability. Only the variability of the lag time is increased 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 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 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 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 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 the European population lack a functional CYP2C19 enzyme and are referred to as poor metabolisers. In these individuals, pantoprazole metabolism is probably mainly catalysed by CYP3A4. After a single dose of 40 mg 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 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 dialysable. Although the main metabolite has a moderately prolonged half-life (2–3 hours), elimination is still rapid, and therefore accumulation does not occur. 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 with that in healthy volunteers. Elderly patients. The slight increase in AUC and Cmax in elderly volunteers compared with younger volunteers is also not clinically significant.

⚠️ 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. 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 its 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, 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 pH-dependent 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 taken into account 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, 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, 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. Serious clinical manifestations of hypomagnesaemia such as fatigue, tetany, delirium, convulsions, dizziness, and ventricular arrhythmia may occur and develop insidiously. In most patients, hypomagnesaemia improved after magnesium replacement therapy and discontinuation of the PPI. For patients expected to be on prolonged treatment or who take PPIs concomitantly with digoxin or medicinal products that may cause hypomagnesaemia (e.g. diuretics), magnesium levels should be measured before starting 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 the elderly or in the presence of other risk factors. Observational studies suggest that PPIs 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 an adequate intake of vitamin D and calcium. Severe cutaneous adverse reactions (SCARs). Severe cutaneous adverse reactions have been reported with 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 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 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 on 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 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 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 therapy. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not take this medicinal product.

Cina

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