What is Coffea Cruda used for?

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

What is the active ingredient in Coffea Cruda?

Homeopatyczny produkt leczniczy

What pharmaceutical form is Coffea Cruda available in?

Coffea Cruda: 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 Coffea Cruda OTC or prescription only?

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

What are the side effects of Coffea Cruda?

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

Does Coffea Cruda interact with other medications?

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

Can Coffea Cruda 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 the excretion of pantoprazole into human breast milk, although such excretion has been reported. A risk to newborns/infants cannot

Coffea Cruda

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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 within 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 achieve symptom relief 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 reduction in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds the enzyme distal 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 therapy. With short-term use, they generally do not exceed the upper limit of normal. During long-term treatment, gastrin levels in most cases double. Excessive increases occur only in isolated cases. Consequently, in a small number of cases during long-term treatment, a slight to moderate increase in specific endocrine (ECL) cells in the stomach is observed (similar to adenomatoid hyperplasia). However, according to studies conducted to date, formation of carcinoid precursor cells (atypical hyperplasia) or gastric neuroendocrine tumors, which were observed in animal studies, has not been reported in humans. Based on the results of animal studies, an effect of long-term (more than one year) pantoprazole treatment on thyroid endocrine parameters cannot be excluded. During treatment with antisecretory agents, serum gastrin levels rise in response to decreased acid secretion. In addition, chromogranin A (CgA) levels increase due to reduced gastric acidity. Elevated CgA levels may interfere with diagnostic investigations for neuroendocrine tumors. 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 therapy. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and peak plasma concentrations are achieved after a single oral dose of 40 mg. The mean peak serum concentration of approximately 2–3 µg/mL is reached approximately 2.5 hours after administration; the concentration remains stable 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 for 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 peak serum concentration, and therefore does not affect bioavailability. Only the variability of the lag time increases 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 metabolized almost exclusively in the liver. The main metabolic pathway is demethylation via CYP2C19 followed by sulfate conjugation; other metabolic pathways include oxidation via 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 elimination half-life does not correlate with the much longer duration of action (acid secretion inhibition). 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. Poor metabolizers. Approximately 3% of Europeans lack functional CYP2C19 enzyme activity and are referred to as poor metabolizers. In these individuals, pantoprazole metabolism is likely catalyzed primarily by CYP3A4. After a single 40 mg dose of pantoprazole, the mean area under the plasma concentration-time curve was approximately 6-fold greater in poor metabolizers than in individuals with functionally active CYP2C19 (extensive metabolizers). Mean peak plasma concentration increased by approximately 60%. These findings do not affect pantoprazole dosing. 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. Only very small amounts of pantoprazole are dialyzable. Although the main metabolite has a moderately prolonged half-life (2–3 hours), elimination is still rapid, so accumulation does not occur. Hepatic impairment. Although in patients with liver cirrhosis (Child-Pugh class A and B) the half-life increases to 7–9 hours and the AUC increases 5- to 7-fold, the peak serum concentration increases only slightly — approximately 1.5-fold compared to 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, especially during long-term treatment. If liver enzymes are elevated, treatment with the medicinal product should be discontinued. Combination therapy. When administering combination therapy, the prescribing information of the respective medicinal products should be followed. Gastric malignancy. The symptomatic response to pantoprazole therapy 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, hematemesis, anemia, melena), and when a gastric ulcer is suspected or present, the possibility of a malignant process should be excluded. If symptoms persist despite adequate treatment, further investigation should be considered. HIV protease inhibitors. Coadministration of pantoprazole with HIV protease inhibitors (such as atazanavir), the absorption of which 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 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 beyond 1 year, patients should be kept under regular medical supervision. Gastrointestinal bacterial infections. Treatment with the 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 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 cases of hypomagnesemia (and associated hypocalcemia and/or hypokalemia), the condition of most patients improved after magnesium replacement therapy and discontinuation of the PPI. Patients requiring long-term therapy, or those taking PPIs concomitantly with digoxin or medications that may cause hypomagnesemia (e.g., diuretics), should have their magnesium levels measured before initiating PPI therapy and periodically during treatment. Bone fractures. Long-term (more than 1 year) high-dose PPI therapy may moderately increase the risk of hip, wrist, and spine fractures, mainly in elderly patients or in the presence of other risk factors. Observational studies suggest that PPI use may increase the overall risk of fractures by 10–40%. Some of this increase may be due 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 in association with pantoprazole use, including erythema multiforme, Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS syndrome), which can 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 monitored closely for cutaneous reactions. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole should be discontinued immediately and alternative treatment considered. Subacute cutaneous lupus erythematosus. PPI use 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 immediate medical advice, 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 PPIs. 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 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.

Coffea Cruda

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