Trombital Forte tabs 150mg + 30.39mg #100

Trombital Forte user manual

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Release form, composition and packaging

Trombital Forte is available in pill form. Covering: film casing. According to the instructions, the preparation contains: • inorganic substance, basic magnesium metal hydroxide; • salicylic ester of acetic acid; • MCC; • starch extracted from corn kernels; • starch extracted from potatoes; • hydroxypropyl methylcellulose; • a mixture of di-, tri-, tetra-ethylene glycol, monoethyl ethers glycols. You can buy or order Trombital Forte in our online pharmacy.

Pharmachologic effect

Magnesium hydroxide in combination with low-dose aspirin therapy combines mechanisms of action to inhibit platelet aggregation, leading to additive effects in reducing stroke in the ESPS2 clinical trial and reducing thrombus formation in human and animal models. The activity of aspirin is due to its ability to inhibit cyclooxygenase (COX). Cyclooxygenase is responsible for the conversion of arachidonic acid to prostaglandin G2 (PGG2), the first step in prostaglandin synthesis. In vivo, aspirin is hydrolyzed to salicylic acid and acetate. However, hydrolysis is not required for the activity of aspirin. Aspirin irreversibly inhibits COX by acetylation of a specific serine fragment. Aspirin appears to inhibit COX in two ways and appears to have a different mechanism of action from other salicylates. The use of aspirin in combination with magnesium hydroxide for the prevention of stroke is often due to its antiplatelet properties. The effects of aspirin on platelet aggregation appear at doses significantly lower than those required for an anti-inflammatory effect.
Aspirin preferentially inhibits platelet-derived COX-1, which reduces the formation of thromboxane A2, a potent vasoconstrictor and platelet agonist. In contrast, aspirin has less inhibitory effect on the COX-1 endothelial cell, which generates prostacyclin, a potent vasodilator and antiplatelet agent. Since COX-1 is more sensitive than endothelial cells, COX-1 is the effect of aspirin, this difference explains the pharmacological effect of very low doses of aspirin to slow platelet aggregation. Inhibition of COX-1 platelets without reducing the number of COX-1 endothelial cells is desirable in patients with coronary artery or cerebrovascular disease. Inhibition of COX-1 platelets leads to a decrease in platelet aggregation, which leads to an increase in bleeding time. Hemostatic effects return to normal 36 hours after the last dose of Trombital Forte. Magnesium hydroxide: Magnesium hydroxide is a non-nitrate coronary vasodilator that inhibits platelet aggregation. The coronary vasodilating effect of magnesium hydroxide includes the accumulation of the endogenous compound adenosine, a potent coronary vasodilator and platelet aggregation inhibitor. Adenosine causes vasodilation directly by stimulating adenosine receptors on the smooth muscle membrane and / or increasing the synthesis of cyclic adenosine monophosphate (cAMP), an inhibitor of platelet function. Thus, adenosine prevents the enzymatic degradation of cAMP by phosphodiesterase. Magnesium hydroxide appears to inhibit adenosine deaminase as well as phosphodiesterase, which increases cAMP levels. The mechanism of action of magnesium hydroxide to inhibit platelet aggregation has not yet been established. The increase in cAMP concentration caused by magnesium hydroxide blocks the release of arachidonic acid from membrane phospholipids and reduces the activity of thromboxane A2. In addition, magnesium hydroxide directly stimulates the release of prostacyclin, which induces adenylate cyclase activity, thereby increasing the concentration of cAMP within platelets and further inhibiting platelet aggregation in response to various stimuli such as PAF (platelet aggregation factor), collagen and ADP (adenosine diphosphate).
Magnesium hydroxide alone does not effectively inhibit platelet aggregation for therapeutic antithrombotic effects in cardiovascular or cerebrovascular disorders. Magnesium hydroxide should not be used in conjunction with an oral anticoagulant (eg, to prevent thrombosis in patients with mechanical valves) or aspirin (eg, for secondary prevention of stroke). Magnesium hydroxide does not alter myocardial oxygen consumption. Intravenous administration of magnesium hydroxide has a vasodilating effect and moderately lowers blood pressure and increases heart rate and cardiac output. Due to poor bioavailability, oral administration of magnesium hydroxide usually does not cause these hemodynamic effects. The combination of aspirin and magnesium hydroxide is given orally. There are no significant differences between aspirin and magnesium hydroxide. The kinetics of the components does not change when they are used together as a drug. Acetylsalicylic acid or aspirin: Aspirin is poorly bound to plasma proteins. Its metabolite, salicylic acid, is strongly bound to plasma proteins, but its binding is concentration dependent (non-linear). At low concentrations (less than 100 μg / ml), approximately 90% of salicylic acid binds to albumin. The binding of salicylic acid is reduced in uremic and hypoalbuminemic conditions, as well as in newborns and pregnant women. Because of the high protein binding of salicylic acid, aspirin should be used with caution in patients receiving other high protein drugs such as warfarin and phenytoin. Salicylic acid is widely distributed in all tissues and body fluids, including the central nervous system, breast milk, and fetal tissues.
Aspirin is rapidly hydrolyzed to salicylic and other metabolites with a half-life of about 20 minutes. Salicylic acid, but not aspirin itself, undergoes Michaelis-Menten kinetics (saturable). At low doses, elimination occurs in the first order, and the elimination half-life remains constant for 2-3 hours. At higher doses, the enzymes responsible for metabolism become saturated, and the apparent half-life can increase to 15-30 hours. Therefore, it may take 5-7 days before a constant concentration is achieved. Salicylic acid and its metabolites are excreted mainly by the kidneys. Almost the entire dose taken is excreted in the urine. About 75% of aspirin and sodium salicylate contained in urine is salicylic acid, and about 15% is in the form of mono- and diglucuronides. The remaining 10% is free salicylic acid. The secretion of salicylic acid is enhanced by alkalinization of the urine, which is used to manage aspirin overdose. When urine pH rises above 6.5, renal clearance of free salicylate increases from less than 5% to> 80%. Thus, removal of serum salicylate is enhanced by hemodialysis.
Magnesium hydroxide: Magnesium hydroxide is distributed throughout the tissues of the body, crosses the placenta and is excreted in breast milk. Approximately 99% of magnesium hydroxide is bound to plasma proteins, mainly alpha-1-acid glycoprotein and albumin. Magnesium hydroxide is very lipophilic, but Trombital Forte does not cross the blood-brain barrier to any significant degree in animal models. Magnesium hydroxide undergoes hepatic metabolism, primarily glucuronidation, and these glucuronide conjugates are found primarily in the feces, although enterohepatic circulation may occur. Renal excretion of magnesium hydroxide is negligible, and urinary excretion of the glucuronide metabolite is low (about 5%). The plasma half-life of Trombital Forte appears to be biphasic and variable, with a half-life of approximately 1 hour and a terminal or beta half-life of 12 hours. When Trombital Forte capsules are taken with food with a high fat content, the AUC for aspirin does not change, and the Cmax for aspirin is reduced by 50%, this effect is not considered clinically significant with a similar level of cyclooxygenase inhibition in the state as compared to the fasting state. Administration of Trombital Forte with a high fat magnesium hydroxide Cmax and AUC values ​​of 20-30% compared with fasting, this effect is not considered to be highly effective.
After oral administration of Trombital Forte twice daily, peak plasma levels of salicylic acid and magnesium hydroxide are reached after 0.63 hours (0.5-1 hours) and 2 hours (range 1-6 hours), respectively. The peak plasma concentration at steady state for salicylic acid is 319 ng / ml (175-63 ng / ml), the maximum plasma concentration of magnesium hydroxide at steady state is 1.98 g / ml (1.01-3.99 g / ml), and the minimum concentration in a steady state is 0.53 g / ml (0.18-1.01 g / ml). Aspirin: Aspirin is increasingly absorbed from the gastrointestinal tract, although its intragastric concentration and the pH of the gastric contents affect the rate of absorption. Thus, longer doses take longer to dissolve. Aspirin is partially hydrolyzed to salicylic acid. The systemic circulation in aspirin has a very low volume of distribution (about 10 liters).

Indications

Trombital Forte is used for: • preventive courses in vivo formation of blood clots inside the blood vessels; • preventive courses in violation of myocardial contractility and a decrease in systolic and minute blood volumes; • preventive courses to prevent heart attacks; • preventive courses of acute blockage (embolism) of a blood vessel by a thrombus after heart surgery; • preventive treatment for conditions that threaten the development of myocardial infarction.

Contraindications

Trombital Forte has a number of contraindications: • individual intolerance to any component of the drug; • intracerebral hemorrhage; • tendency to prolonged, low-intensity bleeding; • ulcerative lesions of the stomach and gastrointestinal tract; • bleeding that occurs in the lumen of the gastrointestinal tract; • chronic inflammatory disease of the respiratory tract while taking medications; • chronic inflammatory airway disease in tandem with nasal polyps; • treatment course with cytostatic drugs from the group of antimetabolites, folic acid antagonists; • first and third trimester of pregnancy; • breast-feeding; • hereditary disease in which not enough cytosolic enzyme is produced, which is included in the pentose phosphate pathway, a metabolic pathway that ensures the formation of cellular NADPH-H from NADP +. NADPH and necessary to maintain the level of reduced glutathione in the cell, the synthesis of fatty acids and isoprenoids; • liver damage; • kidney damage; • chronic form of heart lesions; • children; • adolescents; • persons under the age of 18.

Method of administration and dosage

One capsule of Trombital Forte twice a day (dosage of 150 mg), one in the morning and one in the evening. If unbearable headaches occur, patients can take one capsule of the drug at bedtime, and low-dose aspirin only in the morning. There is no data on results with these modes. Headaches usually last for 1 week. Trombital Forte was studied by physicians in a one-year study of ESPS2 in 6,602 patients with ischemic stroke (76%) or TIA (24%) for 3 months. Oral administration of the drug twice a day (only 400/50 mg per day) is twice as effective as any other agent in the secondary prevention of stroke. Mortality was not significantly reduced with any treatment studied.

Side effects

Trombital Forte has a number of side effects: • GI bleeding; • heart failure; • convulsions; • stomach ulcer; • perforation GI; • hearing loss; • renal failure; • pulmonary edema; • bronchospasm; • coma; • intracranial bleeding; • hematemesis; • pancreatitis; • pancytopenia; • coagulopathy; • aplastic anemia; • disseminated intravascular coagulation; • liver failure; • Reye's syndrome; • renal tubular necrosis; • interstitial nephritis; • proteinuria; • papillary necrosis of the kidneys; • vasculitis; • laryngeal edema; • angioedema; • Stevens-Johnson syndrome; • hyperkalemia; • cerebral edema; • rhabdomyolysis; • fetal death; • bleeding; • melena; • anemia; • amnesia; • hematoma; • hemorrhoids; • hypotension; • jaundice; • cholelithiasis; • hematuria; • hemoptysis; • hyperglycemia; • confusion; • prolonged bleeding; • thrombocytopenia; • thrombocytosis; • platelet dysfunction; • chest pain; • heartbeat; • supraventricular tachycardia; • peripheral vasodilation; • sinus tachycardia; • sore throat; • elevated liver enzymes; • hepatitis; • shortness of breath; • tachypnea; • hyperuricemia; • hypoglycemia; • hypokalemia; • dehydration; • metabolic acidosis; • migraine; • headache; • stomach ache; • dyspepsia; • nausea; • diarrhea; • vomiting; • tiredness; • arthralgia; • back pain; • nose bleed; • cough; • asthenia; • malaise; • purple; • noise in ears; • infection; • itching; • urticaria; • anorexia; • paresthesia; • dizziness; • drowsiness; • agitation; • fever; • fainting; • myalgia; • ecchymosis; • pyrosis; • rash; • alopecia; • hypothermia.

Overdose

In case of overdose, consult a doctor.

Drug interactions

Methylxanthines, due to adenosine antagonism and hence pharmacologically induced coronary vasodilation, have been associated with false negative results during dipyridamole thallium-201 stress testing. It is recommended that you stop taking methylxanthines (caffeine, caffeinated drinks and foods, theophylline, etc.) at least 24 hours before the stress test. Concern is not expected when methylxanthines are used concurrently with chronic dipyridamole therapy. (Moderate) Long-term concomitant use of acetaminophen and salicylates is not recommended. High doses of chronic administration of combined analgesics significantly increase the risk of analgesic nephropathy, renal papillary necrosis and end-stage renal disease. Do not exceed the maximum individual doses when these drugs are administered concurrently for short-term therapy. Long-term concomitant use of acetaminophen and salicylates is not recommended. High doses of chronic administration of combined analgesics significantly increase the risk of analgesic nephropathy, renal papillary necrosis and end-stage renal disease. Do not exceed the maximum individual doses when these drugs are administered concurrently for short-term therapy. If salicylates and sulfonylureas are administered together, patients should be monitored for changes in glycemic control. Salicylates, by inhibiting the synthesis of prostaglandin E2, can increase insulin secretion. Thus, salicylates can lower blood sugar levels and enhance the effects of other antidiabetic agents. This mechanism may explain how salicylates may enhance the clinical effects of sulfonylureas; however, the displacement of sulfonylurea from protein binding sites has thus been reported. In large doses, salicylates uncouple oxidative phosphorylation, hepatic and hepatic glycogen and cause hyperglycemia and glucosuria.

Special instructions

In the ESPS2 study, exposure (AUC) of Trombital Forte in healthy geriatric subjects (over 65 years of age) was approximately 40% higher than in subjects under 55 years of age treated with the combination of active substances. However, no dosage changes are indicated. Geriatric patients may be more susceptible to side effects (GI, renal) due to aspirin therapy, especially at higher doses than is recommended for aspirin. The elderly may also be more susceptible to orthostatic hypotension, which has been reported during drug therapy. According to Beers criteria, the short-acting oral formulation is considered a Potentially Inappropriate Drug (PIM) for use in geriatric patients and should be avoided. The Federal Budgetary Reconciliation Act (OBRA) regulates the use of drugs in long-term care settings. According to OBRA guidelines, platelet inhibitors can cause thrombocytopenia and increase the risk of bleeding. Common side effects include headache, dizziness, and vomiting. Concomitant use of warfarin or NSAIDs may increase the risk of bleeding.

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You don't need a prescription to buy Trombital Forte.