Aluminum hydroxide (dried), magnesium trisilicate, simethicone.
Each uncoated chewable tablet contains: Dried Aluminium Hydroxide BP 300 mg, Magnesium Trisilicate BP 200 mg, Simethicone USP 20 mg.
Excipients/Inactive Ingredients: Mannitol USP, Sucrose IHS, Colour Brilliant blue FCF IHS, Saccharin Sodium BP, Peppermint oil NF, Purified Talc BP, Magnesium Stearate BP, Menthol USP & Purified water BP.
Colour: Brilliant Blue FCF.
Pharmacology: Pharmacodynamics: Peptica C contains Magnesium trisilicate, Dried Aluminium Hydroxide and Simethicone. Antacids provide rapid control of acidity by neutralizing the gastric acid. This action results in increase pH of stomach contents thus providing relief of the symptoms of hyperacidity. Acid concentration within the lumen of oesophagus is also reduced, resulting in an increase in intraesophageal pH.
Magnesium Trisilicate is a relatively weak, nonsystemic antacid and is an effective gastrointestinal adsorbent. The antacid action is exerted slowly, but is prolonged. Magnesium Trisilicate reacts with gastric contents to form a gelatinous Silicon Dioxide (which is said to protect ulcerated mucosal surfaces and promotes healing) and Magnesium Chloride. (Goodman & Gilman 7th Edition).
Peptic activity is inhibited through both Magnesium Trisilicate and Aluminium hydroxide by causing elevation of the gastric pH. Aluminium Hydroxide has a direct antipeptic action as well as a demulcent effect which helps protect the gastrointestinal mucosa and in this way prevents further irritation or erosion and so permits healing.
Simethicone aids in the dispersion and inhibits formation of "mucus-surrounded" gas bubbles in the gastrointestinal tract. This anti-foam action is exerted by changing the surface tension of the gas bubbles so that they coalesce. This permits escape of trapped gas, which then can be eliminated through belching or though passing flatus via the rectum. Simethicone has been widely investigated and used. It has a rapid action and is non-toxic. Being physiologically inert, it has no effect on digestion and is not absorbed through the gastrointestinal mucosa. Infants have been shown to tolerate Simethicone well.
By dispersing gas bubbles with the anti-flatulent, contact with the gastric antacid is facilitated. Coverage of the mucosa by the antacid and demulcent agents is also improved.
Pharmacokinetics: Orally administered Aluminium Hydroxide reacts slowly with the HCL acid in the stomach to form soluble Aluminium Chloride.
The presence of food decreases gastric emptying and prolongs the availability of Aluminium Hydroxide and increase the amount of Aluminium Chloride formed. Any absorbed aluminium is eliminated in the urine.
Aluminium compounds remaining in the gastrointestinal tract form insoluble, poorly Absorbed, Aluminium salts in the intestines including hydroxides, carbonates, phosphates and fatty acid derivatives, which are excreted in the faeces.
Magnesium trisilicate when given orally react with the gastric acid to form soluble magnesium chloride in the stomach. About 10% of Magnesium is slowly absorbed from the gastrointestinal tract and eliminated in the urine, the rest is excreted in the faeces. Simethicone is not absorbed from the gastrointestinal tract.
Toxicology: Preclinical Safety Data: Preclinical Data reveal no special hazard for humans based on conventional studies of pharmacology, repeated dose toxicity, genotoxicity and carcinogenic potential.
For symptomatic relief of gastric Hyperacidity, dyspepsia due to hyperacidity and Heart Burn.
1 to 2 Tablets to be chewed and swallowed, 1-2 hrs after meals or as directed by the physician.
Overdosage with Aluminium and Magnesium may cause flushing, thirst, hypotension and neurotoxicity. Gastric lavage & supportive therapy should be administered. Dialysis may be needed in some patients.
This drug is contraindicated in patients with a history of hypersensitivity to any of its ingredients.
Aluminium may cause nausea, vomiting and constipation. Large doses can cause intestinal obstruction. Excessive or normal doses in patients with low phosphate diets may cause phosphate depletion accompanied by increased resorption and urinary excretion of calcium with the risk of osteomalacia. Osteomalacia, with chronic renal failure on high Aluminium dose as a phosphate binding agent.
Hypermagnesaemia may occur if renal function is impaired. Magnesium Hydroxide and other magnesium salts, in the presence of renal insufficiency, may cause central nervous system depression.
Aluminium and Magnesium may alter the absorption of other medicines from the gastro-intestinal tract if administered concomitantly.
Antacid use may mask the symptoms of internal bleeding secondary to nonsteroidal antiinflammatory drugs (Sing, 1996).
Antacids decrease the absorption of some drugs (eg, tetracyclines, quinolones, propranolol, atenolol, captopril, ranitidine, famotidine, and aspirin); avoid concomitant use of these drugs (Katz & Hallander, 1992).
Magnesium containing antacids may cause diarrhea and potentially lead to dehydration. Combining calcium or aluminum containing antacids with magnesium may reduce the incidence of diarrhea (Katz & Hallander, 1992).
Effects on Ability to Drive and Use Machines: None.
Safety in pregnancy and lactation has not been established.
Aluminium may cause nausea, vomiting and constipation. Large doses can cause intestinal obstruction. Excessive or normal doses in patients with low phosphate diets may cause phosphate depletion accompanied by increased resorption and urinary excretion of calcium with the risk of osteomalacia. Osteomalacia, with chronic renal failure on high Aluminium dose as a phosphate binding agent. Magnesium may cause diarrhoea. Hypermagnesaemia may occur if renal function is impaired. Magnesium Hydroxide and other magnesium salts, in the presence of renal insufficiency, may cause central nervous system depression.
Aluminium and Magnesium may alter the absorption of other medicines from the gastro-intestinal tract if administered concomitantly.
Acetaminophen: The time to attain maximum acetaminophen concentration is significantly delayed by the administration of antacid but the mean plasma peak and maximum plasma concentration of acetaminophen is not affected. Concurrent administration of acetaminophen and antacid also did not alter the elimination half-life of acetaminophen. The delayed absorption of acetaminophen does not have significance in a clinical setting.
Alendronate: Alendronate, a biphosphate, has a high affinity for many multivalent cations. Many antacids contain calcium, magnesium, or aluminum. These cations by binding with alendronate reduce gastrointestinal absorption of alendronate (Prod Info Fosamax, 2003). It is recommended that calcium, magnesium, or aluminum-containing antacids be administered at least one-half hour after alendronate. Patients using alendronate should wait at least one half-hour after taking alendronate before consuming antacids containing calcium, aluminum, or magnesium.
Calcitriol: Summary: The concomitant administration of calcitriol and magnesium-containing antacids may lead to the development of hypermagnesemia (Prod Info Calcijex, 2001). Concurrent administration of calcitriol and antacids containing magnesium is not recommended. If concomitant use cannot be avoided, monitor patient for magnesium intoxication (lethargy, weakness, hyporeflexia, and hypertension).
Digoxin: Simultaneous administration of digoxin and antacids that contain aluminum hydroxide, magnesium hydroxide, and magnesium trisilicate significantly decreased digoxin absorption when digoxin was administered as a tablet (Lanoxin, 2001). No alteration in digoxin absorption was observed following co-administration with calcium carbonate containing antacids. The mechanism responsible for altered digoxin absorption by antacids has not been identified (Brown et al, 1980; D'Arcy & McElnay, 1987). Digoxin serum levels should be monitored if a patient is receiving digoxin and antacids concurrently. The possible sequelae of a drug interaction may be avoided by separating the dosing interval of digoxin and antacids by approximately two hours. The use of digoxin capsules may reduce the interaction but more studies are required to substantiate this possibility.
Ephedrine: The renal elimination of ephedrine and pseudoephedrine are urinary pH dependent. By increasing the urinary pH above 7.5 the renal elimination of either drug may decrease by more than 50%. If the urine remains alkaline for more than 1 to 2 days increased ephedrine toxicity may be observed (Brater et al, 1980; Kuntzman et al, 1971). Monitor for possible ephedrine toxicity (eg, hypertension and tachycardia) and decrease the dose as needed. Patients on ephedrine who frequently require a urinary alkalinizer may need the dose of both drugs to be decreased.
Glipizide: The concomitant use of glipizide or glyburide with magnesium hydroxide antacids has been reported to increase the AUC of either drug (ie, the non-micronized form of these drugs: Diabeta, Micronase) (Neuvonen & Kivisto, 1991; Kivisto & Neuvonen, 1991; Boateng et al, 1991). Concurrent administration of glipizide and antacids is not recommended. If concurrent use cannot be avoided, monitor blood glucose for signs of hypoglycemia upon initiation of antacids. Reduce dose of glipizide as needed on the basis of serum blood glucose concentrations.
Ibuprofen: Summary: Concomitant administration of antacids (oral Maalox 400 mg) and ibuprofen was reported to result in no alterations in the pharmacokinetics of ibuprofen (Gontarz et al, 1987; Prod Info Motrin, 1999).
Mefenamic Acid: Summary: When magnesium hydroxide antacids are given with mefenamic acid and tolfenamic acid an increase in the peak concentration and decrease in the time to peak occurs for these agents. Aluminum hydroxide antacids, however, may lower the peak concentration of tolfenamic acid. Although the peak concentration of the NSAIDs may be lowered, their therapeutic effect is not (Neuvonen & Kivisto, 1988). Concurrent administration of mefenamic acid and antacids, especially those containing magnesium hydroxide or sodium bicarbonate, is not recommended. If concurrent use cannot be avoided, monitor for possible NSAID toxicity (eg, nausea, vomiting, or CNS depression) and adjust the doses accordingly.
Instructions for use, handling and disposal: To be administered orally.
Incompatibilities: Not applicable.
Store at a temperature not exceeding 30°C. Protect from light & moisture.
Shelf-Life: 36 Months from the date of Manufacturing.
A02AF - Antacids with antiflatulents ; Used in the treatment of acid-related disorders.
Chewable tab (light blue-colored, flat, circular, beveled, uncoated, plain on both sides) 4 x 5 x 10's.
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