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MSD Enteric Coated ASA (ASA)
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Pharmacology
ASA has analgesic, antipyretic and anti-inflammatory properties.
In rheumatic diseases, although the analgesic and antipyretic effects are useful, the major purpose for which ASA is used is to reduce the intensity of the inflammatory process. Inhibition of prostaglandin synthesis may be involved in the anti-inflammatory action of ASA.
ASA also alters platelet aggregation and release reaction by inhibiting prostaglandin synthesis. Thromboxane A 2 is an essential step in platelet aggregation. ASA prevents thromboxane A 2 formation by acetylation of platelet cyclooxygenase. This inhibition of prostaglandin synthesis is irreversible and affects platelet function for the life of the platelet.
The enteric coating substantially resists disintegration in aqueous fluids having a pH lower than 3.5 for a period of at least 2hours and is capable of disintegrating in aqueous fluids having a pH of at least 5.5 in from 10to 30minutes. Thus, enteric coating effectively inhibits the release of ASA in the stomach, while allowing the tablet to dissolve in the upper portion of the small intestine for absorption from the duodenal area.
Clinical experience has shown that enteric-coated ASA diminishes or eliminates gastric distress during long-term treatment with high doses of ASA.
Pharmacokinetics: Since this product is enteric-coated, the pharmacological effects are not immediate. Peak serum salicylate concentrations are reached 6to 8hours after single oral administration. This means that MSD Enteric Coated ASA tablets are more useful for chronic administration as in arthritis, than for providing prompt relief of pain and fever.
The plasma half-life of salicylate concentrations is dose-dependent being 3to 6hours at low doses (325mg to 1.3g) and 15to 30hours at high doses.
ASA has analgesic, antipyretic and anti-inflammatory properties.
In rheumatic diseases, although the analgesic and antipyretic effects are useful, the major purpose for which ASA is used is to reduce the intensity of the inflammatory process. Inhibition of prostaglandin synthesis may be involved in the anti-inflammatory action of ASA.
ASA also alters platelet aggregation and release reaction by inhibiting prostaglandin synthesis. Thromboxane A 2 is an essential step in platelet aggregation. ASA prevents thromboxane A 2 formation by acetylation of platelet cyclooxygenase. This inhibition of prostaglandin synthesis is irreversible and affects platelet function for the life of the platelet.
The enteric coating substantially resists disintegration in aqueous fluids having a pH lower than 3.5 for a period of at least 2hours and is capable of disintegrating in aqueous fluids having a pH of at least 5.5 in from 10to 30minutes. Thus, enteric coating effectively inhibits the release of ASA in the stomach, while allowing the tablet to dissolve in the upper portion of the small intestine for absorption from the duodenal area.
Clinical experience has shown that enteric-coated ASA diminishes or eliminates gastric distress during long-term treatment with high doses of ASA.
Pharmacokinetics: Since this product is enteric-coated, the pharmacological effects are not immediate. Peak serum salicylate concentrations are reached 6to 8hours after single oral administration. This means that MSD Enteric Coated ASA tablets are more useful for chronic administration as in arthritis, than for providing prompt relief of pain and fever.
The plasma half-life of salicylate concentrations is dose-dependent being 3to 6hours at low doses (325mg to 1.3g) and 15to 30hours at high doses.
Indications
ASA Has Analgesic, Antipyretic And Anti-inflammatory Properties.
In Rheumatic Diseases, Although The Analgesic And Antipyretic Effects Are Useful, The Major Purpose For Which ASA Is Used Is To Reduce The Intensity Of The Inflammatory Process. Inhibition Of Prostaglandin Synthesis May Be Involved In The Anti-inflammatory Action Of ASA.
ASA Also Alters Platelet Aggregation And Release Reaction By Inhibiting Prostaglandin Synthesis. Thromboxane A 2 Is An Essential Step In Platelet Aggregation. ASA Prevents Thromboxane A 2 Formation By Acetylation Of Platelet Cyclooxygenase. This Inhibition Of Prostaglandin Synthesis Is Irreversible And Affects Platelet Function For The Life Of The Platelet.
The Enteric Coating Substantially Resists Disintegration In Aqueous Fluids Having A PH Lower Than 3.5 For A Period Of At Least 2hours And Is Capable Of Disintegrating In Aqueous Fluids Having A PH Of At Least 5.5 In From 10to 30minutes. Thus, Enteric Coating Effectively Inhibits The Release Of ASA In The Stomach, While Allowing The Tablet To Dissolve In The Upper Portion Of The Small Intestine For Absorption From The Duodenal Area.
Clinical Experience Has Shown That Enteric-coated ASA Diminishes Or Eliminates Gastric Distress During Long-term Treatment With High Doses Of ASA.
Pharmacokinetics: Since This Product Is Enteric-coated, The Pharmacological Effects Are Not Immediate. Peak Serum Salicylate Concentrations Are Reached 6to 8hours After Single Oral Administration. This Means That MSD Enteric Coated ASA Tablets Are More Useful For Chronic Administration As In Arthritis, Than For Providing Prompt Relief Of Pain And Fever.
The Plasma Half-life Of Salicylate Concentrations Is Dose-dependent Being 3to 6hours At Low Doses (325mg To 1.3g) And 15to 30hours At High Doses.
ASA Has Analgesic, Antipyretic And Anti-inflammatory Properties.
In Rheumatic Diseases, Although The Analgesic And Antipyretic Effects Are Useful, The Major Purpose For Which ASA Is Used Is To Reduce The Intensity Of The Inflammatory Process. Inhibition Of Prostaglandin Synthesis May Be Involved In The Anti-inflammatory Action Of ASA.
ASA Also Alters Platelet Aggregation And Release Reaction By Inhibiting Prostaglandin Synthesis. Thromboxane A 2 Is An Essential Step In Platelet Aggregation. ASA Prevents Thromboxane A 2 Formation By Acetylation Of Platelet Cyclooxygenase. This Inhibition Of Prostaglandin Synthesis Is Irreversible And Affects Platelet Function For The Life Of The Platelet.
The Enteric Coating Substantially Resists Disintegration In Aqueous Fluids Having A PH Lower Than 3.5 For A Period Of At Least 2hours And Is Capable Of Disintegrating In Aqueous Fluids Having A PH Of At Least 5.5 In From 10to 30minutes. Thus, Enteric Coating Effectively Inhibits The Release Of ASA In The Stomach, While Allowing The Tablet To Dissolve In The Upper Portion Of The Small Intestine For Absorption From The Duodenal Area.
Clinical Experience Has Shown That Enteric-coated ASA Diminishes Or Eliminates Gastric Distress During Long-term Treatment With High Doses Of ASA.
Pharmacokinetics: Since This Product Is Enteric-coated, The Pharmacological Effects Are Not Immediate. Peak Serum Salicylate Concentrations Are Reached 6to 8hours After Single Oral Administration. This Means That MSD Enteric Coated ASA Tablets Are More Useful For Chronic Administration As In Arthritis, Than For Providing Prompt Relief Of Pain And Fever.
The Plasma Half-life Of Salicylate Concentrations Is Dose-dependent Being 3to 6hours At Low Doses (325mg To 1.3g) And 15to 30hours At High Doses.
Contraindications
Sensitivity to the ingredients; active peptic ulcer; patients who had a bronchospastic reaction to ASA or nonsteroidal anti-inflammatory drugs.
Sensitivity to the ingredients; active peptic ulcer; patients who had a bronchospastic reaction to ASA or nonsteroidal anti-inflammatory drugs.
Safety Information / Warning
ASA is one of the most frequent causes of accidental poisoning in toddlers and infants. ASAshould, therefore, be kept well out of the reach of all children.
ASA is one of the most frequent causes of accidental poisoning in toddlers and infants. ASAshould, therefore, be kept well out of the reach of all children.
Precautions
Salicylates should be administered with caution to patients with asthma and other allergic conditions, with a history of gastrointestinal ulcerations, with bleeding tendencies, with significant anemia or with hypoprothrombinemia.
Salicylates can produce changes in thyroid function tests.
Acute hepatitis has been reported rarely in patients with systemic lupus erythematosus and juvenile rheumatoid arthritis with plasma salicylate concentrations above 25mg/100mL. Patients have recovered upon cessation of therapy.
Regular daily use of alcohol while on ASA daily therapy may increase your risk of developing gastrointestinal bleeding.
Pregnancy: ASA does not appear to have any teratogenic effects. ASA has been found to delay parturition in rats. This effect has also been described with nonsteroidal anti-inflammatory agents which inhibit prostaglandin synthesis.
High doses (3g daily) of ASAduring pregnancy may lengthen the gestation and parturition time.
Because of possible adverse effects on the neonate and the potential for increased maternal blood loss, ASA should be avoided during the last three months of pregnancy.
Children: Recent studies have suggested that ASA usage may cause the development of Reye's syndrome in children and teenagers with acute febrile illnesses, especially influenza and varicella. Although a direct causal relationship has not been established, it is recommended that salicylates be avoided when possible, in children and teenagers with influenza or varicella.
Drug Interactions : Caution is necessary when ASA and anticoagulants are prescribed concurrently, as ASA can depress the concentration of prothrombin in the plasma and may potentiate the action of anticoagulants.
Salicylates may potentiate sulfonylurea hypoglycemic agents. Large doses of salicylates may have a hypoglycemic action, and thus, affect the insulin requirements of diabetics.
Although salicylates in large doses are uricosuric agents, smaller amounts may depress uric acid clearance, and thus decrease the uricosuric effects of probenecid, sulfinpyrazone and phenylbutazone.
Sodium excretion produced by spironolactone may be decreased in the presence of salicylates.
Salicylates also retard the renal elimination of methotrexate.
Salicylates may alter valproic acid (VPA) metabolism and displace VPA from protein binding sites, possibly intensifying the effects of VPA. Caution is recommended when VPA is administered concomitantly with salicylates.
Salicylates should be administered with caution to patients with asthma and other allergic conditions, with a history of gastrointestinal ulcerations, with bleeding tendencies, with significant anemia or with hypoprothrombinemia.
Salicylates can produce changes in thyroid function tests.
Acute hepatitis has been reported rarely in patients with systemic lupus erythematosus and juvenile rheumatoid arthritis with plasma salicylate concentrations above 25mg/100mL. Patients have recovered upon cessation of therapy.
Regular daily use of alcohol while on ASA daily therapy may increase your risk of developing gastrointestinal bleeding.
Pregnancy: ASA does not appear to have any teratogenic effects. ASA has been found to delay parturition in rats. This effect has also been described with nonsteroidal anti-inflammatory agents which inhibit prostaglandin synthesis.
High doses (3g daily) of ASAduring pregnancy may lengthen the gestation and parturition time.
Because of possible adverse effects on the neonate and the potential for increased maternal blood loss, ASA should be avoided during the last three months of pregnancy.
Children: Recent studies have suggested that ASA usage may cause the development of Reye's syndrome in children and teenagers with acute febrile illnesses, especially influenza and varicella. Although a direct causal relationship has not been established, it is recommended that salicylates be avoided when possible, in children and teenagers with influenza or varicella.
Drug Interactions : Caution is necessary when ASA and anticoagulants are prescribed concurrently, as ASA can depress the concentration of prothrombin in the plasma and may potentiate the action of anticoagulants.
Salicylates may potentiate sulfonylurea hypoglycemic agents. Large doses of salicylates may have a hypoglycemic action, and thus, affect the insulin requirements of diabetics.
Although salicylates in large doses are uricosuric agents, smaller amounts may depress uric acid clearance, and thus decrease the uricosuric effects of probenecid, sulfinpyrazone and phenylbutazone.
Sodium excretion produced by spironolactone may be decreased in the presence of salicylates.
Salicylates also retard the renal elimination of methotrexate.
Salicylates may alter valproic acid (VPA) metabolism and displace VPA from protein binding sites, possibly intensifying the effects of VPA. Caution is recommended when VPA is administered concomitantly with salicylates.
Side Effects / Adverse Effects
Gastrointestinal: nausea, vomiting, diarrhea, gastrointestinal bleeding and/or ulceration.
Ear: tinnitus, vertigo, hearing loss.
Hematologic: leukopenia, thrombocytopenia, purpura.
Dermatologic and Hypersensitivity: urticaria, angioedema, pruritus, various skin eruptions, asthma and anaphylaxis.
Miscellaneous: acute reversible hepatotoxicity, mental confusion, drowsiness, sweating and thirst.
Gastrointestinal: nausea, vomiting, diarrhea, gastrointestinal bleeding and/or ulceration.
Ear: tinnitus, vertigo, hearing loss.
Hematologic: leukopenia, thrombocytopenia, purpura.
Dermatologic and Hypersensitivity: urticaria, angioedema, pruritus, various skin eruptions, asthma and anaphylaxis.
Miscellaneous: acute reversible hepatotoxicity, mental confusion, drowsiness, sweating and thirst.
Overdose
Symptoms: In mild overdosage, these may include rapid and deep breathing, nausea, vomiting (leading to alkalosis), hyperpnea, vertigo, tinnitus, flushing, sweating, thirst and tachycardia. (High blood levels of ASA lead to acid-base disturbances including respiratory alkalosis and metabolic acidosis.) Severe cases may show fever, hemorrhage, excitement, confusion, convulsions or coma and respiratory failure.
Treatment: Treatment is essentially symptomatic and supportive. Administer water, universal antidote and remove by gastric lavage or emesis. Force fluids (e.g., salty broth) to replace sodium loss. If the patient is unable to retain fluids orally, the alkalosis can be treated by hypertonic saline i.v. If salicylism acidosis is present, sodium bicarbonate i.v. is preferred because it increases the renal excretion of salicylates. VitaminK is indicated if there is evidence of hemorrhage. Hemodialysis has been used with success.
Respiratory depression may require artificial ventilation with oxygen. Convulsions may best be treated by the administration of succinylcholine and artificial ventilation with oxygen. CNS depressant agents should not be used.
Hyperthermia and dehydration are immediate threats to life and initial therapy must be directed to their correction and to the maintenance of adequate renal function. External cooling with cool water or alcohol should be provided quickly to any child who has a rectal temperature over 40°C.
Symptoms: In mild overdosage, these may include rapid and deep breathing, nausea, vomiting (leading to alkalosis), hyperpnea, vertigo, tinnitus, flushing, sweating, thirst and tachycardia. (High blood levels of ASA lead to acid-base disturbances including respiratory alkalosis and metabolic acidosis.) Severe cases may show fever, hemorrhage, excitement, confusion, convulsions or coma and respiratory failure.
Treatment: Treatment is essentially symptomatic and supportive. Administer water, universal antidote and remove by gastric lavage or emesis. Force fluids (e.g., salty broth) to replace sodium loss. If the patient is unable to retain fluids orally, the alkalosis can be treated by hypertonic saline i.v. If salicylism acidosis is present, sodium bicarbonate i.v. is preferred because it increases the renal excretion of salicylates. VitaminK is indicated if there is evidence of hemorrhage. Hemodialysis has been used with success.
Respiratory depression may require artificial ventilation with oxygen. Convulsions may best be treated by the administration of succinylcholine and artificial ventilation with oxygen. CNS depressant agents should not be used.
Hyperthermia and dehydration are immediate threats to life and initial therapy must be directed to their correction and to the maintenance of adequate renal function. External cooling with cool water or alcohol should be provided quickly to any child who has a rectal temperature over 40°C.
Recommended Dosage
Analgesic/Antipyretic: Patients should be advised not to exceed 4g daily. Single doses should not be administered more frequently than every 4hours.
Adults: Single dose should not exceed 650mg, to be repeated every 4to 6hours; the total daily dosage should not exceed 4000mg ASA unless otherwise advised by a physician, i.e., 12tablets 325mg, or 6tablets 650mg. If the underlying condition requires continued use of ASA for more than 5days, a physician should be consulted.
Children: Only as directed by a physician.
Anti-inflammatory: Because the suppression of inflammation increases with the dose of salicylate even beyond the point of toxicity, the therapeutic objective is to employ as large a dose as possible short of toxicity. Most patients will tolerate blood salicylate levels in the range of 20to 25mg%. The most common reason for failing to obtain a therapeutic response to ASA is the administration of inadequate doses.
The generally accepted way to achieve effective “anti-inflammatory” salicylate blood levels of 20to 25mg% is to titrate the dosage by starting with 2.6to 3.9g daily, according to the size, age and sex of the patient. If necessary, the dosage is then gradually adjusted by daily increments of 0.65g. Optimally, salicylate therapy should be monitored by periodic blood salicylate level determinations. If this is not practical, the appearance of auditory symptoms in the form of tinnitus or deafness are acceptable as an indication of the maximum tolerated salicylate dose.
In adults, the median dose at which tinnitus develops is 4.5g/day, but the range extends from 2.6to 6g/day.
Intermittent administration is ineffective. Patients should be advised not to vary the dose from day to day depending on the level of pain because that often fluctuates independently of the intensity of the inflammation. A continuous regimen of 0.65g 4times daily is considered to be minimum therapy for adults. ASA should be administered 4times daily. For night-time and early morning benefits, the last dose should be given at bedtime.
There is an inverse relation between blood salicylate levels at which auditory symptoms appear and the age of the patient. In the young adult, this is usually in the range of 20to 30mg%. In children, however, the level may be much higher, or the effect apparently absent. Because salicylate toxicity may appear without such warning in children, the usual practice is to give ASA in a daily dose of 50to 80mg/kg of body weight and to follow blood levels aiming for a concentration of about 30mg%.
Rheumatic Fever: A total daily dosage of 80mg/kg of body weight administered in divided doses to allay the pain, swelling and fever.
Cerebral Ischemic Attacks (Men): The recommended dosage is 1300mg/day (650mg twice a day or 325mg 4times a day).
Information for the Patient: See Blue Section--Information for the Patient “MSD Enteric Coated ASA”.
Analgesic/Antipyretic: Patients should be advised not to exceed 4g daily. Single doses should not be administered more frequently than every 4hours.
Adults: Single dose should not exceed 650mg, to be repeated every 4to 6hours; the total daily dosage should not exceed 4000mg ASA unless otherwise advised by a physician, i.e., 12tablets 325mg, or 6tablets 650mg. If the underlying condition requires continued use of ASA for more than 5days, a physician should be consulted.
Children: Only as directed by a physician.
Anti-inflammatory: Because the suppression of inflammation increases with the dose of salicylate even beyond the point of toxicity, the therapeutic objective is to employ as large a dose as possible short of toxicity. Most patients will tolerate blood salicylate levels in the range of 20to 25mg%. The most common reason for failing to obtain a therapeutic response to ASA is the administration of inadequate doses.
The generally accepted way to achieve effective “anti-inflammatory” salicylate blood levels of 20to 25mg% is to titrate the dosage by starting with 2.6to 3.9g daily, according to the size, age and sex of the patient. If necessary, the dosage is then gradually adjusted by daily increments of 0.65g. Optimally, salicylate therapy should be monitored by periodic blood salicylate level determinations. If this is not practical, the appearance of auditory symptoms in the form of tinnitus or deafness are acceptable as an indication of the maximum tolerated salicylate dose.
In adults, the median dose at which tinnitus develops is 4.5g/day, but the range extends from 2.6to 6g/day.
Intermittent administration is ineffective. Patients should be advised not to vary the dose from day to day depending on the level of pain because that often fluctuates independently of the intensity of the inflammation. A continuous regimen of 0.65g 4times daily is considered to be minimum therapy for adults. ASA should be administered 4times daily. For night-time and early morning benefits, the last dose should be given at bedtime.
There is an inverse relation between blood salicylate levels at which auditory symptoms appear and the age of the patient. In the young adult, this is usually in the range of 20to 30mg%. In children, however, the level may be much higher, or the effect apparently absent. Because salicylate toxicity may appear without such warning in children, the usual practice is to give ASA in a daily dose of 50to 80mg/kg of body weight and to follow blood levels aiming for a concentration of about 30mg%.
Rheumatic Fever: A total daily dosage of 80mg/kg of body weight administered in divided doses to allay the pain, swelling and fever.
Cerebral Ischemic Attacks (Men): The recommended dosage is 1300mg/day (650mg twice a day or 325mg 4times a day).
Information for the Patient: See Blue Section--Information for the Patient “MSD Enteric Coated ASA”.
Supplied / Packaging
325mg: Each round, brown, film-coated, unprinted, enteric-coated tablet contains: ASA 325mg. Nonmedicinal ingredients: cellulose acetate phthalate, cornstarch, dietyl phthalate, guar gum, hydrogenated vegetable oil, hydroxypropyl methylcellulose, microcrystalline cellulose, polyvinyl acetate phthalate, red ferric oxide, sodium lauryl sulfate and sucrose. Bottles of 1000 (for dispensing use only).
650mg: Each oval, orange, film-coated, unprinted, enteric-coated tablet contains: ASA 650mg. Nonmedicinal ingredients: cellulose acetate phthalate, cornstarch, dietyl phthalate, guar gum, hydrogenated vegetable oil, hydroxypropyl cellulose, hydroxypropyl methylcellulose, microcrystalline cellulose, sodium lauryl sulfate, sunset yellow aluminum lake and titanium dioxide. Bottles of 1000 (for dispensing use only).
Store at 15to 30°C. Protect from moisture.
325mg: Each round, brown, film-coated, unprinted, enteric-coated tablet contains: ASA 325mg. Nonmedicinal ingredients: cellulose acetate phthalate, cornstarch, dietyl phthalate, guar gum, hydrogenated vegetable oil, hydroxypropyl methylcellulose, microcrystalline cellulose, polyvinyl acetate phthalate, red ferric oxide, sodium lauryl sulfate and sucrose. Bottles of 1000 (for dispensing use only).
650mg: Each oval, orange, film-coated, unprinted, enteric-coated tablet contains: ASA 650mg. Nonmedicinal ingredients: cellulose acetate phthalate, cornstarch, dietyl phthalate, guar gum, hydrogenated vegetable oil, hydroxypropyl cellulose, hydroxypropyl methylcellulose, microcrystalline cellulose, sodium lauryl sulfate, sunset yellow aluminum lake and titanium dioxide. Bottles of 1000 (for dispensing use only).
Store at 15to 30°C. Protect from moisture.
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Brand Name
MSD Enteric Coated ASA
MSD Enteric Coated ASA
Generic Name
ASA
ASA
General Indications
Nonsteroidal Anti-inflammatory Analgesic Antipyretic Platelet
Nonsteroidal Anti-inflammatory Analgesic Antipyretic Platelet
