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PRO-AAS EC is a brand name for Aspirin (also known as Acetylsalicylic Acid), supplied as a tablet (delayed-release). The medicine, its uses, side effects and dosage are the same regardless of brand.
Used for: AND CLINICAL USE ..............................................................................3 CONTRAINDICATIONS ...................................................................................................4 WARNINGS AND PRECAUTIONS…
Verbatim from this product's HC label. Tap a section to expand.
PRO-AAS EC tablets should preferably be taken after meals, with plenty of liquid. Dosing Considerations Please see below for specific dosing instructions for each indication.
Recommended Dose and Dosage Adjustment Platelet aggregation inhibitor:
Suspected Acute Myocardial Infarction: An initial dose of at least 162 mg chewed or crushed to ensure rapid absorption as soon as a myocardial infarction is suspected. The same dose should be given as maintenance over the next 30 days.
After 30 days, consider further therapy based on dosage and administration for prevention of recurrent MI (see Prior Myocardial Infarction). Prevention of a first non-fatal myocardial infarction: 81 - 325 mg once daily, according to the individual needs of the patient, as determined by the physician.
Prior Myocardial Infarction or Unstable Angina Pectoris: 81 - 325 mg daily according to the individual needs of the patient, as determined by the physician. Transient Ischemic Attack and Secondary Prevention of Atherothrombotic Cerebral Infarction: 81 - 325 mg daily according to the individual needs of the patient, as determined by the physician.
Prophylaxis of Venous Thromboembolism after total hip replacement: 162 - 325mg (of PRO-AAS EC 81 mg) daily according to the individual needs of the patient, as determined by the physician. OVERDOSAGE Mild Overdose or Early Poisoning - burning in the mouth, lethargy, nausea, vomiting, tinnitus, sweating, thirst, tachycardia or dizziness.
Moderate Overdose - all of the symptoms from mild overdose plus tachypnea, hyperpyrexia, sweating, dehydration, loss of coordination, restlessness, mental confusion. Severe Overdose - all of the symptoms from moderate overdose plus hypotension, hallucinations, stupor, hypoglycemia, convulsions, cerebral edema, oliguria, renal failure, cardiovascular failure, coma, hemorrhage, metabolic acidosis, respiratory alkalosis and/or failure.
Emergency Management: 1. Immediate transfer to hospital and maintain cardiovascular and respiratory support; 2. pdf Pg. 10 Page 11 of 39 3. Check of acid-base balance and correct if necessary; 4. 2 mmol/L) in children; 5. 0 mmol/L) in children, as renal elimination of salicylates may be slow due to the presence of acidic urine and renal failure.
Many adverse reactions due to ASA ingestion are dose-related. The following is a list of adverse reactions that have been reported in the literature and from both clinical and post-marketing experience. Gastrointestinal (the frequency and severity of these adverse effects are dose-related): nausea, vomiting, diarrhea, gastrointestinal bleeding and/or ulceration, dyspepsia, heartburn, hematemesis, melena, abdominal pain, rarely gastrointestinal inflammation, and intestinal diaphragm disease with frequency not known (especially in long-term treatment).
g. perioperative haemorrhage, hematomas, epistaxis, urogenital bleedings, and gingival bleedings may occur. Serious bleedings, such as gastrointestinal tract hemorrhages, and cerebral hemorrhages are rare. Isolated cases of potentially life threatening bleedings have been reported, especially in patients with uncontrolled hypertension and/or concomitant antihemostatic agents.
Ear: dizziness, tinnitus, vertigo, hearing loss. Dizziness and tinnitus have been reported, which may be indicative of an overdose. Hematologic: leukopenia, thrombocytopenia, purpura, anemia. g. occult microbleeding, acute or chronic bleeding).
Hemolysis and hemolytic anemia in patients with severe forms of glucose-6-phosphate dehydrogenase (G6PD) deficiency has been reported. Dermatologic and hypersensitivity: urticaria, pruritus, skin eruptions, asthma, anaphylaxis, edema, nasal congestion and rhinitus.
Severe allergic reactions, including anaphylactic shock are very rarely reported. Miscellaneous: mental confusion, drowsiness, sweating, thirst. Transient hepatic impairment with increase in liver transaminases has very rarely been reported.
Renal impairment and acute renal failure have been reported. DRUG INTERACTIONS Overview ASA should be used with caution with other products that have anticoagulation or antiplatelet effects, as these effects may be potentiated. Drugs that bind to protein binding sites should also be used cautiously since ASA may displace drugs from their protein binding site.
• Patients who are hypersensitive to ASA, salicylates, non-steroidal anti-inflammatory drugs (NSAIDs), analgesics, antipyretics or other ingredients in the product or component of the container. For a complete listing, see DOSAGE FORMS, COMPOSITION AND PACKAGING section of the product monograph.
• Acute gastrointestinal ulcer • History of gastrointestinal ulcers • Hemorrhagic diathesis • Active or Severe hepatic failure, renal failure, or congestive heart failure • Patients with a history of asthma induced by the administration of salicylates or substances with a similar action, notably non-steroidal anti-inflammatory drugs • Combination with methotrexate at doses of 15mg/week or more (see DRUG INTERACTIONS); • Last trimester of pregnancy (see “Special Populations”) WARNINGS AND PRECAUTIONS General ASA is one of the most frequent causes of accidental poisonings in toddlers and infants.
Tablets or caplets should be kept well out of the reach of children. g. renal vascular disease, congestive heart failure, volume depletion, major surgery, sepsis or major haemorrhagic events) • a history of bleeding tendencies, significant anemia and/or hypothrombinemia • concomitant treatment with anticoagulants (see DRUG INTERACTIONS) • concomitant treatment with NSAIDs, such as ibuprofen and naproxen in patients taking ASA regimen (see DRUG INTERACTIONS) Hypersensitivity ASA may precipitate bronchospasm and induce asthma attacks or other hypersensitivity reactions.
Risk factors are present bronchial asthma, hay fever, nasal polyps, or chronic respiratory disease. g. pdf Pg. 4 Page 5 of 39 Hematologic Due to effect on platelet aggregation, ASA may be associated with an increased risk of bleeding.
Caution is necessary when salicylates and anticoagulants are prescribed concurrently, as salicylates can depress the concentration of prothrombin in the plasma. g. dental extractions).
Not medical advice. Always read the patient information leaflet and follow your prescriber or pharmacist.
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2), acute renal failure, pulmonary edema or CNS symptoms such as: drowsiness, agitation, coma or convulsions; 6. g. half saline) and supplemented with glucose 50 to 100 g/L; 7. Symptomatic treatment. Fatal Dose: varies from 10 to 30 g of ASA.
However, (in one case) 130 g of ASA was ingested without fatal outcome. For management of a suspected drug overdose, contact your regional Poison Control Centre. ACTION AND CLINICAL PHARMACOLOGY Mechanism of Action ASA interferes with the production of prostaglandins in various organs and tissues through acetylation of the enzyme cyclo-oxygenase.
Prostaglandins are themselves powerful irritants and produce headaches and pain on injection in man. Prostaglandins also appear to sensitize pain receptors to other noxious substances such as histamine and bradykinin. By preventing the synthesis and release of prostaglandins in inflammation, ASA may avert the sensitization of pain receptors.
The antipyretic activity of ASA is due to its ability to interfere with the production of prostaglandin E1 in the brain. Prostaglandin E1 is one of the most powerful pyretic agents known. The inhibition of platelet aggregation by ASA is due to its ability to interfere with the production of thromboxane A2 within the platelet.
Thromboxane A2 is, largely, responsible for the aggregating properties of platelets. pdf Pg. 11 Page 12 of 39 Pharmacokinetics Absorption: When ASA is taken orally, it is rapidly absorbed from the stomach and proximal small intestine.
The gastric mucosa is permeable to the non-ionized form of acetylsalicylic acid, which passes through the stomach wall by a passive diffusion process. 10. Absorption in the small intestine occurs at a significantly faster rate than in the stomach.
2 mg % within an hour. Within the same period of time, half or more of the ingested dose is hydrolyzed to salicylic acid by esterases in the gastrointestinal mucosa and the liver, the total plasma salicylate concentration reaching a peak between one or two hours after ingestion, averaging between 3 and 7 mg %.
, all affect absorption.
Distribution:
Distribution of salicylate throughout most body fluids and tissues proceeds at a rapid rate after absorption. Aside from the plasma itself, fluids which have been found to contain substantial amounts of salicylate after oral ingestion include spinal, peritoneal and synovial fluids, saliva and milk.
Tissues containing high concentrations of […]
pdf Pg. 7 Page 8 of 39 general and displacement of methotrexate from its plasma protein binding by salicylates). See CONTRAINDICATIONS.
Drug-Drug Interactions Methotrexate, used at 15 mg/week or less:
Salicylates may retard the elimination of methotrexate by decreasing renal clearance of methotrexate, displacing methotrexate from protein binding sites, and thereby increasing its hematological toxicity. g. warfarin, heparin: Caution is necessary when salicylates and anticoagulants, thrombolytics / other inhibitors of platelet aggregation / hemostasis prescribed concurrently, as salicylates can depress the concentration of prothrombin in the plasma, leading to an increased risk of bleeding.
g. insulin, sulfonylureas: Large doses of salicylates have a hypoglycemic action and may enhance the effect of oral hypoglycemic agents. Diabetics receiving concurrent salicylate and hypoglycemic therapy should be monitored closely; reduction of the sulfonylurea hypoglycemic drug dosage may be necessary.
Diuretics:
Diuretics in combination with acetylsalicylic acid at higher doses leads to decreased glomerular filtration via decreased prostaglandin synthesis. As a result, sodium excretion may be decreased by salicylate administration.
Uricosuric Agents:
Salicylates in large doses are uricosuric agents; smaller amounts may depress uric acid clearance and thus decrease the uricosuric effects of other drugs.
Valproic Acid:
Salicylates may alter valproic acid (VPA) metabolism and may displace VPA from protein binding sites, possibly intensifying the effects of VPA. Caution is recommended when VPA is administered concomitantly with salicylates. Glucocorticoids (systemic), except hydrocortisone used as replacement therapy in Addison’s disease: Decreased blood salicylate levels during corticosteroid treatment and risk of salicylate overdose after this treatment is stopped via increased elimination of salicylates by corticosteroids.
Concurrent use may increase the incidence of gastrointestinal bleeding and ulceration. e. inhibition of vasodilatory prostaglandins leading to decreased glomerular filtration). The potential interaction may be related to the dose of ASA (3 g/day or more).
Selective Serotonin Re-uptake Inhibitors (SSRIs):
Increased risk of upper gastrointestinal bleeding due to possibly synergistic effect. pdf Pg. 8 Page 9 of 39 NSAIDS: ASA and other NSAIDs: The use of other NSAIDs with salicylates at high doses ( 3g/day) may increase the risk of ulcers and gastrointestinal bleeding due to a synergistic effect.
Ibuprofen:
Ibuprofen can interfere with the anti-platelet effect of low dose ASA (81-325 mg per day). Long-term daily use of ibuprofen may render ASA less effective when used for cardioprotection and stroke prevention. To minimize this interaction, regular users of ibuprofen and of low-dose, immediate-release ASA should take the ibuprofen at least one hour after and 11 hours before the daily ASA dose.
g. enteric-coated) ASA is […]
Special Populations Women attempting to conceive:
During the first and second trimester of pregnancy, acetylsalicylic acid containing drugs should not be given unless clearly necessary. If acetylsalicylic acid containing drugs are used by a woman attempting to conceive, or during the first and second trimester of pregnancy, the dose should be kept as low as possible and duration of treatment as short as possible.
Based on the limited published data available, the studies in humans showed no consistent effect of acetylsalicylic acid on impairment of fertility and there is no conclusive evidence from animal studies.
Pregnant Women:
Acetylsalicylic acid inhibits prostaglandin synthesis. Inhibition of prostaglandin synthesis may adversely affect the pregnancy and/or the embryo/foetal development. Data from epidemiological studies raise concern about an increased risk of miscarriage and of malformations after the use of a prostaglandin synthesis inhibitor in early pregnancy.
The risk is believed to increase with dose and duration of therapy. Available data do not support any association between intake of acetylsalicylic acid and an increased risk for miscarriage. For acetylsalicylic acid the available epidemiological data regarding malformation are not consistent, but an increased risk of gastroschisis could not be excluded.
A prospective study with exposure in early pregnancy (1st-4th month) of about 14,800 mother-child pairs has not yielded any association with an elevated rate of malformations. pdf Pg. 5 Page 6 of 39 • possible prolongation of bleeding time, an anti-aggregating effect which may occur even after very low doses; • inhibition of uterine contractions resulting in delayed or prolonged labour.
Consequently, acetylsalicylic acid is contraindicated in the third trimester of pregnancy.
Nursing Women:
ASA and its metabolites pass into breast milk in small quantities. Since no adverse effects on the infant have been observed after occasional use, interruption of breast-feeding is usually unnecessary. However, on regular use or on intake of high doses, breast feeding should be discontinued early.
Pediatrics:
A possible association between Reye's syndrome and the use of salicylates has been suggested but not established. Reye's syndrome has also occurred in many patients not exposed to salicylates. ASA should not be used in children and teenagers for viral infections with or without fever without consulting a physician.
In certain viral illnesses, especially influenza A, influenza B and varicella, there is a risk of Reye’s syndrome, a very rare but possibly life- threatening illness requiring immediate medical action. The risk may be increased when ASA is given concomitantly; however, no causal relationship has been proven.
Should persistent vomiting occur with such diseases; this may be a sign of Reye’s syndrome.
Low Uric Acid Excretion:
At low doses, ASA reduces excretion of uric acid. This can trigger gout in patients who already tend to have low uric acid excretion.
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency:
In […]