Product Overview
[Drug Name]
Generic Name: Enteric-Coated Aspirin Tablets
Trade Name: Shenwei Enteric-Coated Aspirin Tablets, 25mg x 100 Tablets
[Main Ingredient]
The main ingredient of this product is aspirin. Chemical Name: 2-(Acetoxy)benzoic Acid. Molecular Formula: C9H8O4. Molecular Weight: 180.16
[Properties]
This product is an enteric-coated tablet that appears white after removal of the coating.
[Indications/Main Functions]
Antithrombotic: This product inhibits platelet aggregation, preventing thrombosis. It is clinically used to prevent thrombosis after transient ischemic attack, myocardial infarction, atrial fibrillation, prosthetic heart valves, arteriovenous fistula, or other surgical procedures. It can also be used to treat unstable angina.
[Specifications]
25mg x 100 tablets (Shenwei)
[Dosage and Administration]
Oral. 75mg to 160mg once daily, or as directed by a physician.
Adverse Reactions: Generally, adverse reactions are rare. 1. Common gastrointestinal reactions include nausea, vomiting, and upper abdominal discomfort or pain (caused by direct irritation of the gastric mucosa) (incidence 3%-9%), which generally resolve after discontinuation of the drug. 2. Central nervous system: Reversible tinnitus and hearing loss may occur, typically after a certain course of treatment and when blood concentrations reach 200-300 μg/ml. 3. Allergic reactions: These occur in 0.2% of patients and manifest as asthma, urticaria, angioedema, or shock. These reactions usually occur in susceptible individuals, with rapid onset of respiratory distress and, in severe cases, death. This is known as aspirin asthma. Some cases present with a triad of aspirin allergy, asthma, and nasal polyps, often linked to genetic and environmental factors. 4. Liver and kidney damage is dose-dependent, particularly with excessive doses resulting in blood concentrations exceeding 250 μg/ml. These impairments are reversible and resolve after discontinuation of the drug. However, there have been reports of renal papillary necrosis.
[Contraindications]
1. This product is contraindicated in patients allergic to it. 2. It should be contraindicated in the following situations: active ulcer disease or gastrointestinal bleeding caused by other causes; hemophilia or thrombocytopenia; or patients with a history of allergic reaction to aspirin or other nonsteroidal anti-inflammatory drugs, especially those with asthma, angioedema, or shock.
[Drug Interactions]
1. Concomitant use with other nonsteroidal anti-inflammatory analgesics does not enhance efficacy because this product may reduce the bioavailability of other nonsteroidal anti-inflammatory drugs. Furthermore, gastrointestinal side effects (including ulcers and bleeding) may be increased. Furthermore, due to the enhanced inhibition of platelet aggregation, the risk of bleeding in other areas may be increased. Long-term, high-dose concomitant use of this product with acetaminophen may cause renal disease, including renal papillary necrosis, renal or bladder cancer. 2. Concomitant use with any drug that can cause hypoprothrombinemia, thrombocytopenia, decreased platelet aggregation, or gastrointestinal ulcer bleeding may worsen coagulopathy and increase the risk of bleeding. 3. Concomitant use with anticoagulants (such as dicoumarol and heparin) or thrombolytics (such as streptokinase and urokinase) may increase the risk of bleeding. 4. Urine alkalinizing drugs (such as sodium bicarbonate) and antacids (when used in large amounts over a long period of time) may increase urinary excretion of this drug, reducing blood concentrations. However, discontinuation of alkalinizing drugs after a stable blood concentration of this drug may increase blood concentrations to toxic levels. Carbonic anhydrase inhibitors can alkalinize urine but can cause metabolic acidosis, which not only reduces blood concentrations but also increases the amount of this drug penetrating into brain tissue, thereby increasing toxic reactions. 5. Uricidizing drugs can reduce the excretion of this drug, increasing blood concentrations. Adding uricidifying drugs to patients whose blood concentrations of this drug have stabilized may result in elevated blood concentrations and increased toxic reactions. 6. Glucocorticoids (also known as steroids) can increase the excretion of salicylates. To maintain blood concentrations of this drug when used concomitantly, the dose of this drug should be increased if necessary. Long-term coadministration of this product with hormones, especially when used in large quantities, increases the risk of gastrointestinal ulcers and bleeding. Therefore, concurrent use of these two drugs is currently not recommended clinically. 7. The hypoglycemic effect of insulin or oral hypoglycemic drugs may be enhanced and accelerated by coadministration with this product. 8. Coadministration with methotrexate (MTX) may reduce protein binding of methotrexate and its renal excretion, leading to increased blood concentrations and potentially increased toxicity. 9. The uricosuric effect of probenecid or sulfinpyrazone may be reduced by coadministration with this product; this reduction is significant at blood salicylate concentrations of 50 μg/ml, and even more so at 100-150 μg/ml. Furthermore, probenecid may reduce the renal clearance of salicylates, thereby increasing their blood concentrations.
[Precautions]
1. Hypersensitivity reactions: Allergic reactions to this product may also result in hypersensitivity to another salicylate or non-salicylate NSAID, but this is not always the case. Be vigilant about the possibility of cross-sensitivity and two potential diagnostic interferences: 1) When the daily dose exceeds 2.4g, the copper sulfate urine glucose test may produce a false-positive result. The glucose enzyme urine glucose test may produce a false-negative result. 2) It may interfere with the urine ketone body test. 3) When the blood drug concentration exceeds 130μg/ml, the colorimetric method for measuring serum uric acid may produce a falsely high value, but the uricase method is not affected. 4) This drug may interfere with the fluorescence method for measuring urinary 5-hydroxyindoleacetic acid (5-HIAA). 5) The results of urinary vanillylmandelic acid (VMA) may be high or low depending on the method used. 6) Because this drug inhibits platelet aggregation, it may prolong bleeding time. Doses as low as 40 mg/day can also affect platelet function, but there have been no reports of low doses (<150 mg/day) causing bleeding in clinical practice; 7) In liver function tests, when the blood concentration is 250 μg/ml, alanine aminotransferase, aspartate aminotransferase and serum alkaline phosphatase may have abnormal changes, which can be restored when the dose is reduced; 8) High-dose application, especially when the blood concentration is 300 μg/ml, can prolong the prothrombin time; 9) Daily dosage exceeds 5g and serum cholesterol is low; 10) Because this product acts on the renal tubules, it increases potassium excretion, which can lead to decreased blood potassium; 11 When high-dose application of this product, serum thyroxine (T4) and triiodothyronine (T3) can be measured by radioimmunoassay. Lower results are obtained; 12) Due to competitive renal tubular excretion with phenolsulfonphthalein, this drug reduces phenolsulfonphthalein excretion (i.e., PSP excretion test). 3. Use with caution in the following conditions: 1) Patients with asthma or other allergic reactions; 2) Those with glucose-6-phosphate dehydrogenase deficiency (this drug may occasionally cause hemolytic anemia); 3) Those with gout (this drug may affect the effects of other uricosuric drugs and may cause uric acid retention at low doses); 4) Patients with impaired liver function may experience worsening hepatotoxicity and bleeding tendency. Patients with hepatic insufficiency and cirrhosis are more susceptible to renal adverse reactions; 5) Patients with cardiac insufficiency or hypertension may experience heart failure or pulmonary edema with high-dose use; 6) Patients with renal insufficiency may experience increased risk of renal toxicity; 7) Patients with thrombocytopenia. 4. Regular monitoring of hematocrit, liver function, and serum salicylate levels is recommended for long-term, high-dose use.
[Pediatric Use]
Pediatric patients, especially those with fever and dehydration, are prone to toxic reactions. The use of this product in children with acute febrile illnesses, especially influenza and chickenpox, may be associated with the development of Reye's syndrome, which is rare in China.
[Use in Elderly Patients]
Elderly patients are more susceptible to toxic reactions due to decreased renal function.
[Overdose]
1. Mild: This is a salicylic acid reaction, manifested by headache, dizziness, tinnitus, deafness, vomiting, diarrhea, confusion, sweating, rapid breathing, thirst, involuntary movements of the hands and feet (more common in the elderly), and visual impairment. 2. Severe: Hematuria, convulsions, hallucinations, severe mental disturbances, dyspnea, and unexplained fever may occur. Mental and respiratory disturbances are more pronounced in children. In overdose, laboratory tests may reveal abnormal electroencephalograms (EEGs), acid-base disturbances (respiratory alkalosis and metabolic acidosis), hypoglycemia or hyperglycemia, ketonuria, hyponatremia, hypokalemia, and proteinuria.
[Pharmacology and Toxicology]
Pharmacology: ① Analgesic effect: This drug primarily inhibits the synthesis of prostaglandins and other substances that sensitize pain to mechanical or chemical stimuli (such as bradykinin and histamine). It is a peripherally acting analgesic. However, the possibility of central analgesia (possibly acting on the hypothalamus) cannot be ruled out. ② Anti-inflammatory effect: The exact mechanism is still unclear. It may be because this product acts on inflamed tissues and exerts an anti-inflammatory effect by inhibiting the synthesis of prostaglandins or other substances that can cause inflammatory reactions (such as histamine). Inhibition of the release of lysosomal enzymes and leukocyte chemotaxis may also be related to it. ③ Antipyretic effect: It may act on the hypothalamic thermoregulatory center to cause peripheral vasodilation, increased skin blood flow, sweating, and increased heat dissipation, thereby exerting an antipyretic effect. This central effect may be related to the inhibition of prostaglandin synthesis in the hypothalamus. ④ Anti-rheumatic effect: In addition to antipyretic and analgesic effects, the anti-rheumatic mechanism of this product lies mainly in its anti-inflammatory effect. Inhibition of platelet aggregation: It works by inhibiting platelet cyclooxygenase and reducing the production of prostaglandins.
