Aspirin 500 Mg 20 Tablets

Aspirin 500 Mg 20 Tablets

ACTION AND MECHANISM

- [ANALGESIC], [ANTIPIRETIC], [ANTI-INFLAMMATORY] and [ANTI-AGGREGANT PLATELET].
* Analgesic action: produces analgesia by acting at the central level on the hypothalamus and at the peripheral level, blocking the generation of painful impulses, by blocking the synthesis of prostaglandins mediated by the inhibition of cyclooxygenase.
* Anti-inflammatory action: inhibits the synthesis of prostaglandins and other mediators of inflammation.
* Antipyretic action: reduces the abnormally high temperature by acting on the thermoregulatory center of the hypothalamus and producing peripheral vasodilation. Vasodilation increases sweating and therefore heat loss.
* Antiplatelet action: It causes irreversible inhibition (acetylation) of the cyclooxygenase enzyme, which intervenes in the synthesis of common precursors of thromboxanes (proaggregates) and prostacyclin, PGI2 (antiplatelet). The predominance of the antiplatelet action is due to the fact that prostacyclin is synthesized by vascular endolethial cells, capable of producing new cyclooxygenase molecules after initial inactivation by acetylsalicylic acid. In contrast, platelets (which are cell fractions and therefore lack a nucleus) are unable to produce new cyclooxygenase molecules, so no precursors of thromboxanes are synthesized.

PHARMACOKINETICS

Oral route:
- Absorption: After oral administration of acetylsalicylic acid, absorption is rapid and complete (absorption of the microencapsulated form is delayed, but continues until completion). Absorption is lower in the initial stages of Kawasaki disease, and then returns to normal values. Cmax is reached, generally within 1-2 hours with single doses. It can be faster with liquid dosage forms.
Lysine acetylsalicylate is a prodrug of acetylsalicylic acid, with better solubility than acetylsalicylic acid. It allows reaching plasma concentrations faster than with conventional forms of acetylsalicylic acid.
Food: Food slows the rate of absorption, but not the final amount absorbed.
- Distribution: Acetylsalicylic acid and salicylic acid bind partially with serum proteins, and mainly with albumin. The degree of binding to plasma proteins is 80-90%. Aspirin and salicylic acid are distributed in the synovial fluid, the central nervous system, and saliva. Salicylic acid easily crosses the placenta, and at high doses, it passes into breast milk.
- Metabolism: Suffers extensive liver metabolism.
- Elimination: The half-life of acetylsalicylic acid is very short (15-20 minutes) since it is rapidly transformed in the digestive mucosa, liver and plasma into salicylic acid by deacetylation, with its half-life of 2-3 hours. Salicylic acid from the hydrolysis of acetylsalicylic acid or salicylates is eliminated with the urine, part metabolized as salicylic acid (80%) and part as conjugates with glucuronides (15%) and glycine. The rate of formation of glycine and glucuronic acid metabolites is saturable. The proportion that is excreted unchanged is pH-dependent (acidic urine: 5%; alkaline urine: up to 85%).
Dialysis: salicylates and their metabolites are rapidly cleared by hemodialysis (there are data for salicylates clearance of 35-100 ml / minute). Peritoneal dialysis clearance is lower and slower.

INDICATIONS

- [FEVER]. Symptomatic treatment of febrile states of any nature.
- [PAIN]. Treatment of pain of mild to moderate intensity, such as [HEADACHE], [DENTALGIA], [DYSMENORRHEA], [CONTRACTURE] muscle or [LOW BACKGROUND].

POSOLOGY

500 mg of acetylsalicylic acid corresponds to 900 mg of lysine acetylsalicylate.
1000 mg of acetylsalicylic acid corresponds to 1800 mg of lysine acetylsalicylate.
- Adults and adolescents over 16 years of age, oral:
* Analgesic and antipyretic: 500 mg / 4-6 hours.
The use of acetylsalicylic acid is subject to the appearance of painful or feverish symptoms, so treatment will be suspended when these disappear.
The maximum recommended dose is 4 g / 24 hours.
- Children and adolescents under 16 years of age, oral: Acetylsalicylic acid is contraindicated in these patients due to the risk of Reye's syndrome.

DOSAGE IN KIDNEY INSUFFICIENCY

* ClCr <10 ml / min: Avoid use.
* Hemodialysis: Dialyzable (50-100%).

DOSAGE IN LIVER INSUFFICIENCY

* Avoid in severe liver failure.

RULES FOR CORRECT ADMINISTRATION

It is recommended to administer acetylsalicylic acid after meals or with milk, especially if gastric damage is observed or in prolonged treatments. In patients treated with high doses on a chronic basis, it is suggested to administer most of the total daily dose at bedtime, together with some food.
The chewable tablets can be taken with or without drinks.
The effervescent tablets will be dissolved in half a glass of water.
The sachets must be dissolved in water, milk or fruit juices.
If the pain continues or worsens after 10 days of treatment, or if the fever does so after 3 days, it is recommended to stop the treatment and see a doctor.

CONTRAINDICATIONS

- Hypersensitivity to any component of the drug, such as [SALICYLATE ALLERGY]. Cross-hypersensitivity reactions have been described with other NSAIDs or with tartrazine, therefore it is not recommended in the case of [NSAID ALLERGY] or azo dyes. These hypersensitivity reactions are especially frequent in patients with [ASTHMA], [NASAL POLYPS] or [IDIOPATIC CHRONIC URTICARIA], therefore, given their seriousness, potentially fatal, it is recommended to avoid the use of acetylsalicylic acid in these patients.
- [PEPTIC ULCER] active, chronic or recurrent, or in any other process that increases the risk of [GASTROINTESTINAL HEMORRHAGE], as well as in patients with a history of bleeding or [GASTRIC PERFORATION] associated with treatment with acetylsalicylic acid. Aspirin has an ulcerogenic effect, which increases the risk of upper gastrointestinal bleeding and gastric perforation.
- [COAGULATION DISORDERS], especially [HEMOPHILIA] or [HYPOPROTHROMBINEMIA], as well as [VITAMIN K DEFICIT]. Acetylsalicylic acid exerts an antiplatelet effect, thereby increasing the risk of bleeding in these patients.
- Severe renal failure (CLcr <30 ml / minute) or severe liver failure (Child-Pugh C).
- Children under 16 years of age with febrile processes, flu or chickenpox, since in these cases the intake of acetylsalicylic acid has been associated with the appearance of Reye's syndrome.
- Third trimester of pregnancy.

PRECAUTIONS

- [RENAL INSUFFICIENCY]. Always use the lowest dose that is effective. ASA is excreted in the urine, so in case of kidney failure, accumulation could occur, with the risk of poisoning. In addition, ASA has occasionally led to a transient decrease in kidney function, and conditions such as interstitial nephritis and nephrotic syndrome. Dosage readjustment may be necessary. It is recommended to avoid its use in patients with severe renal insufficiency (CLcr <30 ml / minute), as well as in patients with decreased albumin levels (See Contraindications).
- [LIVER FAILURE]. Always use the lowest effective dose, due to the accumulation of ASA that is metabolized in the liver. In addition, in patients with liver failure, bleeding is more frequent, due to the decrease in the production of clotting factors. It is recommended to avoid the use of acetylsalicylic acid in patients with severe hepatic impairment (Child-Pugh class C) (See Contraindications).
- [DIABETES]. ASA could lead to hypoglycemia when administered in high doses. It is recommended to monitor blood glucose levels before and after high-dose treatment with ASA.
- [GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY]. The administration of high doses of ASA, greater than 1 g per day, has been associated on rare occasions with the appearance of hemolytic anemia, so extreme precautions are recommended.
- [ARTERIAL HYPERTENSION] or [HEART FAILURE] not controlled. ASA could lead to fluid retention, which could worsen these diseases, especially in cases in which there is no previous treatment, or in which it has not been able to control the disease.
- [DROP]. The AAS could compete with the urates in their elimination, being able to increase their levels. Caution is advised in patients with gout.
- [SURGERY]. It is recommended to suspend the administration of ASA at least 5-7 days before a surgical intervention, including dental extractions, due to the risk of bleeding during the operation. The chewable tablets should not be used within seven days after tooth extraction, tonsillectomy, or oral cavity surgery.
- Gastric damage. Acetylsalicylic acid can lead to the appearance of erosion of the gastric mucosa, which could progress to a peptic ulcer, and in more serious situations to gastric bleeding and / or gastric perforation. This adverse reaction can appear at any time during treatment, even in patients without a history of peptic ulcer, so be very vigilant in case symptoms appear, such as burning, abdominal pain, general unjustified weakness, cold sweat, dizziness, hypotension , melena or hematemesis. Precautions should be greater in patients with a history of peptic ulcer. If symptoms of peptic ulcer or gastric bleeding appear, it is advisable to suspend treatment (See Contraindications).
Concomitant treatment with medications that increase the risk of bleeding, especially upper gastrointestinal bleeding, such as corticosteroids, non-steroidal anti-inflammatory drugs, antidepressants such as selective serotonin reuptake inhibitors, antiplatelet agents, anticoagulants, should be avoided. Treatment should be interrupted in the event of the appearance of melena, hematemesis, hypotension, cold sweats, abdominal pain and dizziness
and seek medical advice immediately.
- Alcohol. Alcohol should not be ingested as it increases the gastrointestinal adverse effects of acetylsalicylic acid, and is a triggering factor in chronic irritation. In cases of chronic alcoholism it can cause gastric bleeding.
- [BRONCHIAL SPASM]. In the case of pre-existing risk factors such as: asthma, hay fever, nasal polyps or chronic respiratory failure, bronchospasm can occur and induce asthma attacks or other hypersensitivity reactions. Likewise, it can occur in patients with other allergic manifestations, such as skin reactions, itching or hives.

ADVICE TO THE PATIENT

- It is recommended to administer acetylsalicylic acid after meals.
- It is advisable to avoid the intake of alcoholic beverages during the treatment.
- Symptoms such as burning, abdominal pain, general unwarranted weakness, cold sweat, dizziness, hypotension, bloody vomiting or blackish stools should be reported to the doctor.
- If the patient is going to undergo a dental extraction or other type of surgery, the treatment should be suspended 5-7 days before the intervention.
- It is advisable to avoid the use of chewable tablets in the 7 days after dental extractions, tonsillectomies or surgery of the oral cavity.
- If the pain and / or fever continue after 10 and 3 days respectively of treatment, it is advisable to see a doctor.
- Do not use in children and adolescents under 16 years of age.

SPECIAL WARNINGS

>> Do not use in children under 16 years of age as the use of acetylsalicylic acid has been associated with Reye's Syndrome, a rare but serious disease.
- It is recommended to control blood glucose in diabetic patients receiving high doses of acetylsalicylic acid.
- It is recommended to monitor kidney function and hematocrit in patients receiving high doses of salicylates for prolonged periods of time.
- In patients treated with oral anticoagulants or heparin, it is advisable to monitor coagulation.
- It is advisable to control blood pressure in hypertensive patients, since ASA could interfere with the effects of many antihypertensive drugs.

INTERACTIONS

- Acetazolamide. ASA has led to increases in acetazolamide levels of up to 80-200%, probably due to displacement of plasma protein binding. There is a risk of poisoning, so it is recommended to avoid administration. Furthermore, acetazolamide could lead to systemic acidosis, which could delay the elimination of salicylates. Although no cases of this interaction have been recorded with other carbonic anhydrase inhibitors, it cannot be ruled out.
- Urinary acidifiers (ascorbic acid, ammonium chloride, methionine) or urinary alkalinizers (absorbable antacids). ASA is a weak acid whose elimination in urine depends on urinary pH. Those drugs that lower the pH will decrease renal elimination, while those that increase the pH will lead to increased elimination.
- Tiludronic acid. The interaction has been detected in pharmacokinetic terms, since ASA could decrease the bioavailability of tiludronate by up to 50% when taken within one hour of tiludronate. It is recommended to distance the administrations of these drugs at least 2 hours.
- Valproic acid. There have been cases of increased levels of valproate associated with the administration of ASA. The interaction could be due to competition between both drugs for the same renal elimination mechanism. Posology readjustment may be necessary.
- NSAIDs. Co-administration of ASA with other NSAIDs, including coxibes, could increase the risk of peptic ulcer and gastric bleeding. In addition, it has been proven that ASA could reduce the plasma levels of other NSAIDs, especially those with an arylpropionic structure such as ibuprofen.
-Aliskiren. Possible reduction of the antihypertensive effect of aliskiren (NSAIDs act on the renin-angiotensin system). In patients with compromised renal function (dehydrated or elderly), deterioration of renal function may be precipitated (possible acute renal failure, usually reversible). Caution, especially in the elderly, monitoring the antihypertensive effect and kidney function.
- Antacids. Antacids may delay and decrease the absorption of ASA. Additionally, absorbable antacids may increase the elimination of ASA.
- Antiplatelet agents. Clopidogrel and ticlopidine could potentiate the antiplatelet effects of ASA. For its part, dipyridamole has increased in pharmacokinetic studies an increase in Cmax and AUC of 31.5% and 37% respectively, probably due to the inhibition of metabolism, with the consequent risk of toxicity. In the case of prasugrel, concomitent administration is indicated, since the efficacy and safety of prasugrel was studied in patients receiving ASA.
- Oral anticoagulants. ASA has led to a potentiation of the effects of anticoagulants such as acenocoumarol, with the consequent risk of bleeding, especially of gastric origin. This interaction could be due to the hypoprothrombinemic effects of ASA at high doses (more than 3 g) or to the inhibition of platelet aggregation. The administration of punctual doses of ASA does not appear to pose a great risk. However, it is advisable to avoid association in patients treated with ASA for long periods, using salicylates or other NSAIDs without antiplatelet effects, and if this is not possible, to exercise extreme caution and control the INR.
- Antiulcer. Pharmacokinetic studies have shown that the increase in gastric pH produced by h3 antihistamines or hydrogen ions pump inhibitors could increase the absorption of ASA, with the possible risk of poisoning. In the case of patients receiving high doses of ASA, a decrease in dosage may be necessary.
- Barbiturates. ASA could increase barbiturate concentrations, with the consequent risk of poisoning.
- Beta-blockers. Administration of ASA at high doses, greater than 2 g, has resulted in a decrease in the antihypertensive effects of beta-blockers. Although the cause is unknown, it could probably be due to inhibition of prostaglandin synthesis, which appear to mediate the antihypertensive effects of beta-blockers. It is therefore recommended to avoid treatment with high doses of ASA in patients treated with a beta-blocker.
- Cyclosporine. NSAIDs may increase cyclosporine nephrotoxicity. It is recommended to periodically evaluate kidney function, especially in the elderly.
- Corticosteroids. There is an increased risk of damage to the gastric mucosa. Furthermore, it appears that corticosteroids could reduce plasma levels of ASA, although the mechanism is unclear. However, it is believed that it could be due to an increase in glomerular filtration and a decrease in tubular reabsorption. For its part, ASA could displace corticosteroids from their protein binding, leading to toxic effects.
- Digoxin. ASA could increase digoxin concentrations, increasing the risk of poisoning. Dosage readjustment may be necessary.
- Diuretics. In several trials it has been shown that ASA could slightly reduce the diuretic effects of drugs such as furosemide, and the natriuretics of spironolactone. In addition, the appearance of acute renal failure could be more frequent, especially in dehydrated patients treated with thiazide diuretics.
- Ototoxic drugs. ASA could increase the ototoxicity of drugs such as aminoglycosides, cisplatin, erythromycin, furosemide, or vancomycin, especially at high doses.
- Phenytoin. ASA could, at high doses, displace phenytoin from its protein binding sites, leading to toxic effects. However, symptoms of this interaction do not usually appear, since free phenytoin undergoes a redistribution in the tissues, decreasing its plasma concentrations. It is recommended to monitor the patient.
- Griseofulvin. Griseofulvin could intensely decrease the absorption of ASA, so it is recommended to avoid the association.
- Heparin. A large number of cases of patients have been described in which the administration of heparin together with ASA resulted in a potentiation of the anticoagulant effects, with an increased risk of bleeding. Although heparin has been associated with ASA to reduce mortality associated with postoperative thromboembolism, the risk in each patient must be evaluated, and their coagulation parameters must be controlled.
- Ibuprofen. Experimental data suggest that ibuprofen may inhibit the effect of
low-dose ASA on platelet aggregation when administered concomitantly. However, there is no clinical evidence and it is likely that there is no relevant effect with the occasional use of ibuprofen.
- ACEI. There are studies in which it has been possible to verify an antagonistic effect of NSAIDs at doses greater than 1 g, on ACE inhibitors, probably due to the inhibition of prostaglandin synthesis, which have vasodilator effects. Regular monitoring of blood pressure is recommended.
- SSRI. There is an increased risk of bleeding in general, and gastric in particular, so it is recommended to avoid the association.
- Lithium. ASA could decrease lithium clearance, increasing the risk of poisoning. Dosage readjustment may be necessary.
- Methotrexate. Numerous cases have been described in which the administration of ASA potentiated the effects of methotrexate. The effects could be due to the displacement of methotrexate from its protein binding sites by ASA, or due to decreased renal clearance due to inhibition of tubular secretion. This effect is especially important in elderly patients with kidney failure. Extreme precautions are recommended, given the risk of severe pancytopenia.
- Nitroglycerin. In pharmacokinetic studies, it has been shown that ASA could increase plasma nitroglycerin levels by up to 54%, perhaps due to decreased hepatic flux and nitroglycerin metabolism. On the contrary, prolonged treatments with ASA led to an increase in the need for nitroglycerin for the same effect, perhaps due to a decrease in the production of vasodilator prostaglandins. It is recommended to monitor the patient.
- Pentazocine. A case of reversible renal toxicity of ASA has been described when adding pentazocine. It is recommended to evaluate the renal function of the patient.
- Sulfonylureas. The administration of ASA at high doses, greater than 2 g, could potentiate the hypoglycemic effects of sulfonylureas. The mechanism is unknown, but ASA could displace sulfonylureas from their binding sites to plasma proteins, while it could reduce the renal elimination of some of them, such as chlorpropamide. It is recommended to monitor blood glucose, especially when starting and ending treatment with ASA, adjusting the sulfonylurea dosage if necessary.
- Uricosuric. ASA has uricosuric effects at high doses, greater than 3 g, but at low doses, it has been shown that it can antagonize the effects of probenecid or sulfinpyrazone. In addition, uricosuric drugs may decrease the elimination of AAS. A buildup of uric acid and ASA can occur. It is therefore recommended to avoid association.
- Verapamil. Cases of potentiation of the antiplatelet effects of ASA by verapamil have been described. Monitoring the patient is recommended.
- Zafirlukast. In pharmacokinetic studies it has been shown that ASA could increase the levels of zafirlukast up to 45%, with the possible risk of toxicity. It is recommended to monitor the patient.
- Zidovudine. Zidovudine plasma concentrations can be increased by competitively inhibiting glucuronidation or directly by inhibiting
hepatic microsomal metabolism , reaching toxic levels. Caution must be exercised. It also increases the toxicity of acetylsalicylic acid.
- Food. Pharmacokinetic studies have shown that the administration of ASA after meals could reduce absorption by up to 50%. Therefore, if rapid effects are desired, it is advisable to administer ASA on an empty stomach. However, administration with meals reduces the risk of gastric irritation.
- Ethyl alcohol. There is an increased risk of gastric damage, so it is recommended to avoid alcohol consumption, especially in the 8-10 hours after a dose of ASA. Those patients who ingest more than three alcoholic beverages daily should avoid the use of ASA, replacing it with another NSAID.

PREGNANCY

FDA Category D. Animal studies with salicylates have reported teratogenic and embryocidal effects. Salicylates quickly cross the placenta. Epidemiological studies suggest an increased risk of miscarriage and congenital malformations (including cardiac malformations and gastroschisis). During the first and second trimesters of pregnancy, acetylsalicylic acid should not be administered unless strictly necessary, with the lowest possible dose and the shortest possible duration of treatment. During the third trimester of pregnancy, the use of prostaglandin synthesis inhibitors can expose the fetus to cardiopulmonary toxicity (with premature closure of the ductus arteriosus and pulmonary hypertension) and renal failure, which can lead to renal failure and oligohydroamniosis. Likewise,It can expose the mother and the child, at the end of pregnancy, to a possible prolongation of the bleeding time, an antiplatelet effect that can occur even at very low doses and to an inhibition of uterine contractions leading to a delay or prolongation of labor. Chronic treatment with high doses of salicylates during late pregnancy can prolong and complicate labor and increase the risk of maternal or fetal bleeding. Therefore, salicylates should only be taken during pregnancy after a strict benefit-risk assessment, being contraindicated during the third trimester of pregnancy.antiaggregant effect that can occur even at very low doses and an inhibition of uterine contractions leading to a delay or prolongation of labor. Chronic treatment with high doses of salicylates during late pregnancy can prolong and complicate labor and increase the risk of maternal or fetal bleeding. Therefore, salicylates should only be taken during pregnancy after a strict benefit-risk assessment, being contraindicated during the third trimester of pregnancy.antiaggregant effect that can occur even at very low doses and an inhibition of uterine contractions leading to a delay or prolongation of labor. Chronic treatment with high doses of salicylates during late pregnancy can prolong and complicate labor and increase the risk of maternal or fetal bleeding. Therefore, salicylates should only be taken during pregnancy after a strict benefit-risk assessment, being contraindicated during the third trimester of pregnancy.salicylates should only be taken during pregnancy after a strict evaluation of the benefit-risk ratio, being contraindicated during the third trimester of pregnancy.salicylates should only be taken during pregnancy after a strict evaluation of the benefit-risk ratio, being contraindicated during the third trimester of pregnancy.
Animal studies have shown reproductive toxicity.

LACTATION

Acetylsalicylic acid, as well as other salicylates, are excreted in human milk in low amounts. There is a potential risk of effects on platelet function in the newborn, although these have not been reported with the use of ASA. In general, it is recommended to suspend breastfeeding in nursing mothers with long-term therapy and / or high doses; however, it has been observed that occasional single doses do not appear to have significant risk to the infant.

CHILDREN

The use of salicylates, particularly ASA, in children under 16 years of age with acute febrile illnesses, especially influenza and chickenpox, is associated with the development of Reye's syndrome (encephalopathy of hepatic origin, with a high mortality rate). This syndrome is very rare, it only appears in children and adolescents. The risk disappears once they stop taking ASA. Therefore, as a preventive measure, it should not be used in this circumstance. Children with fever or dehydration may also be more susceptible to other forms of salicylate toxicity. Special monitoring of serum salicylate levels is recommended in children with Kawasaki disease,since therapeutic concentrations of salicylates in plasma can be difficult to achieve as the absorption of ASA is altered during the initial febrile stages of the disease; As the feverish state passes, absorption improves, so if the dose is not readjusted, salicylate toxicity can occur.

SENIORS

Geriatric patients may be more sensitive to the toxic effects of salicylates, possibly due to decreased kidney function. Lower doses may be required, especially for long-term use.

ADVERSE REACTIONS

Adverse reactions are described according to each frequency range, being considered very common (> 10%), common (1-10%), uncommon (0.1-1%), rare (0.01-0.1%) , very rare (<0.01%) or of unknown frequency (cannot be estimated from the available data).
- Hematological: Common: [BLEEDING] (increased risk), perioperative bleeding, [HEMATOMA],, [GINGIVAL HEMORRHAGE], [GENITOURINARY HEMORRHAGE], [HYPOPROTHROMBINEMIA] (with high doses). Uncommon: [ANEMIA]. Rare: chronic post-hemorrhagic anemias due to bleeding or hidden bleeding, which will present typical symptoms such as [ASTENIA], [PALE], hypoperfusion. Very rare: [BRAIN HEMORRHAGE], especially in patients with uncontrolled hypertension taking concomitant anticoagulant agents.
- Respiratory: Common: [BRONCHIAL SPASM] paroxysmal, [DYSNEA] severe, [RHINITIS], [ASTHMA], [NASAL CONGESTION]. Very rare: [ANAPHYLAXY].
- Digestive: Common: [GASTRIC ULCER], [DUODENAL ULCER], [MELENA], [HEMATEMESIS], [ABDOMINAL PAIN], [DYSPEPSIA], [NAUSEA], [VOMITING]. Rare: [INFLAMMATION] gastrointestinal. Very rare: [GASTRIC PERFORATION]
- Dermatological: Frequent: [URTICARIA], [EXANTEMATIC ERUPTIONS], [ANGIOEDEMA], [PRURITO]. Unknown frequency: [EXCESS SWEATING].
- Hepatic: Uncommon: [HEPATITIS] (particularly in patients with juvenile arthritis). Very rare: [HEPATIC INSUFFICIENCY] transient with [INCREASED TRANSAMINASES].
- Neurological / psychological: Unknown frequency: [HEADACHE], [DIZZINESS], [CONFUSION].
- Optics: Unknown frequency: [TINNITUS], [DEAF].
- Genitourinary: Unknown frequency: [ACUTE RENAL INSUFFICIENCY], [ACUTE TUBULOINTERSTICIAL NEPHRITIS].
- General: Uncommon: [REYE'S SYNDROME] (in children under 16 years of age with febrile processes, flu or chickenpox).
In patients with a history of hypersensitivity to acetylsalicylic acid and other non-steroidal anti-inflammatory drugs, anaphylactic or anaphylactoid reactions may occur. This could also happen in patients who have not previously shown hypersensitivity to these drugs.

OVERDOSE

With doses of more than 100 mg / kg / day for more than two days it can cause salicylism. It is possible to differentiate between chronic toxicity and acute toxicity. Signs of salicism appear when plasma salicylate concentrations exceed 300 mg / l.
- Symptoms: Symptoms of overtoxification are: dizziness, vertigo, ringing in the ears, nausea, vomiting, deafness, sweating, headaches and confusion, vasodilation and hyperventilation, blurred vision, and occasionally diarrhea. Vasodilation and sweating are the result of an accelerated metabolism. Symptoms of chronic toxicity can be controlled by reducing the dose.
In acute toxicity, it is the alteration in the acid-base balance that can influence the toxicity of salicylates, changing their distribution between plasma and tissues. The most common presentation for children is metabolic acidosis. Stimulation of respiration produces hyperventilation and respiratory alkalosis. Impaired oxidative phosphorylation produces metabolic acidosis. In children up to four years of age, the metabolic component tends to predominate, while in older children and adults respiratory alkalosis is more common. The absorption of ASA may be decreased due to slow gastric emptying, stomach stone formation, or as a result of the ingestion of enteric-coated preparations.
- Treatment: There is no antidote to salicylate poisoning. In the event of an overdose, the patient should be kept under observation for at least 24 hours, since the symptoms and levels of salicylate in the blood may not become evident for several hours. Overdose is treated with gastric lavage, forced alkaline diuresis, repeated administration of activated charcoal, and supportive therapy with administration of fluids and electrolytes. Restoration of acid-base balance may be required along with hemodialysis in acute cases. 

Aspirin Leaflet 500 Mg 20 Ta