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Posology
The recommended dosage is 1 tablet once daily or as directed by the Physician.
Special population
Renal Impairment: Patients who have been diagnosed with renal impairment must seek medical advice before taking this medication. The restrictions
related to the use of paracetamol products in patients with renal impairment are primarily a consequence of the paracetamol content of the drug.
Hepatic Impairment : Patients who have been diagnosed with liver impairment must seek medical advice before taking this medication. The restrictions
related to the use of Paracetamol products in patients with hepatic impairment are primarily a consequence of the paracetamol content of the drug.
Method of administration : For oral administration only.
Patient should be advised to swallow the tablet whole, not be chewed or crushed.
Contraindicated in patients with:
Known hypersensitivity to acetaminophen (Paracetamol) or any of the other ingredients/components of the product.
Severe and active hepatic impairment.
Warning
Taking more than daily dose may cause serious liver damage or allergic reactions (e.g. swelling of the face, mouth and throat, difficulty in breathing, itching or rash).
Do not exceed the recommended dose.
Immediate medical advice should be sought in the event of an overdose, even if you feel well, because of the risk of delayed, serious liver damage.
If symptoms persist consult your doctor.
Do not use with any other products containing acetaminophen.
Keep all medicines out of the reach of children.
Care is advised in the administration of paracetamol to patients with severe renal or severe hepatic impairment. The hazards of overdose are greater in those with non-cirrhotic alcoholic liver disease.
Do not exceed the stated dose.
Do not take with any other paracetamol-containing products. If symptoms persist for more than 3 days or get worse consult with the physician.
Hepatotoxicity
Acetaminophen (Paracetamol) has been associated with cases of acute liver failure, at times resulting in liver transplant and death. Most of the cases of liver injury are associated with the use of acetaminophen at doses that exceed 4,000 milligrams per day, and often involve more than one acetaminophencontaining product. Cases of hepatic dysfunction/failure have been reported in patients with depleted glutathione levels, such as those who are severely malnourished, anorexic, have a low body mass index are chronic heavy users of alcohol or have sepsis. In patients with glutathione depleted states the use of paracetamol may increase the risk of metabolic acidosis. Paracetamol should be given with care to patients with impaired kidney or liver function.
Where analgesics are used long-term (>3 months) with administration every two days or more frequently, headache may develop or worsen. Headache induced by overuse of analgesics (MOH medication-overuse headache) should not be treated by dose increase. In such cases, the use of analgesics should be discontinued in consultation with the doctor. Care is advised in the administration of paracetamol to patients with alcohol dependency, severe renal or severe hepatic impairment. The hazards of overdose are greater in those with non-cirrhotic alcoholic liver disease. Acetaminophen provides symptomatic relief only, additional therapy to treat the cause of the pain or fever should be instituted when necessary.
The hepatotoxicity of Paracetamol, particularly after overdosage, may be increased by drugs which induce liver microsomal enzymes such as barbiturates, tricyclic antidepressants, and alcohol.
Chronic alcohol intake can increase the hepatotoxicity of paracetamol overdose and may have contributed to the acute pancreatitis reported in one patient who had taken an overdose of paracetamol. Acute alcohol intake may diminish an individual’s ability to metabolize large doses of paracetamol, the plasma half-life of which can be prolonged.
Cholestyramine:
The speed of absorption of paracetamol is reduced by cholestyramine. Therefore, the cholestyramine should not be taken within one hour if maximal analgesia is required.
Metoclopramide and Domperidone:
The absorption of paracetamol is increased by metoclopramide and domperidone. However, concurrent use need not be avoided.
Imatinib:
Restriction or avoidance of concomitant regular paracetamol use should be taken with imatinib.
Warfarin:
The anticoagulant effect of warfarin and other coumarins may be enhanced by prolonged regular use of paracetamol with increased risk of bleeding; occasional doses have no significant effect.
Chloramphenicol: Increased plasma concentration of chloramphenicol.
Antivirals:
Regular use of Paracetamol possibly reduces metabolism of Zidovudine (increased risk of neutropenia).
The use of drugs that induce hepatic microsomal enzymes such as anticonvulsants and oral contraceptives may increase the extent of metabolism of paracetamol resulting in reduced plasma concentrations of the drug and a faster elimination rate.
Pregnancy
A large amount of data on pregnant women indicates neither malformative, nor feto/neonatal toxicity. Epidemiological studies on neurodevelopment in children exposed to paracetamol in utero show inconclusive results. If clinically needed, paracetamol can be used during pregnancy however it should be used at the lowest effective dose for the shortest possible time and at the lowest possible frequency.
It is considered to be the analgesic of choice in pregnant patients. Although it crosses placenta, paracetamol is considered to be safe in normal therapeutic doses for short-term use as a minor analgesic/antipyretic in pregnancy.
Lactation
It is not recommended for use by lactating mothers. It is excreted in breast milk. Maternal ingestion of paracetamol in normal therapeutic doses does not appear to present a risk to the nursing infant. Available published data do not contraindicate breast feeding.
It is unlikely to impair a patient’s ability to drive or use machinery.
Fixed drug eruption (FDE) has been reported with Paracetamol
Adverse effects of paracetamol are rare but hypersensitivity including skin rash may occur. There have been reports of blood dyscrasias including thrombocytopenia and agranulocytosis, but these were not necessarily causality related to paracetamol. Very rare cases of serious skin reactions have been reported.
Cases of acute pancreatitis have been reported. Paracetamol has been widely used and reports of adverse reactions are rare, and are generally associated with overdosage. Allergic reactions occur occasionally.
Chronic hepatic necrosis has been reported in a patient who took daily therapeutic doses of paracetamol for about a year and liver damage has been reported after daily ingestion of excessive amounts for shorter periods. A review of a group of patients with chronic active hepatitis failed to reveal differences in the abnormalities of liver function in those who were long-term users of paracetamol nor was the control of the disease improved after paracetamol withdrawal.
Low level transaminase elevations may occur in some patients taking therapeutic doses of paracetamol; these are not accompanied with liver failure and usually resolve with continued therapy or discontinuation of paracetamol.
Nephrotoxic effects are uncommon and have not been reported in association with therapeutic doses, except after prolonged administration.
Post-marketing data
Blood and lymphatic system disorders: Very rare: Thrombocytopaenia.
Immune System disorders: Very rare: Anaphylaxis cutaneous hypersensitivity reactions including, among others, skin rashes, angioedema, Stevens- Johnson syndrome and Toxic Epidermal Necrolysis.
Respiratory, thoracic and mediastinal disorders: Very rare: Bronchospasm in patients sensitive to aspirin and other NSAIDs.
Hepatobiliary disorders: Very rare: Hepatic dysfunction.
Reporting of side effects or suspected adverse reaction: If you get or experience any side effects, talk to your doctor or pharmacist or report to indiadrugsafety@akums.in. You can also report side effects directly via the National Pharmacovigilance Program of India by calling on 1800 180 3024. By reporting side effects, you can help provide more information on the safety of this product.
Liver damage is possible in adults who have taken 10g or more of paracetamol. Ingestion of 5g or more of paracetamol may lead to liver damage if the patient has risk factors.
Risk Factors: If the patient: A, Is on long term treatment with carbamazepine, phenobarbital, phenytoin, primidone, rifampicin, St John’s Wort or other drugs than induce liver enzymes. Or B, Regularly consumes ethanol in excess of recommended amounts. Or C, is likely to be glutathione depleted e.g. eating disorders, cystic fibrosis, HIV, starvation, cachexia.
Symptoms of paracetamol overdosage in the first 24 hours are pallor, nausea, vomiting, anorexia and abdominal pain. Liver damage may become apparent 12 to 48 hours after ingestion. Abnormalities of glucose metabolism and metabolic acidosis may occur. In severe poisoning, hepatic failure may progress to encephalopathy, haemorrhage, hypoglycaemia, cerebral oedema, and death. Acute renal failure with acute tubular necrosis, strongly suggested by loin pain, haematuria and proteinuria, may develop even in the absence of severe liver damage. Cardiac arrhythmias and pancreatitis have been reported.
Immediate treatment is essential in the management of paracetamol overdose. Despite a lack of significant early symptoms, patients should be referred to hospital urgently for immediate medical attention. Symptoms may be limited to nausea or vomiting and may not reflect the severity of overdose or the risk of organ damage.
Treatment: In cases of overdose, methods of reducing the absorption of ingested drug are important. Gastric lavage is essential even if several hours have elapsed. Prompt administration of 50g activated charcoal and 500ml iced mannitol 20% by mouth, may reduce absorption. If the history suggests that 15g Paracetamol or more has been ingested, administer one of the following antidotes:
Acetylcysteine 20% i.v.:
Administer intravenously, 20% acetlcysteine immediately without waiting for positive urine test or plasma level results: initial dose of 150mg/kg over 15 minutes, followed by continuous infusion of 50mg/kg in 500ml 5% glucose/dextrose over 4 hours and 100mg/kg in 1L 5% glucose/dextrose over 16 hours; or
Oral Methionine:
2.5g immediately followed by three further doses of 2.5g at four hourly intervals. For a 3 year old child, 1g methionine every four hours for four doses has been used; or
Oral Acetylcysteine 5%:
140mg/kg as a loading dose, then 70mg/kg every 4 hours for a total of 17 maintenance doses. If more than ten hours have elapsed since the overdosage was taken, the antidote may be in ineffective.
Pharmacodynamic properties
Pharmacotherapeutic group: Other analgesics and antipyretics, Anilides.
Paracetamol is a centrally acting analgesic and antipyretic with minimal anti-inflammatory properties.
Analgesic:
The mechanism of analgesic action has not been fully determined. Paracetamol may act predominantly by inhibiting prostaglandin synthesis in the central nervous system (specifically cyclooxygenase (COX)-2) and, to a lesser extent, through a peripheral action by blocking pain-impulse generation. The peripheral action may also be due to inhibition of prostaglandin synthesis or to inhibition of the synthesis or actions of other substances that sensitize pain receptors to mechanical or chemical stimulation.
Antipyretic:
Paracetamol act centrally on the hypothalamic heat-regulating center to produce peripheral vasodilatation resulting in increased blood flow through the skin, sweating and heat loss. Paracetamol reduces fever by inhibiting the formulation and release of prostaglandins in the CNS and by inhibiting endogenous pyrogens at the hypothalamic thermoregulator center.
Pharmacokinetic properties
Following oral administration paracetamol is rapidly absorbed.
Paracetamol absorption takes place mainly in the small intestine and therefore the rate of absorption is depending on the rate of gastric emptying. It has been shown that drugs which delay gastric emptying also delay the absorption of paracetamol whereas metoclopramide (a drug which increases the rate of gastric emptying) accelerates absorption of the analgesic through the total amount absorbed doses not increase.
The presence of food in the stomach has also been reported to reduce the rate of absorption of paracetamol. Alterations in gastric pH have no appreciable effect on paracetamol absorption.
During absorption, the amount of paracetamol which is inactivated is negligiable and it has been shown that paracetamol dose not affect gastric mucosal permeability and does not produce mucosal bleeding.
Peak plasma concentrations are reached 1 hour after absorption. The plasma half-life is 1 to 3 hours.
Paracetamol penetrates the brain and is present in breast milk of human.
Paracetamol is metabolized by the microsomal enzyme system of the liver. This metabolism is mainly to the glucuronide and sulphate conjugates, accounting for approximately 49% and 26% of the ingested dose respectively. About 4% is excreted as free paracetamol. Other minor pathways include the production of catechol derivatives and cysteine conjugates (via glutathione). Paracetamol excretion is rapid and occurs via the urine.
Not known.