Formulary
Paracetamol (Acetaminophen): Uses, Dosing, Side Effects and Indian Brand Names
Paracetamol is the most commonly used analgesic and antipyretic globally, acting primarily through central COX inhibition. It lacks anti-inflammatory activity and is hepatotoxic in overdose, with N-acetylcysteine being the specific antidote.
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Clinically reviewed by Awaiting clinical review
Paracetamol (Acetaminophen): Uses, Dosing, Side Effects and Indian Brand Names
Paracetamol is the most commonly used analgesic and antipyretic globally, acting primarily through central COX inhibition. It lacks anti-inflammatory activity and is hepatotoxic in overdose, with N-acetylcysteine being the specific antidote.
NEET PG High-Yield: NAPQI is the toxic metabolite produced by CYP2E1 -- detoxified by glutathione conjugation. N-acetylcysteine (NAC) is the antidote (replenishes glutathione). Paracetamol is safe in pregnancy (Category B), in peptic ulcer patients, and in aspirin allergy. It has NO anti-inflammatory or antiplatelet activity -- a common differentiator question.
Clinical overview
Paracetamol is the most widely used analgesic and antipyretic drug worldwide and in India. It is the first-line drug for mild to moderate pain and fever across all age groups, from neonates to the elderly. Unlike NSAIDs, paracetamol does not cause gastric erosion, does not affect platelet function, and is safe in patients with peptic ulcer disease and bleeding disorders. It lacks clinically significant anti-inflammatory activity, which distinguishes it from NSAIDs and makes it insufficient for inflammatory conditions like rheumatoid arthritis. The major toxicity concern is hepatotoxicity in overdose. Paracetamol is metabolised by conjugation (glucuronidation and sulphation) at therapeutic doses, but a small fraction undergoes CYP2E1-mediated oxidation to the highly reactive toxic metabolite NAPQI (N-acetyl-p-benzoquinone imine). At therapeutic doses, NAPQI is detoxified by glutathione conjugation. In overdose (>150 mg/kg), glutathione stores are depleted, and NAPQI causes centrilobular hepatic necrosis, potentially leading to fulminant liver failure. N-acetylcysteine (NAC) is the specific antidote, replenishing glutathione. The Rumack-Matthew nomogram guides treatment decisions based on timed plasma paracetamol levels. In India, paracetamol is available OTC and is a component of numerous fixed-dose combination analgesics. Its safety in pregnancy (Category B) makes it the analgesic of choice during pregnancy.
Pharmacological class
Paracetamol (Acetaminophen) belongs to the Non-opioid analgesic and antipyretic (para-aminophenol derivative) class. Paracetamol's exact mechanism remains incompletely understood. It inhibits cyclooxygenase (COX) centrally, particularly a COX-3 isoform (a splice variant of COX-1), reducing prostaglandin synthesis in the CNS but not in peripheral tissues. This explains its analgesic and antipyretic effects without significant anti-inflammatory or antiplatelet activity. It may also modulate serotonergic descending pain pathways and interact with the endocannabinoid system via its metabolite AM404.
Indian brand names and formulations
Available as: Crocin (GlaxoSmithKline/Haleon), Dolo (Micro Labs), Calpol (GlaxoSmithKline), Metacin (IPCA Laboratories), Pacimol (Ipca).
Tablets (325 mg, 500 mg, 650 mg), Oral suspension/syrup (120 mg/5 mL, 250 mg/5 mL), Drops (100 mg/mL for infants), IV infusion (1 g/100 mL), Rectal suppositories (80 mg, 170 mg, 325 mg), Effervescent tablets
Regulatory status
Paracetamol (Acetaminophen) is classified under OTC (Over the Counter) in India under the Drugs and Cosmetics Act, 1940. Paracetamol is available over the counter in India and does not require a prescription for sale. It is listed in the NLEM 2022 and WHO Model List of Essential Medicines. Some fixed-dose combinations containing paracetamol with other drugs may fall under Schedule H.
Indications
- Mild to moderate pain (headache, toothache, musculoskeletal pain)
- Fever (antipyretic of choice in all age groups)
- Osteoarthritis (first-line analgesic per guidelines)
- Post-operative pain (as part of multimodal analgesia)
- Pain and fever in patients with peptic ulcer disease, bleeding disorders, or aspirin allergy
- Analgesic of choice during pregnancy and breastfeeding
Dosing
Adults: 500-1000 mg every 4-6 hours, maximum 4 g/day (3 g/day in chronic alcohol users or hepatic impairment). Children: 10-15 mg/kg every 4-6 hours (max 60 mg/kg/day). Neonates: 10 mg/kg every 6-8 hours. IV infusion (Perfalgan): 1 g over 15 minutes, up to 4 g/day. Rectal suppositories: 15-20 mg/kg. Overdose threshold: >150 mg/kg (or >7.5 g in adults) warrants assessment with the Rumack-Matthew nomogram.
Contraindications
- Severe hepatic impairment or active liver disease
- Known hypersensitivity to paracetamol
- Severe renal impairment (reduce dose and extend interval)
- Chronic alcoholism (increased NAPQI production via CYP2E1 induction)
Adverse effects
- Hepatotoxicity (dose-dependent; most important adverse effect, primarily in overdose)
- Acute liver failure (fulminant hepatic necrosis in severe overdose)
- Rarely: thrombocytopenia, leucopenia
- Hypersensitivity reactions (rare: urticaria, angioedema)
- Chronic nephropathy with long-term heavy use (controversial)
- No significant GI toxicity at therapeutic doses (unlike NSAIDs)
Drug interactions
- Warfarin -- chronic paracetamol use (>2 g/day for >1 week) may increase INR
- Alcohol (chronic use) -- induces CYP2E1, increasing NAPQI production and hepatotoxicity risk even at therapeutic doses
- CYP2E1 inducers (isoniazid) -- increased risk of hepatotoxicity
- Metoclopramide -- increases paracetamol absorption rate (useful in migraine)
- Cholestyramine -- reduces paracetamol absorption
Pregnancy and lactation
Category B. Considered the safest analgesic and antipyretic during pregnancy across all trimesters. No established teratogenicity in humans. It is the recommended first-line analgesic by ACOG, FOGSI, and WHO during pregnancy. Unlike NSAIDs, it does not cause premature closure of ductus arteriosus or oligohydramnios.
Exam-style clinical scenario
A 20-year-old college student presents to the emergency department 6 hours after ingesting 30 tablets of paracetamol 500 mg (15 g total) in a suicidal attempt. She has nausea but no jaundice. LFTs are currently normal. What is the immediate management? Answer: This is a potentially lethal overdose (>150 mg/kg). Begin IV N-acetylcysteine (NAC) immediately using the standard 3-bag protocol (150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours). NAC replenishes glutathione and is most effective within 8 hours of ingestion. The 4-hour plasma paracetamol level plotted on the Rumack-Matthew nomogram determines if treatment should continue. Normal LFTs at 6 hours do NOT exclude impending hepatotoxicity -- liver damage peaks at 72-96 hours.
Cost in India
INR 10-30 per strip of 10 tablets (500 mg); Dolo-650: INR 25-30; IV 1g: INR 40-80
Clinical governance
Author: MedNext Editorial Team. Clinical reviewer: Awaiting clinical review. Jurisdiction: India (Drugs and Cosmetics Act, 1940). Sources: CIMS India, Indian Pharmacopoeia. Publication state: Awaiting clinical review. Correction: Report errors at support@mednext.academy.
Frequently Asked Questions
Why is paracetamol safe in peptic ulcer patients while NSAIDs are not?
Paracetamol predominantly inhibits COX in the CNS and has negligible inhibition of COX-1 in peripheral tissues including the gastric mucosa. Since gastric mucosal protection depends on COX-1-derived prostaglandins (PGE2, PGI2), paracetamol does not impair this protective barrier, unlike NSAIDs which inhibit peripheral COX-1 and reduce gastric mucosal blood flow, bicarbonate and mucus secretion.
What is the Rumack-Matthew nomogram?
The Rumack-Matthew nomogram is a graph that plots serum paracetamol concentration against time after ingestion (from 4 to 24 hours) to determine the risk of hepatotoxicity and the need for NAC treatment. A level above the treatment line (starting at 150 mcg/mL at 4 hours in the original line, or 100 mcg/mL in the modified treatment line used in many protocols) indicates the need for NAC therapy.
Why does chronic alcohol use increase paracetamol hepatotoxicity?
Chronic alcohol consumption induces CYP2E1, the enzyme responsible for converting paracetamol to the toxic metabolite NAPQI. Simultaneously, chronic alcohol use depletes hepatic glutathione stores (glutathione is needed to detoxify NAPQI). This dual mechanism -- increased NAPQI production and decreased detoxification capacity -- makes chronic alcoholics vulnerable to hepatotoxicity even at therapeutic doses of paracetamol (the safe limit is reduced to 2 g/day).
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