Paracetamol was licensed for assumedly safe worldwide usage in 1955 and is debatably the most common form of pain relief, headache palliative and hyperthermia medication used in both pediatric and adult populations in the Americas. Acetaminophen as it is commonly referred to in the United States is a component of very numerous treatment protocols for a wide range of ailments worldwide. Its patency permits has given rise to newer names in various countries using such names as paracetamol and panda. Although fatal and nonfatal liver based injuries, (some microscopic and others macroscopic) have been reported since 1966 due to overdose medications (usually self inflicted) due to self medications. Despite these problems, it's a reasonably safe drug when taken within its therapeutic dose range. Paracetamol poisoning is portrayed as a foremost causative factor in the emergence of acute liver damage in the Americas. It is note worthy that certain factors tend to favor the emergence of paracetamol induced liver damage like chronic use of alcohols, certain enzyme inducing drugs, and associated liver parenchymal diseases even under the circumstances of a normal therapeutic usage of the drug-paracetamol / acetaminophen. Certain questions beg for answers. Are there new findings from decades of pharmacovigilance? Is there a possibility of genetic mutations observed? Is paracetamol still steadfastly safe as portrayed in pregnancy as has been documented since 1966? These are some questions seeking updates.
No takes yet. Share an insight, caveat, or question.
L. Njoku Amara Chiemezie (2016) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: