From a BMJ online release (March 17, 2020):
“The finding in two randomised trials that advice to use ibuprofen results in more severe illness or complications helps confirm that the association seen in observational studies is indeed likely to be causal. Advice to use paracetamol (acetaminophen) is also less likely to result in complications.”
Scientists and senior doctors have backed claims by France’s health minister that people showing symptoms of covid-19 should use paracetamol (acetaminophen) rather than ibuprofen, a drug they said might exacerbate the condition.
Ian Jones, a professor of virology at the University of Reading, said that ibuprofen’s anti-inflammatory properties could “dampen down” the immune system, which could slow the recovery process. He added that it was likely, based on similarities between the new virus (SARS-CoV-2) and SARS I, that covid-19 reduces a key enzyme that part regulates the water and salt concentration in the blood and could contribute to the pneumonia seen in extreme cases. “Ibuprofen aggravates this, while paracetamol does not,” he said.
Researchers matched 7,743 people with osteoarthritis with 23,229 healthy people who rarely or never took NSAIDs. People with osteoarthritis had a 42% higher risk of heart failure and a 17% higher risk of coronary artery disease compared with healthy people. After controlling for a range of factors that contribute to heart disease (including high body mass index, high blood pressure, and diabetes), they concluded that 41% of the increased risk of heart disease related to osteoarthritis was due to the use of NSAIDs.
Antibiotic resistance is a global threat for public health. It is widely acknowledged that antibiotics at sub-inhibitory concentrations are important in disseminating antibiotic resistance via horizontal gene transfer. While there is high use of non-antibiotic human-targeted pharmaceuticals in our societies, the potential contribution of these on the spread of antibiotic resistance has been overlooked so far. Here, we report that commonly consumed non-antibiotic pharmaceuticals, including nonsteroidal anti-inflammatories (ibuprofen, naproxen, diclofenac), a lipid-lowering drug (gemfibrozil), and a β-blocker (propanolol), at clinically and environmentally relevant concentrations, significantly accelerated the conjugation of plasmid-borne antibiotic resistance genes.
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