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Pharma News - diclofenac - UGT2B17  May 01, 2023  7 months, 1 week, 20 hours, 1 minute ago

BREAKING NEWS! Pharma News: A Common Painkiller's Hidden Danger Uncovered - Millions at Risk From Using Diclofenac!

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BREAKING NEWS! Pharma News: A Common Painkiller's Hidden Danger Uncovered - Millions at Risk From Using Diclofenac!
Pharma News - diclofenac - UGT2B17  May 01, 2023  7 months, 1 week, 20 hours, 1 minute ago
Pharma News: New research has unveiled the potential reason behind the alarming side effects of a widely-used painkiller, diclofenac, putting millions of people at risk for severe complications. A misunderstood enzyme responsible for metabolizing the drug may be the key factor leading to serious health consequences, including heart damage.

In a groundbreaking study, scientists have discovered a significant link between the poorly understood drug-metabolizing enzyme UGT2B17 and the severe side effects associated with diclofenac. This revelation could pave the way for identifying at-risk individuals and tailoring safer dosing guidelines for specific demographic groups, potentially saving countless lives.
Diclofenac, a popular pain and inflammation treatment for arthritis patients, was previously available over the counter in the US until 2013. The U.S.FDA restricted its use to prescription-only after mounting evidence of its potential to cause heart damage. Despite this, over 10 million prescriptions are written for it annually in the US, and it remains a popular over-the-counter medication in Asia, Africa, and the Middle East according to latest Pharma News reports.
A ticking time bomb, the painkiller continues to pose a risk to the millions of arthritis patients, many of whom are already at risk of heart disease. The danger is exacerbated when diclofenac is consumed, increasing the likelihood of heart attack and stroke.
The study team from the Washington State University (WSU) had previously found that the enzyme UGT2B17, crucial in diclofenac metabolism, varied significantly in expression. The enzyme's presence is notably lower in women compared to men, possibly accounting for the heightened risk of heart damage in female patients. It is also virtually absent in children under nine and exhibits significant ethnicity-based differences.
In their latest study, the study team utilized human liver and intestinal samples, along with computer-based modeling, to quantify the enzyme's contribution to diclofenac metabolism. They discovered that UGT2B17 is a major player, suggesting that low levels of this enzyme may be responsible for the heart damage linked to the drug.
This groundbreaking discovery has shed light on why certain individuals experience heart toxicity from diclofenac. The study highlights the crucial role of UGT2B17 in the drug's metabolism and underscores the enzyme's varying expression levels as a possible reason for the diverse reactions to diclofenac, leading to toxicity in some and ineffectiveness in others.
Interestingly, the study team found that the enzyme primarily metabolizes diclofenac in the intestine, as opposed to other related enzymes that are active in the liver. Consequently, the effects are specific to oral diclofenac tablets, which provide the fastest absorption and pain relief.
This revolutionary finding could lead to the implementation of genetic testing, allowing healthcare providers to assess safety risks before prescribing diclofenac. In countries where the drug is still available over the counter, drug regulatory authorities should consider conducting efficacy testing to determine the optimal dose for the ir local markets.
The study team are currently working on confirming their findings through a pilot clinical trial. The next step will involve partnering with large hospitals to study the relationship between diclofenac and heart damage using patients' electronic medical records.
Stay tuned as this groundbreaking discovery continues to unfold, potentially saving millions of lives and prompting a reevaluation of one of the world's most widely-used painkillers.
The study findings were published in the peer reviewed journal: Clinical Pharmacology & Therapeutics.
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