EXPERT REACTION: Popping ibuprofen could prolong back pain

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Researchers looked at blood cells of people with low back pain, finding that short-lived inflammation in the body prevented pain from lasting three months - and that using anti-inflammatories like ibuprofen could actually delay recovery. People who took anti-inflammatory drugs were 1.76 times more likely to have pain persist for three months. The team says their research should inform how we treat common pain, and these meds need more scrutiny over their use for back pain and other pain conditions.

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These comments have been collated by the Science Media Centre to provide a variety of expert perspectives on this issue. Feel free to use these quotes in your stories. Views expressed are the personal opinions of the experts named. They do not represent the views of the SMC or any other organisation unless specifically stated.

Dr Bronwyn Lennox Thompson, Senior Lecturer, Academic Coordinator Postgraduate Programmes in Pain & Pain Management, University of Otago, Christchurch

The information content of an organism is recorded in the DNA of its genome and expressed through transcription. Here, mRNA serves as a transient intermediary molecule in the information network, whilst non-coding RNAs perform additional diverse functions. A transcriptome captures a snapshot in time of the total transcripts present in a cell. Transcriptomics technologies provide a broad account of which cellular processes are active and which are dormant.

A variety of genes are involved in many biological processes, one of which may be involved in a person transitioning between acute (short-term) pain to chronic (ongoing or persistent) pain. Some forms of chronic pain may be a disorder in the way the nervous system and the immune system interact, involving neuroinflammation. In acute pain, immune cells converge on damaged tissue (inflammation) and also influence the nervous system. Once activated, these cells enable the release of substances to temporarily alter the peripheral and the central nervous system, as well as cells adjacent to the damaged area. Support cells in the central nervous system are also activated, and control substances that enhance signal transmission in the spinal cord and brain. Both sets of cells (immune cells and support cells) may be involved in the transition from acute pain to chronic pain.

In this study, the researchers investigated molecular mechanisms in peripheral blood immune cells across the whole human transcriptome, and found that acute inflammatory responses appear to protect against developing chronic pain, in people with low back pain. They repeated the same investigation in people with temporomandibular disorder (jaw joint pain) with similar findings.

The researchers used experimental data from rats to understand how the processes developed over time, and followed up with human data from the UK Biobank to look at the impact of using anti-inflammatory drugs for acute pain on long-term outcomes. They found that those people who used anti-inflammatory drugs reported a 1.76 fold greater risk of developing chronic low back pain (at three months), while those who didn’t use anti-inflammatory drugs recovered. The elevated risk was maintained for up to 7 years.

The number of neutrophils (a type of white blood cell) present in the blood stream differentiated between those who used anti-inflammatory drugs, and those who used other pain relieving medications, antidepressants or did not use any medication. Those who used anti-inflammatory drugs showed lower levels of neutrophils over time.

The authors conclude that, while it’s early in this investigation, short-term activity where the number of neutrophils rises briefly due to inflammation in acute pain is beneficial, while blocking this action by using anti-inflammatory medications appears to delay recovery. The authors argue that it’s important to understand the long-term effects of using anti-inflammatory drugs for acute low back pain, as it may lead to poorer outcomes over time.

Last updated:  11 May 2022 3:33pm
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Science Translational Medicine
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Organisation/s: McGill University, Queen’s University (Canada), University of Parma (Italy), Radboudumc (Netherlands), University of North Carolina (US), etc.
Funder: This work was supported by Pfizer Canada Professorship in Pain Research (to L.D.); Canadian Excellence Research Chairs grant CERC09 (to L.D.); Canadian Institutes of Health Research grant 136975 (to P.A.T.); Canadian Institutes of Health Research Foundation grant 154281 (to J.S.M.); National Institute of Dental and Craniofacial Research grant R56DE025298 (to A.G.N. and G.D.S.); National Institute of Dental and Craniofacial Research grant U01DE017018 (to A.G.N., G.D.S., and L.D.); Canadian Institutes of Health Research grants PJT-173288, PJT-169671, and SCA-145102 (to N.G.); European Commission in the context of the Seventh Framework Program grant 602736 (to C.D. and M.A.); and Canadian Institutes of Health Research Strategy for Patient-Oriented Research in Chronic Pain grant SCA-145102 (to L.D.).
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