News briefs

Cate Swannell
Med J Aust 2017; 206 (3): 102. || doi: 10.5694/mja17.n2002
Published online: 20 February 2017

NSAIDs don’t stop back pain

A systematic review from the George Institute for Global Health has found that non-steroidal anti-inflammatory drugs (NSAIDs) commonly used to treat back pain provide little benefit, but cause side effects. Published in the Annals of Rheumatic Disease, the review, which examined 35 trials involving more than 6000 people, found that only one in six patients treated with NSAIDs achieved any significant reduction in pain. Patients taking NSAIDs were 2.5 times more likely to suffer from gastro-intestinal problems such as stomach ulcers and bleeding. Most clinical guidelines currently recommend NSAIDs as the second line analgesics after paracetamol, with opioids coming at third choice. Lead author Associate Professor Manuela Ferreira said the review highlighted an urgent need to develop new therapies to treat back pain. “When you factor in the side effects which are very common, it becomes clear that these drugs are not the answer to providing pain relief to the many millions of Australians who suffer from this debilitating condition every year.”

Gene discovery could prevent onset of MD

An international group including researchers from the Walter and Eliza Hall Institute of Medical Research has found that mutations in a gene called SMCHD1 can cause a rare syndrome called bosma arhinia microphthalmia syndrome (BAMS), in which the nose fails to form during embryonic development. The same gene is also faulty in people with an inherited form of muscular dystrophy called facioscapulohumeral muscular dystrophy type 2 (FSHD2). Published in Nature Genetics, the research compared the genetic changes in SMCHD1 causing BAMS and FSHD. They found that FSHD2 was caused when the protein SMCHD1 was damaged and can no longer function normally. They also found that in children with BAMS the opposite happened – the nose fails to develop in instances where SMCHD1 is activated. “This is really exciting because it gives us clues about how to design medicines that boost SMCHD1’s activity to protect the body from the development of FSHD2,” one of the authors said.

  • Cate Swannell



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