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High on drugs: lessons from opiates in pancreatitis
  1. Vijay P Singh
  1. Department of Medicine, Mayo Clinic, Scottsdale, Arizona, USA
  1. Correspondence to Vijay P Singh, Division of Gastroenterology and Hepatology, Mayo Clinic, Scottsdale, Arizona, USA; singh.vijay{at}mayo.edu

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The current opiate epidemic, the widespread clinical utilisation of opiates, along with the controversies that revolve around their use, mandate that we take a fresh look at the risks and benefits of this invaluable yet potentially hazardous class of drugs. Pancreatitis is a common illness in which opiates are used extensively for pain control. With the well-known overlap between the complications of acute pancreatitis and opiate use, that is, ileus and bacterial translocation, and the difficulty in identifying the underlying causality in a clinical scenario, it is appropriate that this dilemma be approached using animal models. Additionally, the recent paradigm1 that chronic pancreatitis (for which opioids may be used for long periods) evolves from recurrent acute attacks reinforces the need to weigh the risks this usage may create apart from opiate abuse.

In the study entitled ‘Morphine worsens the severity and prevents pancreatic regeneration in mouse models of acute pancreatitis’, Balrass et al2 present a clinically relevant argument of the multiple ways in which opiates may be worsening the outcomes of acute pancreatitis (AP). They postulate three mechanisms: (1) increased bacterial translocation, (2) a temporal delay in the reparative inflammatory response and (3) a delay in the regenerative response. Additionally, they note that morphine worsens pancreatic necrosis and acute inflammation in mechanistically distinct models. These effects of morphine are prevented in μ-opioid receptor knockout mice.

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