The role of oxycodone/naloxone in the management of patients with pain and opioid-induced constipation

ABSTRACT

Introduction: Common opioid adverse effects (AE) of the gastrointestinal tract include opioid-induced constipation (OIC) and opioid-induced bowel dysfunction (OIBD) with traditional laxatives being of limited efficacy, having AEs and not addressing the pathophysiology of OIC or OIBD. Targeted treatment comprises of PAMORA (peripherally acting mu-opioid receptor antagonists) and a combination of an opioid receptor agonist with its antagonist, namely prolonged-release oxycodone with prolonged-release naloxone (OXN) tablets at a fixed ratio of 2:1. Oxycodone provides analgesia, whereas naloxone prevents binding or displaces it from opioid receptors located in the gut wall.

Areas covered: The authors review the role of OXN in the management of patients with pain and OIC. A literature search was performed using the search terms ‘oxycodone/naloxone’ and ‘opioid-induced constipation’ using the PubMed database up to October 2018.

Expert opinion: OXN delivers analgesia comparable (or superior versus placebo and in observational studies) to oxycodone alone and other opioids with a limited or decreased disturbing effect on bowel function. OXN in daily doses of up to 160 mg/80 mg provides effective analgesia with little negative impact on bowel function. OXN may be successfully used in patients with chronic pain, to prevent or treat symptoms of OIC and OIBD.

KEYWORDS:

• Opioid–induced constipation
• opioid–induced bowel dysfunction
• opioid receptor antagonist
• oxycodone/naloxone
• chronic pain

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

One referee declares that they are an employee of Mundipharma Pharmaceuticals BV. Peer reviewers on this manuscript have no other relevant financial relationships or otherwise to disclose.

Additional information

Funding

This manuscript has not been funded.