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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-.

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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].

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Last Update: November 24, 2020.



The opioids are a large class of medications related in structure to the natural plant alkaloids found in opium that are derived from the resin of the opium poppy, Papaver somniferum. The natural alkaloids are also referred to as opiates and include morphine and codeine. Synthetic derivatives include heroin, fentanyl, hydromorphone, methadone, buprenorphine and others. The opioids are highly potent and effective analgesics, but most have a high potential for dependency and abuse.

Opioids act by engagement of specific cell surface receptors; the opiate receptors, which are designated µ [mu], κ [kappa] and δ [delta]. These receptors are found predominantly in the central nervous system, brain and spinal column, but are also present on vascular, cardiac, lung, gut and even peripheral blood mononuclear cells. Engagement of the opiate receptors generates a series of intracellular signals, including inhibition of adenylate cyclase, decreased opening of calcium channels, increased potassium currents and activation of protein kinase C (PKC). The major effect of these pathways is reduction in cell excitability and neurotransmission. The natural ligands for the opiate receptors are the so-called endogenous opioid peptides such as the enkephalins, endorphins and endomorphins.

The opioids have a variety of clinical effects, but are predominantly known and used for their profound pain relieving effects. Other effects that are often linked to opiate analgesia include euphoria, changes in mood, drowsiness and mental clouding. However, the distinctive feature of the analgesia induced by the opioids is the lack of loss of consciousness. The pain is often described as less intense, but still present although better tolerated. Thus, the opioids do not decrease or treat the cause of the painful stimulus, but rather decrease its perception.

Other effects of opioids include respiratory depression, decreased gastrointestinal motility, sedation, nausea, vomiting, constipation and intestinal bloating. Opioids also have direct cardiovascular effects, decreasing blood pressure, causing vasodilation and decreasing cardiac work.

Most opioids have similar effects and side effects, although pharmacokinetic differences, tissue distribution, and receptor type specificity probably account for the variation in effects of the various synthetic and semisynthetic derivatives of morphine. Morphine is considered the prototype opiate, against which other agents are measured for their analgesic effects as well as adverse side effects.

The opioids can be categorized into subclasses on the basis of their chemical structure as opium alkaloids (opiates: codeine, morphine), semisynthetic derivatives of the natural alkaloids (hydrocodone, hydromorphone, oxycodone, buprenorphine), and various classes of synthetic opioids such as the anililopiperidines (fentanyl, alfentanil, sufentanil, remifentanil), diphenylpropylamine derivatives (propoxyphene, dextropropoxyphene, methadone, diphenoxylate, loperamide), and others (pentazocine, butorphanol, nalbuphine, levorphanol, tramadol), and, the opioid antagonists (nalmefene, naloxone and naltrexone). They can also be informally classified based upon their major use such as anesthesia (fentanyl, alfentanil, remifentanil, sufentanil), severe pain (morphine, hydromorphone, levorphanol, meperidine), moderate-to-severe acute or chronic pain (transdermal or transbuccal fentanyl, codeine, oxycodone, hydrocodone, levorphanol, methadone), diarrhea (loperamide, diphenoxylate), and cough (codeine, hydrocodone). Finally, opioids can be categorized on the basis of their action as full agonists, partial agonists or mixed agonists/antagonists, and antagonists of opiate receptors.

Opioid receptor antagonists are used to reverse the effects of opioids and are invaluable in the management of opioid overdose (naloxone, naltrexone, nalmefene). Specialized opioid antagonists can be used to reverse unwanted opioid effects, such as constipation in patients with chronic pain on long-term opioids. These agents (naldemedine, naloxegol) are generally modified so as not to cross the blood brain and reverse the central nervous system effects of opiates.

Opioids are rare causes of drug induced liver disease and are not mentioned in large case series of clinically apparent liver injury caused by medications. In physiological, pain relieving doses, opioids have not been implicated in causing clinically apparent liver injury, acute liver failure, chronic hepatitis or vanishing bile duct syndrome. However, overdoses of the more potent opioids have been linked to cases of acute liver injury, usually with a precipitous onset and pattern of acute toxicity with marked elevations in serum aminotransferase levels and early onset of signs of hepatic failure. This syndrome has been best characterized after buprenorphine overdose or abuse, but likely occurs with others. It is possible that the implicated opioids are not directly toxic to the liver, but cause ischemic liver injury due to respiratory failure, cardiovascular collapse, shock and anoxia that can occur with severe opioid overdose. The clinical syndrome resembles acute hepatic necrosis and liver failure, but is rapidly reversible and rarely the primary cause of death from overdose.

A special form of liver injury linked to opioid use occurs with their fixed drug combinations with acetaminophen. These combinations are commonly used for moderate to moderately severe pain and can lead to abuse. If taken too frequently, acetaminophen doses may reach toxic levels, particularly with overuse for several days in the face of malnutrition, alcohol abuse or intercurrent illness. These other stresses can lower hepatic glutathione levels and predispose to acetaminophen hepatotoxicity. This constellation of events is referred to as inadvertent or unintended acetaminophen overdose or more colloquially as a “therapeutic misadventure”. Because of their potential for hepatotoxicity, opioid combinations in which the dose of acetaminophen is greater than 325 mg per tablet or capsule were discontinued.

References to the safety and hepatotoxic potential of the various opiate agonists are given together at the end of this overview section. References to the opioids and the opiate antagonists used to treat substance abuse are given separately with each agent (buprenorphine, methadone, nalmefene, naloxone, naltrexone). The opioids are discussed individually or as groups of agents and links to each are given below.

Full and partial agonists:

Opiate antagonists:


References updated: 24 November 2020

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    (Among 1036 patients with opioid use disorder treated with buprenorphine/naloxone in short [18 day] or long [52 week] courses, serum ALT elevations above 3 times ULN arose in 76 patients [7%], most instances occurring with either acute or chronic HCV infection and rates of ALT elevations were similar with either short and long term use, as well as after discontinuation of the medication).
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    (Concise review of the mechanism of action, efficacy and safety of naloxegol shortly after its approval for use in the US; mentions dose related gastrointestinal side effects, but not ALT elevations or hepatotoxicity).
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    (32 year old Chinese man was found unconscious after an opioid overdose and developed severe acidosis, respiratory failure and shock with evidence of cardiac, muscle, renal and hepatic injury [bilirubin not given, ALT 61 rising to 330 U/L, CPK 454 U/L, myoglobin 2000 ng/mL], with ultimate recovery, the liver injury most likely due to ischemic hepatitis).
  • Tetrault JM, Tate JP, Edelman EJ, Gordon AJ, Lo Re V 3rd, Lim JK, Rimland D, et al. Hepatic safety of buprenorphine in HIV-infected and uninfected patients with opioid use disorder: the role of HCV-infection. J Subst Abuse Treat. 2016;68:62–7. [PMC free article: PMC4976086] [PubMed: 27431048]
    (Among 666 patients [mostly men] identified in a Veterans Administration electronic medical database who were started on buprenorphine and were monitored, 14 developed “drug-induced liver injury”, all of whom had received a potentially hepatotoxic medication [93%] or had preexisting HCV infection [7%], and there was no overall “substantial” change in serum ALT, AST or bilirubin levels).
  • Pergolizzi JV, Raffa RB, Marcum Z, Colucci S, Ripa SR. Safety of buprenorphine transdermal system in the management of pain in older adults. Postgrad Med. 2017;129:92–101. [PubMed: 27929709]
    (Review of the literature on the safety and efficacy of buprenorphine in elderly patients mentions that liver abnormalities were rare [<1%] and ALT values above 3 times ULN occurred in 0.2% of both elderly and younger adults).
  • Ward A, Del Campo M, Hauser K. Complications with oxycodone and naloxone. Aust Prescr. 2017;40:156–7. [PMC free article: PMC5601970] [PubMed: 28947855]
    (Three patients on long term oxycodone who had significant liver dysfunction had symptoms of withdrawal probably due to increase in systemic levels of naloxone, but liver tests did not worsen).
  • Lau F, Gardiner M. Oxycodone/naloxone: An unusual adverse drug reaction. Aust Fam Physician. 2017;46:42–3. [PubMed: 28189131]
    (52 year old woman with chronic liver disease was switched from regular oxycodone to a fixed combination of oxycodone and naloxone and rapid developed withdrawal symptoms suspected to be due to the loss of first-pass clearance of naloxone by the liver dysfunction).
  • Cantrell FL, Sherrard J, Andrade M, Schaber B, McIntyre IM. A pediatric fatality due to accidental hydromorphone ingestion. Clin Toxicol (Phila). 2017;55:60–2. [PubMed: 27775447]
    (3 year old boy was found to be dead and autopsy revealed no abnormalities except for presence of hydromorphone in blood and liver, his mother having a prescription for the drug found that several pills were missing).
  • Paul ABM, Simms L, Mahesan AM. Intentional heroin administration resulting in homicide in a 10-month old infant. Forensic Sci Int. 2018;290:e15–e18. [PubMed: 30017664]
    (10 month of girl was found dead at home and autopsy revealed high levels of morphine in blood and liver as well as a single needle puncture mark in the left antecubital fossa; liver histopathology was referred to as unremarkable).
  • Opioids for pain. Med Lett Drugs Ther. 2018;60(1544):57–64. [PubMed: 29664446]
    (Concise review of the mechanism of action, efficacy, safety and costs of opioids used for pain relief, discusses adverse events or short and long term use, but makes no mention of ALT elevations or hepatotoxicity).
  • Concheiro M, Chesser R, Pardi J, Cooper G. Postmortem toxicology of new synthetic opioids. Front Pharmacol. 2018;9:1210. [PMC free article: PMC6212520] [PubMed: 30416445]
    (Summary of the chemical structures, pharmacology, relative potency and toxicology of the major synthetic opioids implicated in the ongoing opioid overdose epidemic; no discussion of hepatic injury).
  • Pattullo V, Pattullo GG, Strasser SI. Adverse effects of modified release oxycodone/naloxone in patients with moderate to severe liver impairment. Med J Aust. 2018;209:279–80. [PubMed: 30208822]
    (Letter stressing the complications of oxycodone/naloxone therapy in patients with moderate or severe liver impairment marked by a decrease in analgesic effect and risk of withdrawal symptoms due to systemic absorption and lack of hepatic clearance of naloxone, a potent opiate antagonist).
  • Kinnunen M, Piirainen P, Kokki H, Lammi P, Kokki M. Updated clinical pharmacokinetics and pharmacodynamics of oxycodone. Clin Pharmacokinet. 2019;58:705–25. [PubMed: 30652261]
    (Oxycodone is a full opioid agonist relatively selective for the µ receptor which is actively transported across the blood-brain barrier and is extensively metabolized by the liver via CYP3A4 [45%] and CYP 2D6 [29%], and plasma levels can be increased by CYP 3A4 inhibitors and renal dysfunction and to a lesser degree by CYP 2D6 inhibitors and hepatic dysfunction).


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