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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.



Buprenorphine is a sublingually and transdermally available, semisynthetic opioid analgesic, which is used as an analgesic and for management of opioid dependence. Therapy with buprenorphine is associated with mild and transient serum enzyme elevations, and with moderate-to-severe clinically apparent liver injury when abused by intravenous administration or the sublingual formations.


Buprenorphine (bue" pre nor' feen) is a semisynthetic opioid that is 25 to 50 times more potent than morphine and has been used as an analgesic as well as therapy of opioid addiction. Buprenorphine is a partial µ-opioid receptor agonist and a κ-receptor antagonist accounting for its benefit for opioid deterrence. Buprenorphine competes with morphine and heroin for the µ receptor, but is only a partial agonist and has a “ceiling” effect. Buprenorphine was approved for treatment of opioid addiction in 2004 and is a schedule III controlled substance. Current indications include treatment of moderate-to-severe pain (parenterally in low doses <1 mg) and opiate addiction (in various formulations in higher doses 2 to 16 mg daily). Buprenorphine is available as 2 and 8 mg tablets for sublingual administration generically and under the brand name Subutex, and in 1 mL ampules of 0.3 mg/mL for intravenous (iv) or intramuscular (im) injection generically and under the brand name Buprenex. More recently, buccal film formulations, transdermal patches (Butrans and generics), once monthly prolonged release injections (Sublocade) and once every 6 months implants injected subcutaneously (Probuphine) with buprenorphine have become available as therapy for opioid dependence. Buprenorphine is also available in fixed combination with naloxone (tablets and buccal films: 2 mg/0.5 mg and 8 mg/2 mg) for sublingual administration generically and under the brand name Suboxone. Naloxone is not absorbed orally, but provides full opioid antagonism if the combination is administer intravenously, as might occur with intentional abuse. Oral naloxone may also help to alleviate the gastrointestinal side effects of opioids such as constipation, nausea, vomiting and abdominal bloating. Finally, parenteral forms of buprenorphine are used for moderate-to-severe pain and administered iv or im, the typical dose being 0.3 mg every 6 hours as needed. Common side effects of buprenorphine include headache, dizziness, fatigue, sedation, dry mouth, urinary retention, diaphoresis, orthostatic hypotension, biliary spasm and withdrawal symptoms. Rare but potentially severe adverse reactions include life threatening respiratory and CNS depression, hepatotoxicity, adrenal insufficiency, interactions with other sedative medications, unintentional pediatric exposure and neonatal opioid withdrawal syndrome. Buprenorphine should be prescribed only by a health care provider with training in opioid dependency and managing the dosing and side effects of buprenorphine and naloxone.


Buprenorphine therapy has been associated with a low rate of serum enzyme elevations during treatment, although the populations studied (opioid dependent) often have coexisting chronic liver diseases which complicate such assessments. Nevertheless, rates of ALT elevations during treatment with buprenorphine (with or without naloxone) have been minimally or no greater than with comparator arms (methadone).

In addition, there have been several reports and case series of acute, clinically apparent liver injury arising within 2 to 20 weeks of starting buprenorphine, usually (but not invariably) following misuse and intravenous administration of sublingual tablets. However, some cases occurred in patients who denied intravenous use and were on conventional sublingual doses. In most cases, the pattern of serum enzyme elevations was hepatocellular and the presentation resembled acute toxic hepatic necrosis. Immunoallergic features (fever, rash and eosinophilia) were not present, nor were autoantibodies detected. Almost all patients with this injury had concurrent chronic hepatitis C, and several appeared to resolve the chronic infection with the acute liver injury (Case 1). Strikingly, most patients were able to continue buprenorphine without recurrence, some of whom admitted to continued intravenous abuse.

Likelihood score: B[HD] (likely rare cause of clinically apparent liver injury usually associated with overdose or misuse).

Mechanism of Injury

Buprenorphine undergoes extensive first pass hepatic extraction and is metabolized primarily by the cytochrome P450 system (CYP 3A4). The low doses used and rapid metabolism may account for its relative lack of hepatotoxicity when used in conventional doses. The appearance of an acute hepatic necrosis after intravenous injection of the sublingual tablets is likely due to direct toxicity of these high parenteral doses. The occurrence of this syndrome largely in patients with concurrent hepatitis C remains unexplained. Clearance of hepatitis C during this toxic injury raises the issue of whether the acute injury is actually due to an exacerbation of hepatitis C or whether the severe acute toxic injury can induce viral clearance.

Outcome and Management

The severity of liver injury attributed to buprenorphine has ranged from mild-to-severe hepatitis, and fatal instances have been reported. Interestingly, most patients subsequently tolerated restarting buprenorphine at doses used prior to the toxic event, and some patients continued to misuse it by intravenous injection, but did not have recurrence of the liver injury.

Drug Class: Substance Abuse Treatment Agents; Opioids


Case 1. Acute liver injury attributed to buprenorphine use in a patient with chronic hepatitis C.(1)

A 33 year old male injection drug user with chronic hepatitis C (HCV genotype 1a) developed jaundice, abdominal pain and fever shortly after injecting 3 to 5 crushed and dissolved tablets of buprenorphine (8 mg, meant for sublingual administration) intravenously. He was known to have chronic hepatitis C, but had never been treated for the infection which was considered mild. He had no other history of liver disease but consumed alcohol regularly. He took no other medications. On admission, laboratory tests showed a serum bilirubin of 29.6 mg/dL with marked elevations in serum aminotransferase levels (ALT 4132 U/L, AST 3947 U/L) and mild increases in alkaline phosphatase (347 U/L) and GGT (127 U/L; normal <50) (Table). The prothrombin index was 43% of control (INR 1.7). A transjugular liver biopsy showed panlobular necrosis, diffuse lobular inflammation, and marked cholestasis indicative of acute hepatic injury. In addition, there was moderate portal fibrosis and portal inflammation suggestive of an underlying chronic hepatitis C. Tests for hepatitis A and B and HIV were negative. Anti-HCV was present, but serum HCV RNA was present at very low levels (15 IU/mL). Jaundice resolved within a week and serum enzymes fell rapidly. Sublingual buprenorphine was restarted without a change in the pattern of recovery. In follow up 3 months later, serum ALT levels were normal and HCV RNA was undetectable. When seen almost a year later, he admitted to continuing to self-inject buprenorphine, yet serum ALT levels were still normal and HCV RNA was undetectable.

Key Points

Medication:Buprenorphine (24 mg intravenously)
Pattern:Hepatocellular (R=31)
Severity:4+ (jaundice and prolongation of INR)
Latency:Short, specific time not provided
Recovery:Rapid, within 1-2 months
Other medications:None

Laboratory Values

Time After
Alk P
2 days254628826.9Prothrombin time 18 sec
2 weeks132802.2Buprenorphine restarted
4 monthsNormalHCV RNA negative
10 months11HCV RNA negative
Normal <40 <104 <1.2


The clinical presentation of acute hepatic necrosis shortly after intravenous abuse of buprenorphine has been reported in several case reports and single center series of as many as 7 cases. Intriguingly, virtually all patients reported with this syndrome had a preexisting chronic hepatitis C, although many were HCV RNA negative at the time of the acute illness. The current case documents the loss of HCV RNA during the acute hepatic injury attributed to buprenorphine. Two explanations are possible. First, that the acute toxic hepatic injury caused an interruption in the replication of HCV or triggered host immune responses (the innate immune system and interferon production), resulting in clearance of hepatitis C. A second explanation is that the acute illness was due to an exacerbation of the chronic HCV infection, which led to an acute hepatitis C-like clearance of virus. The role of hepatitis C in this reaction is perhaps demonstrated best by the absence of recurrence of liver injury when buprenorphine was restarted and even when abused intravenously in high doses. The combination of buprenorphine with naloxone (a full µ opioid receptor antagonist) was developed to discourage such intravenous abuse.



Buprenorphine – Generic, Buprenex®, Subutex® (SL Tablets)

Buprenorphine/Naloxone – Generic, Suboxone®


Substance Abuse Treatment Agents


Product labeling at DailyMed, National Library of Medicine, NIH


Buprenorphine 52485-79-7 C29-H41-N-O4 image 135002732 in the ncbi pubchem database


Peyrière H, Tatem L, Bories C, Pageaux GP, Blayac JP, Larrey D. Hepatitis after intravenous injection of sublingual buprenorphine in acute hepatitis C carriers: report of two cases of disappearance of viral replication after acute hepatitis. Ann Pharmacother. 2009;43:973–7. [Modified from Case 1.] [PubMed: 19383935]


References updated: 24 November 2020

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