What is the safety and efficacy data of naltrexone for alcohol use disorder in liver transplant recipients?

Comment by InpharmD Researcher

Based on limited data, the safety and efficacy of naltrexone for alcohol use disorder (AUD) in liver transplant recipients remains inadequately defined and potentially controversial. A case report describes a liver transplant patient with pain that led to hospitalization, which resolved upon cessation of naltrexone (see Table 1). While additional data not specific to liver transplant patients suggest the risk of liver injury from naltrexone is low, older studies highlight its potential for hepatotoxicity and a lack of substantial efficacy. Consequently, its use in this complex population requires great caution until more data is available.

Background

The 2018 guidelines from the American Psychiatric Association on pharmacological treatment of patients with alcohol use disorder (AUD) states that while naltrexone have been extensively reviewed in placebo-controlled and some head-to-head trials for the treatment of AUD, there remains a significant need for further investigation into other pharmacotherapies for AUD. More comprehensive data is needed regarding the efficacy, effectiveness, and safety profile, including adverse events, of both existing and novel pharmacotherapies for AUD in populations with co-occurring psychiatric disorders, other substance use disorders, and various medical conditions. These medical conditions include obesity, major cardiac diseases, chronic kidney disease, significant liver conditions like cirrhosis, and individuals who have undergone liver transplantation. Such research is critical to understanding and optimizing treatment strategies for these complex patient populations. [1]

A 2021 publication examines the challenges and management strategies for patients with severe alcoholic hepatitis (AH) who undergo early liver transplantation (LT). The authors discuss the grim prognosis of severe AH, traditionally associated with a high mortality rate even with corticosteroid therapy and expert medical management. They highlight the significance of early liver transplantation, performed without the conventional 6-month pre-transplant alcohol abstinence, which has gained traction due to high mortality in severe AH patients unresponsive to medical treatment. The paper presents data from both European and U.S. centers, showcasing varied outcomes based on strict candidate selection and regional practices. European studies, such as one described by Mathurin et al., reported survival rates post-transplantation of 77% at 6 months and 71% at 2 years, whereas U.S. data, analyzed by Lee et al., indicated a 94% 1-year survival rate and 84% at 3 years, signifying a notable survival benefit. The 2021 article emphasizes the critical nature of minimizing alcohol relapse post-transplant to optimize patient and graft survival. It details the various approaches employed, such as multidisciplinary psychosocial evaluations involving social workers and addiction specialists to assess relapse risk. Furthermore, the paper highlights the role of post-transplant monitoring for alcohol use disorder, advocating for a combination of pharmacologic therapies, such as naltrexone and acamprosate, and behavioral treatments like cognitive behavioral therapy and motivational interviewing. The research underscores the need for personalized care strategies and integrated treatment models to effectively manage alcohol use disorder and enhance transplant outcomes in this high-risk patient population. [2]

A 2007 review discusses the evidence for pharmacological treatment of alcohol dependence in liver transplant recipients, focusing on disulfiram, naltrexone, and acamprosate. Naltrexone, while initially promising, shows little to no substantial effect on alcohol dependence based on large cooperative studies and has a rare potential for liver toxicity. Specifically, three studies were discussed that focused on liver transplant and non-transplant patients. One study in alcohol dependence liver transplant patients could not recruit the adequate number of patients due to the low but possible risk of liver injury. Two large prospective studies only observed a small benefit with naltrexone in non-transplant patients, which included a Veterans Affairs cooperative study where naltrexone was administered as an adjunct to standard psychosocial treatment. The authors conclude that naltrexone is a controversial agent with potential for damaging effects on the liver, suggesting its conventional use is not recommended. [3]

According to the LiverTox database, naltrexone is typically given to patients with a high background rate of liver disease (injection drug use or alcoholism) and has been associated with variable rates of serum enzyme elevations (0% to 50%), with values above 3 times the upper limit of normal occurring in approximately 1% of patients and occasionally leading to drug discontinuation. However, several studies have found that the rate of alanine aminotransferase (ALT) elevations during naltrexone therapy is similar to that with placebo. Notably, most serum aminotransferase elevations during naltrexone therapy are mild and self-limiting and often resolve even with continuation of therapy. While there have been rare reports of acute, clinically apparent liver disease in patients taking naltrexone, the role of the medication in liver injury has not always been clear. Additionally, no clear description of the clinical features of the injury are given. Overall, while naltrexone has often been considered hepatotoxic, it has not been definitively linked to cases of clinically apparent liver injury. [4]

A recent review published in 2022 discussing treatment of alcohol use disorder in patients with liver disease suggests using naltrexone with caution in cirrhosis patients since the medication is metabolized via the liver. Mild liver injury has been reported in approximately 1% of patients, but there have been no proven cases of clinically apparent liver injury. [5]

A 2025 article examines the utilization of naltrexone for treating AUD in patients with liver disease, highlighting misconceptions surrounding its hepatotoxicity. A comprehensive review of literature up to 2023, including a systematic review of 118 clinical trials with 20,976 participants, corroborates the efficacy of oral naltrexone (50 mg/day) in reducing alcohol consumption, with a number needed to treat (NNT) of 18 for preventing any return to drinking and 11 for heavy drinking. Despite this, only a small fraction of individuals with AUD receive pharmacotherapy in the United States. The findings from a retrospective cohort study of 9,131 Veterans Affairs patients with alcohol-associated cirrhosis reveal improved survival rates associated with naltrexone or acamprosate exposure, with longer medication exposure correlating with further survival benefits. The 2025 discussion extends to the safety of naltrexone, particularly following the FDA's removal of the black box warning for hepatotoxicity in 2013, noting minimal evidence of progression to liver disease. Significant outcomes from the COMBINE trial show only a minimal proportion of participants experiencing liver enzyme elevation on naltrexone without ensuing liver failure. Furthermore, a retrospective analysis of 2,940 Veterans Affairs patients with cirrhosis demonstrated a decrease in liver enzyme levels with naltrexone, with no episodes of liver decompensation or death attributable to the medication. Therefore, the evidence bases for naltrexone's safety include patients with Child-Pugh B cirrhosis, suggesting that hospitalization presents a critical opportunity for intervention, reducing heavy alcohol use, and preventing further liver complications through timely naltrexone initiation. [6]

References:

[1] Reus VI, Fochtmann LJ, Bukstein O, et al. The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. Am J Psychiatry. 2018;175(1):86-90. doi:10.1176/appi.ajp.2017.1750101
[2] Ting PS, Gurakar A, Wheatley J, Chander G, Cameron AM, Chen PH. Approaching Alcohol Use Disorder After Liver Transplantation for Acute Alcoholic Hepatitis. Clin Liver Dis. 2021;25(3):645-671. doi:10.1016/j.cld.2021.03.008
[3] Beresford TP, Martin B. The evidence for drug treatment of alcohol dependence in liver transplant patients. Current Opinion in Organ Transplantation. 2007;12(2):176-181. doi:10.1097/MOT.0b013e32803fb77d
[4] LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Naltrexone. [Updated 2020 Mar 24]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK548583/
[5] Nielsen AS, Askgaard G, Thiele M. Treatment of alcohol use disorder in patients with liver disease. Curr Opin Pharmacol. 2022;62:145-151. doi:10.1016/j.coph.2021.11.012
[6] Kee DP, Buyske JJ, Calcaterra SL. Things We Do for No Reason™: Avoiding naltrexone for alcohol use disorder in liver disease. J Hosp Med. 2025;20(7):768-771. doi:10.1002/jhm.13569

Relevant Prescribing Information

Hepatotoxicity
Cases of hepatitis and clinically significant liver dysfunction were observed in association with naltrexone hydrochloride exposure during the clinical development program and in the postmarketing period. Transient, asymptomatic hepatic transaminase elevations were also observed in the clinical trials and postmarketing period. When patients presented with elevated transaminases, there were often other potential causative or contributory etiologies identified, including pre-existing alcoholic liver disease, hepatitis B and/or C infection, and concomitant usage of other potentially hepatotoxic drugs. Although clinically significant liver dysfunction is not typically recognized as a manifestation of opioid withdrawal, opioid withdrawal that is precipitated abruptly may lead to systemic sequelae, including acute liver injury. Patients should be warned of the risk of hepatic injury and advised to seek medical attention if they experience symptoms of acute hepatitis. Use of naltrexone hydrochloride should be discontinued in the event of symptoms and/or signs of acute hepatitis. [4]
Hepatic Impairment
An increase in naltrexone AUC of approximately 5- and 10-fold in patients with compensated and decompensated liver cirrhosis, respectively, compared with subjects with normal liver function has been reported. These data also suggest that alterations in naltrexone bioavailability are related to liver disease severity. [4]

References:

[4] Naltrexone hydrochloride. Prescribing information. Chartwell RX, LLC; 2022.

Literature Review

A search of the published medical literature revealed 6 studies investigating the researchable question:

What is the safety and efficacy data of naltrexone for alcohol use disorder in liver transplant recipients?

Level of evidence

C - Multiple studies with limitations or conflicting results  Read more→



Please see Tables 1-6 for your response.


 

A case report of naltrexone for alcoholism in a liver transplant recipient: side effects and safety

Design

Case report

Case presentation

A 52-year-old male patient presented with hepatitis C and alcoholic cirrhosis who experienced severe pain following the initiation of naltrexone as part of a double-blind study. The patient, having fractured his foot shortly before receiving his liver transplant, began the study treatment two months post-transplant. Within a week, he reported significant lower back and torso pain. Despite resting and using nonsteroidal anti-inflammatory drugs and muscle relaxants for seven weeks, his pain escalated, necessitating hospitalization and intravenous morphine administration. After discontinuing the study drug, naltrexone, the patient's pain diminished, prompting a discussion about the drug's role in exacerbating his symptoms. The mechanism by which naltrexone might have contributed to pain was examined through a previous understanding of the drug's interaction with the endogenous opiate system. 

Study Author Conclusions

In summary, we have found naltrexone to be a safe option for the treatment of alcoholism in stable patients who have had a recent liver transplant and in those with cholestatic liver disease needing treatment for pruritis. However, clinicians should be aware that patients with preexisting injuries or pain who receive chronically administered naltrexone may experience an unmasking or exacerbation of pain. Therefore, because of the long halflife of naltrexone and its metabolites, effective opioid analgesia would not be expected until approximately three days after stopping naltrexone. Patients receiving naltrexone must be fully informed of this possibility and carry this information on a wallet card or identification bracelet

 

References:

Weinrieb RM, O'Brien CP. A case report of naltrexone for alcoholism in a liver transplant recipient: side effects and safety. Am J Addict. 2004;13(5):495-497. doi:10.1080/10550490490512870

 

Naltrexone for alcohol use disorder: Hepatic safety in patients with and without liver disease

Design

Retrospective, observational, single-center, cohort study

N= 160

Objective

To evaluate the safety of naltrexone in those with liver disease (LD)

Study Groups

Without LD (n = 60)

With LD (n = 100)

Inclusion Criteria

Patients with prescriptions of naltrexone for alcohol use disorder (AUD)

Exclusion Criteria

Patients with naltrexone prescriptions for indications other than AUD; patients with other known chronic liver diseases including chronic hepatitis B or C infection

Methods

This was a retrospective study from a single center in California. Of 160 patients prescribed naltrexone for AUD, 100 (63%) had LD, and 47 (47%) of those with LD had cirrhosis (47% decompensated).

Duration

2015 to 2019

Outcome Measures

Differences in mean AST, ALT, ALP, and Tbili at three time points (before, during, and after naltrexone) were assessed overall and by group (without LD, LD without cirrhosis, and cirrhosis)

Mortality including deaths from all causes and alcohol-related hospitalizations included hospitalizations for alcohol withdrawal, alcohol-associated hepatitis, alcohol-induced gastrointestinal bleed or pancreatitis, and decompensated cirrhosis.

Baseline Characteristics

 

Without LD (n = 60)

With LD (n = 100)

p-value 

Age, years (IQR)

46 (34–56) 51(41–58)  0.05
Male gender

70%

86% 0.01

Ethnicity

Black

Caucasian

Asian

Unknown

Hispanic

 

10%

8%

3%

73%

52%

 

13%

2%

1%

1%

71%

0.03

Comorbidities

Psychiatric history

Diabetes

Hyperlipidemia

 

80%

7%

12%

 

39%

21%

17%

 

<0.001

0.02

0.36

BMI, kg/m2 (IQR)

27 (24–29)

28 (23–31)

0.61

Oral naltrexone formulation

88%

95% 0.40

Naltrexone dose prescribed

25 mg/day

50 mg/day

380 mg/month

 

3%

85%

12%

 

5%

90%

5%

0.27

>30 days of naltrexone

70%

63%

0.40

Alcohol-related hospitalization after naltrexone

7%

26%

0.003

Results

 

Without LD (n = 60) With LD (n = 100)  

ALT, IU/L

Baseline

During treatment

After treatment

 

22

25

25

 

39

32

28

 

AST, IU/L

Baseline

During treatment

After treatment

 

25

27

27

 

59

46

39

 

ALP, IU/L

Baseline

During treatment

After treatment

 

70

65

97

 

98

94

100

 

Total bilirubin, mg/dL

Baseline

During treatment

After treatment

 

0.40

0.52

0.19

 

0.86

0.82

0.54

 

Mortality: Follow-up of 10 months (IQR, 4–18), eight patients died. Cumulative 2-year survival in patients without LD was 97.7% (95% CI, 84.6–99.7) compared to 95.4% (95% CI, 82.8–98.8; p = 0.93) for those with LD alone, 90.8% (95% CI, 73.5–97.0; p = 0.52) for those with cirrhosis, and 81.3% (95% CI, 51.2–93.8; p = 0.25) for those with decompensated cirrhosis

Alcohol-related hospitalizations: 30 patients (19%) had at least one subsequent alcohol-related hospitalization and no hospitalizations related to naltrexone hepatoxicity. Cumulative incidence of 2-year alcohol-related hospitalizations after naltrexone prescriptions was 8.2% (95% CI, 2.7–24.0) for those without LD compared to 27.7% for LD alone (95% CI, 16.6–44.0; p = 0.09), 40.5% for LD with cirrhosis (95% CI, 24.8–61.6; p = 0.006), and 41.7% (95% CI, 23.3–66.6; p = 0.005) for decompensated cirrhosis.  Alcohol-related hospitalization rates were highest among those with LD and shorter naltrexone prescriptions (45.3%; 95% CI, 28.6–66.0) and lowest in those without LD and shorter naltrexone prescriptions (0%) (p < 0.001)

Adverse Events

Not disclosed

Study Author Conclusions

Naltrexone is safe for patients with underlying liver disease with a very low incidence of liver enzyme elevations and no evidence of hepatotoxicity.

InpharmD Researcher Critique

Some limitations in this study include liver enzyme elevations, severe liver enzyme elevations, transient elevations, and clinically meaningful hepatoxicity were detected only if laboratory values were checked. Adherence or gaps in prescriptions were not measured. Naltrexone prescriptions outside of the hospital system were not assessed.

Drinking history was not recorded in health records. Information regarding patient visits outside of the network hospital was lacking. The cohort was composed mainly of Hispanic subjects and this will limit the generalizability to the population. The cohort of decompensated individuals with cirrhosis was small, limiting the power of this analysis. The potential confounding effect of psychotherapy was not captured.

Some strengths in this study include hepatologists were not involved in prescribing naltrexone for those with LD, it is less likely that selection was based on liver disease severity. 



References:

Ayyala D, Bottyan T, Tien C, et al. Naltrexone for alcohol use disorder: Hepatic safety in patients with and without liver disease. Hepatology Communications. 2022;6(12):3433-3442.

 

Incidence and Progression of Alcohol-Associated Liver Disease After Medical Therapy for Alcohol Use Disorder

Design

Retrospective, observational, single-center, cohort study

N= 9635

Objective

To ascertain whether medical addiction therapy was associated with an altered risk of developing alcohol-associated liver disease (ALD) in patients with alcohol use disorder (AUD)

Study Groups

Treated (n=3906)

Untreated (n=5729)

Inclusion Criteria

Patients with ALD who had at least 1 of the following International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) diagnosis codes: alcoholic hepatitis (K70.1), alcoholic cirrhosis of liver (K70.3), alcoholic hepatic failure (K70.4), alcoholic fibrosis and sclerosis (K70.2), other cirrhosis (K74.69), or unspecified cirrhosis (K74.60); received 3 prescriptions for at least 1 of the following: disulfiram, acamprosate, naltrexone, gabapentin, topiramate, or baclofen

Exclusion Criteria

None explicitly stated

Methods

Eligible patients were from a research institution in Massachusetts. Information was collected for patients meeting the inclusion criteria. The ICD-10 diagnosis codes used were alcohol abuse (F10.1) or alcohol dependence (F10.2). The cohort of patients was split into those treated with medical addiction therapy or not.

Duration

The mean duration of therapy for patients in the treated group was 4.1 years, whereas the mean follow-up duration from AUD diagnosis was 9.8 years in the treated group and 8.8 years in the untreated group.

Outcome Measures

Incidence of ALD and hepatic decompensation after medication addiction therapy

Baseline Characteristics

 

Treated (n= 3906)

Untreated (n= 5729)

Mean Age, years

55 ± 15.3 54.7 ± 59.5

Female

44.4% 36.2%

White

84.8% 82.5%
Viral hepatitis

16.2%

9.9%
Nonalcohol substance use disorder

49.8%

27.6%

Results

Any pharmacotherapy (e.g., gabapentin, topiramate, baclofen, naltrexone, disulfiram, or acamprosate) was associated with decreased odds of developing ALD after therapy (aOR, 0.37; 95% CI, 0.31-0.43; p< 0.001).

Naltrexone therapy was independently associated with decreased odds of developing ALD (aOR, 0.67; 95% CI, 0.46-0.95; p= 0.03) after medical addiction therapy.

The only agent that was not associated with decreased odds of ALD development was disulfiram (aOR, 0.86; 95% CI, 0.43-1.61; p= 0.66).

Any pharmacotherapy (e.g., gabapentin, topiramate, baclofen, naltrexone, disulfiram, or acamprosate) was associated with decreased odds of developing hepatic decompensation after therapy (aOR, 0.35; 95% CI, 0.23-0.53; p< 0.001).

Naltrexone therapy was independently associated with reduced incidence of hepatic decompensation in patients with cirrhosis (aOR, 0.27; 95% CI, 0.10-0.64; p= 0.005).

Baclofen (p= 0.91), acamprosate (p= 0.06), and disulfiram (p= 0.24) were the only studied agents not significantly associated with decreased hepatic decompensation; these three agents were associated with increased odds of developing hepatic decomensation.

Adverse Events

N/A

Study Author Conclusions

Naltrexone is currently contraindicated in severe liver disease given the concern for hepatotoxicity and the precipitation of liver failure in these vulnerable patients. The results of this study suggest a benefit of naltrexone: it is a factor in not only preventing ALD but also limiting hepatic decompensation in patients with established cirrhosis.

InpharmD Researcher Critique

This study is not generalizable due to the patient population being majority white and there was not a balanced population of females and males. There were no subgroup analyses based on each studied medication and it was unreported if polypharmacy occurred with the studied agents. As a retrospective single-center study, there is a potential for confounding variables to influence these results. There was also no documentation on adherence to AUD pharmacotherapy.



References:

Vannier AGL, Shay JES, Fomin V, et al. Incidence and Progression of Alcohol-Associated Liver Disease After Medical Therapy for Alcohol Use Disorder. JAMA Netw Open. 2022;5(5):e2213014. Published 2022 May 2. doi:10.1001/jamanetworkopen.2022.13014

 

Pharmacokinetics of Long-Acting Naltrexone in Subjects With Mild to Moderate Hepatic Impairment

Design

Randomized, double-blinded, parallel-group, multicenter, placebo-controlled, phase 3 study

N= 250

Objective

To evaluate the efficacy and safety of XR-NTX in treating patients who were dependent on opioids

Study Groups

Naltrexone XR (n=126)

Placebo (n=124)

Inclusion Criteria

Diagnosis of opioid dependence; actively seeking treatment; recently received inpatient (up to 30 days) treatment for opioid detoxification

Exclusion Criteria

Patients with evidence of decompensated liver disease (e.g., ascites, jaundice, encephalopathy, or esophageal varices); an ALT or AST greater than three times the ULN at screening; baseline or total bilirubin greater than 10% above the ULN; patients with evidence of AIDS-defining illness; positive naloxone text during the study

Methods

Participants were randomized 1:1 to receive extended-release naltrexone 380 mg injections or placebo once monthly. To evaluate the safety of naltrexone XR, liver enzymes were compared with that of the placebo group in patients with liver disease and HIV infection. Liver enzymes were collected at baseline and before patients revived their monthly injections.

Duration

July 3, 2008, through October 5, 2009

Outcome Measures

Abnormal laboratory tests and incidence of treatment-emergent adverse events

Frequency of liver enzyme elevations (three times the Upper limit of Normal[ULN])

Baseline Characteristics

 

Naltrexone XR (n=126)

Placebo (n=124)

 

Age, years (mean SD)

29.4 ± 4.8 29.7 ± 3.6  

Male

88.0%  

Hepatitis C

HIV positive

88.8%

42%

 

While individual baseline characteristics were not reported for each group, the authors state they were equally distributed.

Results

Endpoint

Naltrexone XR (n=126)

Placebo (n=124)

p-value

ALT elevation

Baseline

Week 4

Week 12

Week 24

Any post-baseline elevation

 

0

10.7%

3.5%

4.4%

19.6%

 

0

6.2%

6.7%

4.2%

12.9%

0.876

AST elevation

Baseline

Week 4

Week 12

Week 24

Any post-baseline elevation

 

0

8.7%

2.3%

2.9%

14.0%

 

0

6.2%

3.3%

3.8%

10.6%

0.713

GGT elevation

Baseline

Week 4

Week 12

Week 24

Any post-baseline elevation

 

18.3%

17.5%

12.6%

8.8%

23.4%

 

20.2%

14.8%

13.3%

10.4%

21.2%

0.811

Adverse Events

Common Adverse Events: not reported

Discontinued due to Adverse Events: 2 patients dropped out of the study when the liver enzymes were three times the ULN

Study Author Conclusions

Naltrexone extended release can be used safely in eligible patients with opioid dependence, including those with underlying mild to moderate chronic HCV and/or HIV infections. 

InpharmD Researcher Critique

Patients with liver impairments usually have fluctuations in liver enzymes, making it a challenge to interpret the liver enzyme results. However, this data was able to provide trends from both baseline and post-baseline levels. One limitation is the large amount of dropouts or exclusions during the 24-week trial. Other limitations may be due to the population of White Russian males at a single center, reducing the extrapolatability of these results to other populations.

It is also possible that any ALT elevations observed were adaptations rather than true liver injuries. Elevations in ALT occasionally resolve spontaneously in patients taking potentially hepatotoxic drugs.

 

References:

Turncliff RZ, Dunbar JL, Dong Q, et al. Pharmacokinetics of long-acting naltrexone in subjects with mild to moderate hepatic impairment. J Clin Pharmacol. 2005;45(11):1259-1267. doi:10.1177/0091270005280199

Safety and Effectiveness of Naltrexone in the Management of Alcohol Use Disorder in Patients With Alcohol-associated Cirrhosis: First Clinical Observation From Indian Cohort
Design

Observational study

N= 86

Objective To study the safety, effectiveness, and tolerability of Naltrexone in the management of alcohol use disorder in patients with alcohol-associated cirrhosis
Study Groups All patients (n= 86)
Inclusion Criteria Patients with alcohol-associated cirrhosis who continued alcohol consumption until the month prior to hospital visit and failed abstinence with up to 30 mg/day of Baclofen
Exclusion Criteria Liver decompensation (presence of jaundice, ascites, hepatic encephalopathy) in the 2 months prior to inclusion
Methods

Naltrexone was started at 50 mg/day after acute withdrawal management. Baseline liver parameters were compared with those at 4 weeks. Effectiveness was determined by reduction in AUDIT scores, craving, number and days of drinking. Self-report of side effects was noted.

Duration 4 weeks
Outcome Measures

Reduction in liver parameters (AST, ALT, SAP, GGT, Serum Bilirubin, INR, MELD score)

Baseline Characteristics   All patients (n= 86)
Age, years 41.03 (±8.56)
CTP A 65 (75.61%)
CTP B 19 (22.08%)
CTP C 2 (2.31%)
MELD score 16.62 (±7.69)
AUD severity - Mild 11 (12.8%)
AUD severity - Moderate 47 (54.7%)
AUD severity - Severe 38 (32.5%)
AUDIT score (range) 24.13 (±5.04)
Comorbid TUD - Smoking 23 (26.76%)
Comorbid TUD - Smokeless 12 (13.95%)
Comorbid TUD - Combined 20 (23.25%)
Comorbid TUD - None 31 (36.04%)
Comorbid psychiatric disorder - Anxiety 27 (31.39%)
Comorbid psychiatric disorder - Depression 14 (16.29%)
Comorbid psychiatric disorder - Others 1 (1.26%)
Comorbid psychiatric disorder - None 44 (51.16%)
Results   Baseline (±SD) Post Naltrexone (±SD) p-Value
AST (IU/L) 89.86 (±51.52) 57.61 (±26.61) 0.17
ALT (IU/L) 50.19 (±22.14) 27.08 (±10.55) 0.10
SAP (IU/L) 121.81 (±20.29) 98.19 (±30.96) 0.15
GGT (IU/L) 166.93 (±133.54) 139.88 (±73.38) 0.26
S. Bilirubin (mg/dl) 4.31 (±3.24) 1.98 (±1.25) <0.01
INR 1.49 (±0.46) 1.32 (±0.33) <0.01
MELD 16.32 (±5.77) 12.13 (±1.23) 0.41
Adverse Events No severe side effects or new onset of jaundice/worsening ascites were reported. Specific side effect profile was not found in clinical records
Study Author Conclusions The reduction in all liver parameters and AUDIT scores and craving after treatment with Naltrexone supports its safety and utility in the management of alcohol use disorder in alcohol-related liver cirrhosis.
Critique The study was not specific to liver transplant patients.
References:

Varshney M, Kaur A, Sarin SK, Shasthry SM, Arora V. Safety and Effectiveness of Naltrexone in the Management of Alcohol Use Disorder in Patients With Alcohol-associated Cirrhosis: First Clinical Observation From Indian Cohort. J Clin Exp Hepatol. 2025;15(2):102447. doi:10.1016/j.jceh.2024.102447

Safety and Tolerability of Injectable Extended-Release Naltrexone for the Management of Alcohol Use Disorder in Advanced Alcohol-Associated Liver Disease
Design

Retrospective case series

N= 14

Objective To describe the clinical experience with XR-NTX in individuals with advanced ALD, evaluating its safety, tolerability and impact on liver function and alcohol use
Study Groups All patients (n= 14)
Inclusion Criteria Adults (≥21 years) with a diagnosis of ALD who received at least one dose of XR-NTX between January 2023 and March 2025, with clinical, radiologic or histologic diagnosis of ALD and initiated on XR-NTX for AUD treatment according to DSM-5 criteria
Exclusion Criteria Other causes of chronic liver disease, HIV infection, nutritional disorders, acute hepatic decompensation (MELD > 25), opioid use disorder or concurrent opioid therapy, concurrent use of oral naltrexone, severe hypersensitivity to naltrexone, major systemic illness, history of liver transplantation
Methods Retrospective review of electronic medical records for adults with ALD who received XR-NTX 380 mg IM. Safety assessed based on adverse events and liver biochemistry. Alcohol use evaluated using PEth levels. Data collected over a minimum follow-up of 12 weeks.
Duration January 2023 to March 2025
Outcome Measures

Primary: Tolerability and safety of XR-NTX measured via Model for End- Stage Liver Disease (MELD) and Child-Pugh score

Secondary: Changes in surrogate markers of liver function

Baseline Characteristics   All patients (n= 14)
Age, median years (IQR) 51 [44–65]
Male 9 (64%)
Non-Hispanic White 5 (36%)
Hispanic or Latino 5 (36%)
Asian 1 (7%)
Other 3 (21%)
Body mass index, kg/m2 (IQR) 28.8 [24.1–35.4]
Type 2 diabetes mellitus 2 (14%)
Arterial hypertension 5 (36%)
Hyperlipidemia 4 (29%)
Alcohol consumption, g/week (IQR) 882 [392–1190]
Current smokers 4 (29%)
Former smokers 5 (36%)
Liver fibrosis stage F0–1 2 (14%)
Liver fibrosis stage F2 1 (7%)
Liver fibrosis stage F3 2 (14%)
Liver fibrosis stage F4 9 (64%)
Results   Baseline (N= 14) End follow-up (N= 12) p-Value
MELD 7 (6–10) 8 (6–10) 0.688
Child-Pugh 6 (6–8) 7 (5–8) 0.500
AST (U/L) 43 (26–49) 31 (19–44) 0.625
ALT (U/L) 28 (16–51) 16 (11–17) 0.139
Total bilirubin (mg/dL) 0.9 (0.6–1.4) 1.0 (0.6–1.1) 0.264
Albumin (g/dL) 4.3 (4.0–4.5) 4.2 (3.6–4.5) 0.883
Phosphatidylethanol (ng/mL) 207 (33–401) 94 (5–571) 0.557
Adverse Events Four patients (29%) experienced mild adverse effects (injection site pain, nausea and vomiting, fatigue and sexual side effects); none had hepatotoxicity or hepatic decompensation
Study Author Conclusions In this case series, XR-NTX was well tolerated in patients with advanced ALD, without evidence of hepatotoxicity or liver decompensation.
Critique

The study provides preliminary evidence of the safety of XR-NTX in patients with advanced ALD, but the small sample size and single-center design limit the generalizability of the findings. The retrospective nature may introduce selection bias, and the lack of a control group limits the ability to attribute changes directly to XR-NTX. Additionally, reliance on self-reported alcohol use and inconsistent PEth testing may affect the accuracy of alcohol consumption assessment.

 

References:

Díaz LA, Collier S, Yin J, Loomba R. Safety and Tolerability of Injectable Extended-Release Naltrexone for the Management of Alcohol Use Disorder in Advanced Alcohol-Associated Liver Disease. Aliment Pharmacol Ther. 2025;62(7):692-698. doi:10.1111/apt.70237