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Pharmacotherapy for Alcohol Use Disorder in Patients with Hepatic Impairment

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Pharmacotherapy for Alcohol Use Disorder in Patients with Hepatic Impairment Savvy Psychopharmacology Pharmacotherapy for alcohol use disorder in patients with hepatic impairment Courtney V. Eatmon, PharmD, BCPP, and Kelley Trent, PharmD r. S, age 64, presents for an outpa- partially explain the higher prevalence of tient follow-up after a recent hospital viral hepatitis among persons with alco- M discharge for alcohol detoxification. hol use disorder (AUD) compared with the He reports a long history of alcohol use, which general population. Alcoholic liver disease has resulted in numerous hospital admissions. (ALD) progresses through several stages, He has recently been receiving care from a beginning with hepatic steatosis and pro- gastroenterologist because the results of labo- gressing through alcohol-related hepatitis, Vicki L. Ellingrod, ratory testing suggested hepatic impairment fibrosis, cirrhosis, and potentially hepatocel- PharmD, FCCP (Table 1,1 page 26). Mr. S says that an friend of lular carcinoma.3 Department Editor his was able to stop drinking by taking a medi- cation, and he wonders if he can be prescribed Liver markers of alcohol use a medication to help him as well. Although biological markers can be used A chart review shows that Mr. S recently in clinical practice to screen and monitor underwent paracentesis, during which 6 liters of fluid were removed. Additionally, an abdomi- Practice Points nal ultrasound confirmed hepatic cirrhosis. • The risk of alcoholic liver disease (ALD) increases with daily alcohol According to the World Health Organization, consumption; however, it is also alcohol consumption contributes to 3 mil- dependent on genetic predisposition, lion deaths annually.2 The highest proportion age, gender, comorbid hepatitis B or C infection, and other risk factors. of these deaths (21.3%) is due to alcohol- associated gastrointestinal complications, • Liver function tests must be interpreted including alcoholic and infectious hepati- carefully along with a full clinical picture because these tests are not specific to liver tis, pancreatitis, and cirrhosis. Because the injury, and the degree of liver enzyme liver is the primary site of ethanol metabo- elevation does not always correspond with lism, it sustains the greatest degree of tis- the degree of liver injury. sue injury with heavy alcohol consumption. • Although not specific, alterations in serum Additionally, the association of harmful use albumin level and international normalized of alcohol with risky sexual behavior may ratio are better correlated to actual liver Savvy Psychopharmacology function as the disease progresses. is produced in partnership Dr. Eatmon is Clinical Pharmacy Specialist, Substance Use with the College Disorders, Lexington Veterans Affairs Health Care System, and • Of the 3 FDA-approved medications for of Psychiatric Assistant Professor, Department of Pharmacy Practice and Science, the treatment of alcohol use disorder, only and Neurologic University of Kentucky, Lexington, Kentucky. Dr. Trent is a PGY-2 acamprosate is considered safe for use in Pharmacists Psychiatric Pharmacy Resident, Lexington Veterans Affairs Health patients with severe ALD. cpnp.org Care System, Lexington, Kentucky. mhc.cpnp.org (journal) Disclosures • Baclofen is the only medication that has The authors report no financial relationships with any companies been tested specifically in patients with whose products are mentioned in this article, or with manufacturers advanced ALD and may promote abstinence of competing products. and reduce return to use. Current Psychiatry doi: 10.12788/cp.0068 Vol. 20, No. 1 25 Savvy Psychopharmacology Table 1 advanced cirrhosis may have liver enzyme levels that appear normal. However, the Hepatic laboratory values for Mr. S pattern of elevation in transaminases can Liver Mr. S’s Reference be helpful in making a diagnosis of liver function test values range dysfunction; using the ratio of AST to ALT AST 216 U/L 17 to 59 U/L may aid in diagnosing ALD, because AST ALT 99 U/L 20 to 35 U/L is elevated more than twice that of ALT in ALP 194 U/L 44 to 147 U/L >80% of patients with ALD.1,3,4 GGT 76 U/L 9 to 48 U/L Table 2,1,3,4 (page 27) shows the pro- Total bilirubin 1.6 mg/dL 0.2 to 1.3 mg/dL gression of ALD from steatohepatitis to ALP: alkaline phosphatase; ALT: alanine aminotransferase; alcoholic hepatitis to cirrhosis. In steatohep- AST: aspartate aminotransferase; GGT: gamma-glutamyl transferase atitis, transaminitis is present but all other Source: Reference 1 biomarkers normal. In alcoholic hepatitis, Clinical Point transaminitis is present along with elevated The risk of alkaline phosphatase, elevated bilirubin, and elevated international normalized alcoholic liver for alcohol abuse, making a diagnosis of ratio (INR). In alcoholic cirrhosis, the AST- disease increases ALD can be challenging. Typically, a history to-ALT ratio is >2, and hypoalbuminemia, with daily alcohol of heavy alcohol consumption in addition to hyperbilirubinemia, and coagulopathy consumption, but certain physical signs and laboratory tests for (evidenced by elevated INR) are present, liver disease are the best indicators of ALD. consistent with long-term liver damage.1,3,4 also depends on However, the clinical assessment can be con- other risk factors founded by patients who deny or minimize FDA-approved medications how much alcohol they have consumed. Three medications—acamprosate, naltrex- Furthermore, physical and laboratory find- one, and disulfiram—currently are FDA- ings may not be specific to ALD. approved for treating AUD.5,6 Additionally, Liver enzymes, including aspartate ami- several other medications have shown notransferase (AST), alanine aminotransfer- varying levels of efficacy in treating patients ase (ALT), and gamma-glutamyltransferase with AUD but are not FDA-approved for (GGT), have historically been used as the this indication (Table 3,5-8 page 28). basis of diagnosing ALD. In addition to ele- Acamprosate is thought to create a bal- vated bilirubin and evidence of macrocytic ance of inhibitor and excitatory neurotrans- anemia, elevations in these enzymes may mitters by functioning as a glutamate suggest heavy alcohol use, but these val- antagonist and gamma-aminobutyric acid ues alone are inadequate to establish ALD. (GABA) agonist. This is speculated to aid Gamma-glutamyltransferase is found in cell in abstinence from alcohol. Data suggests membranes of several body tissues, includ- that acamprosate may be more effective ing the liver and spleen, and therefore is not for maintaining abstinence than for induc- specific to liver damage. However, elevated ing remission in individuals who have not GGT is the best indicator of excessive alcohol yet detoxified from alcohol. Because of its consumption because it has greater sensitiv- renal excretion, acamprosate is the only ity than AST and ALT.1,3,4 FDA-approved medication for AUD that is Discuss this article at Although these biomarkers are helpful in not associated with liver toxicity. The most www.facebook.com/ diagnosing ALD, they lose some of their util- commonly reported adverse effect with MDedgePsychiatry ity in patients with advanced liver disease. acamprosate use is diarrhea. Patients with severe liver dysfunction may Naltrexone, a mu-opioid receptor antago- not have elevated serum aminotransferase nist, is available in both tablet and long-act- levels because the degree of liver enzyme ing IM injection formulations. Naltrexone elevation does not correlate well with the blocks the binding of endorphins created by Current Psychiatry 26 January 2021 severity of ALD. For example, patients with alcohol consumption to opioid receptors. Savvy Psychopharmacology Table 2 Progression of alcoholic liver disease Liver function test Alcoholic steatohepatitis Alcoholic hepatitis Alcoholic cirrhosis AST 174 U/L (H) 260 U/L (H) 109 U/L (H) ALT 86 U/L (H) 94 U/L (H) 39 U/L ALP 87 U/L 192 U/L (H) 169 U/L (H) GGT 52 U/L (H) 94 U/L (H) 204 U/L (H) Total protein 6.6 gm/dL 8.6 gm/dL (H) 6.7 gm/dL Albumin 3.7 g/dL 4.6 g/dL 2.8 g/dL (L) Total bilirubin 1.0 mg/dL 1.8 mg/dL (H) 3.8 mg/dL (H) INR 1.11 1. 3 (H) 2.45 (H) ALP: alkaline phosphatase; ALT: alanine aminotransferase; AST: aspartate aminotransferase; GGT: gamma- glutamyltransferase; INR: international normalized ratio Clinical Point Source: References 1,3,4 Liver function tests must be interpreted carefully along with This results in diminished dopamine release Off-label medications for AUD a full clinical picture and is speculated to decrease reward and Additional pharmacotherapeutic agents because these tests positive reinforcement with alcohol con- have been evaluated in patients with AUD. are not specific to sumption, leading to fewer heavy drinking Baclofen, topiramate, gabapentin, and days. Due to hepatic metabolism, naltrex- ondansetron have shown varying levels liver injury one use carries a risk of liver injury. Cases of efficacy and pose minimal concern in of hepatitis and clinically significant liver patients with ALD. dysfunction as well as transient, asymp- Baclofen. Although findings are con- tomatic, hepatic transaminase elevations flicting, baclofen is the only agent that has have been observed in patients who receive been specifically studied for treating AUD naltrexone. Because of the absence of first- in patients with ALD. A GABA B recep- pass metabolism, long-acting IM naltrexone tor antagonist, baclofen is currently FDA- may produce less hepatotoxicity than the approved for treating spasticity. In a series oral formulation. When the FDA approved of open-label and double-blind studies, both formulations of naltrexone, a “black- baclofen has been shown to effectively box” warning was issued concerning the reduce alcohol intake, promote abstinence, risk of liver damage; however, these warn- and prevent relapse.5,6 Further studies ings have since been removed from their identified a possible dose-related response, respective prescribing information. noting that 20 mg taken 3 times daily may Disulfiram inhibits acetaldehyde dehydro- confer additional response over 10 mg taken genase, resulting in elevated acetaldehyde 3 times daily.5,6 Conversely, the ALPADIR concentrations after consuming alcohol.
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