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Case Report Diphenhydramine as a Cause of Drug-Induced Liver Injury Yunseok Namn, 1 Yecheskel Schneider, 1 Isabelle H. Cui, 2 and Arun Jesudian 1 1 Department of Gastroenterology and Hepatology, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY, USA 2 Department of Pathology, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY, USA Correspondence should be addressed to Yunseok Namn; [email protected] Received 18 November 2016; Accepted 10 January 2017; Published 26 January 2017 Academic Editor: Melanie Deutsch Copyright © 2017 Yunseok Namn et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Unites States and accounts for 10% of acute hepatitis cases. We report the only known case of diphenhydramine-induced acute liver injury in the absence of concomitant medications. A 28-year-old man with history of 13/14-chromosomal translocation presented with fevers, vomiting, and jaundice. Aspartate-aminotransferase and alanine-aminotransferase levels peaked above 20,000 IU/L and 5,000 IU/L, respectively. He developed coagulopathy but without altered mental status. Patient reported taking up to 400 mg diphenhydramine nightly, without concomitant acetaminophen, for insomnia. He denied taking other medications, supplements, antibiotics, and herbals. A thorough workup of liver injury ruled out viral hepatitis (including A, B, C, and E), autoimmune, toxic, ischemic, and metabolic etiologies including Wilson’s disease. A liver biopsy was consistent with DILI without evidence of iron or copper deposition. Diphenhydramine was determined to be the likely culprit. is is the first reported case of diphenhydramine-induced liver injury without concomitant use of acetaminophen. 1. Introduction Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Unites States, accounting for nearly 50% of cases and 10% of acute hepatitis cases [1–3]. Other etiologies of acute liver injury include viral, autoimmune, metabolic, and ischemic etiologies. When acute liver injury progresses to fulminant hepatic failure, it is associated with high mortality [4, 5]. erefore, prompt recognition of the underlying etiology and initiation of treatment are of paramount importance. Medications such as acetaminophen, antiepileptics, and antibiotics are well known causes of DILI; however, thousands of drugs, herbs, and toxins can cause idiosyncratic liver injury. We report the first case of diphenhydramine-induced liver injury without concomitant use of acetaminophen. 2. Case A 28-year-old man with history of chromosomal translo- cation 13/14 and no prior liver disease presented to the hospital with complaint of fevers, nonbloody emesis, and dark urine. History revealed ingestion of diphenhydramine 400mg nightly, taken for insomnia, over the previous 4 months; the medication was inspected in the hospital and confirmed not to contain acetaminophen. He denied use of herbal compounds, supplements, teas, and any other medication. e patient endorsed rare alcohol consumption and rare intranasal cocaine use in the distant past. Family history was notable for possible statin-induced liver disease and hereditary angioedema. Vital signs on presentation were within normal limits. Physical exam revealed icteric conjunctiva, a 15 cm liver pal- pable 3 cm below the right costal margin, nonpalpable spleen, normal mentation, and neurologic exam without asterixis. Initial laboratory studies revealed aspartate aminotrans- ferase (AST) 10,425 IU/L, alanine aminotransferase (ALT) 2,471 IU/L, alkaline phosphatase (ALP) 65 IU/L, total biliru- bin 2.7 mg/dL (direct 1.4 mg/dL), INR 2.6, and a hemoglobin level of 12.7 g/dL; the remainder of the laboratory studies were normal, including creatinine, blood glucose, and lactate. Hepatology and toxicology consultations were requested, and empiric intravenous N-acetylcysteine (NAC) was initiated. By day two, his transaminases and coagulopathy worsened, Hindawi Case Reports in Hepatology Volume 2017, Article ID 3864236, 4 pages https://doi.org/10.1155/2017/3864236
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  • Case ReportDiphenhydramine as a Cause of Drug-Induced Liver Injury

    Yunseok Namn,1 Yecheskel Schneider,1 Isabelle H. Cui,2 and Arun Jesudian1

    1Department of Gastroenterology and Hepatology, Weill Cornell Medical College, New York Presbyterian Hospital,New York, NY, USA2Department of Pathology, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY, USA

    Correspondence should be addressed to Yunseok Namn; [email protected]

    Received 18 November 2016; Accepted 10 January 2017; Published 26 January 2017

    Academic Editor: Melanie Deutsch

    Copyright © 2017 Yunseok Namn et al.This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

    Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Unites States and accounts for 10%of acute hepatitis cases. We report the only known case of diphenhydramine-induced acute liver injury in the absence ofconcomitantmedications. A 28-year-oldmanwith history of 13/14-chromosomal translocation presentedwith fevers, vomiting, andjaundice. Aspartate-aminotransferase and alanine-aminotransferase levels peaked above 20,000 IU/L and 5,000 IU/L, respectively.He developed coagulopathy but without altered mental status. Patient reported taking up to 400mg diphenhydramine nightly,without concomitant acetaminophen, for insomnia. He denied taking other medications, supplements, antibiotics, and herbals. Athorough workup of liver injury ruled out viral hepatitis (including A, B, C, and E), autoimmune, toxic, ischemic, and metabolicetiologies including Wilson’s disease. A liver biopsy was consistent with DILI without evidence of iron or copper deposition.Diphenhydramine was determined to be the likely culprit. This is the first reported case of diphenhydramine-induced liver injurywithout concomitant use of acetaminophen.

    1. Introduction

    Drug-induced liver injury (DILI) is the most common causeof acute liver failure in theUnites States, accounting for nearly50% of cases and 10% of acute hepatitis cases [1–3]. Otheretiologies of acute liver injury include viral, autoimmune,metabolic, and ischemic etiologies. When acute liver injuryprogresses to fulminant hepatic failure, it is associated withhigh mortality [4, 5]. Therefore, prompt recognition ofthe underlying etiology and initiation of treatment are ofparamount importance.Medications such as acetaminophen,antiepileptics, and antibiotics are well known causes ofDILI; however, thousands of drugs, herbs, and toxins cancause idiosyncratic liver injury. We report the first case ofdiphenhydramine-induced liver injury without concomitantuse of acetaminophen.

    2. Case

    A 28-year-old man with history of chromosomal translo-cation 13/14 and no prior liver disease presented to thehospital with complaint of fevers, nonbloody emesis, and

    dark urine. History revealed ingestion of diphenhydramine400mg nightly, taken for insomnia, over the previous 4months; the medication was inspected in the hospital andconfirmed not to contain acetaminophen. He denied useof herbal compounds, supplements, teas, and any othermedication. The patient endorsed rare alcohol consumptionand rare intranasal cocaine use in the distant past. Familyhistory was notable for possible statin-induced liver diseaseand hereditary angioedema.

    Vital signs on presentation were within normal limits.Physical exam revealed icteric conjunctiva, a 15 cm liver pal-pable 3 cm below the right costal margin, nonpalpable spleen,normal mentation, and neurologic exam without asterixis.Initial laboratory studies revealed aspartate aminotrans-ferase (AST) 10,425 IU/L, alanine aminotransferase (ALT)2,471 IU/L, alkaline phosphatase (ALP) 65 IU/L, total biliru-bin 2.7mg/dL (direct 1.4mg/dL), INR 2.6, and a hemoglobinlevel of 12.7 g/dL; the remainder of the laboratory studieswere normal, including creatinine, blood glucose, and lactate.Hepatology and toxicology consultationswere requested, andempiric intravenous N-acetylcysteine (NAC) was initiated.By day two, his transaminases and coagulopathy worsened,

    HindawiCase Reports in HepatologyVolume 2017, Article ID 3864236, 4 pageshttps://doi.org/10.1155/2017/3864236

    https://doi.org/10.1155/2017/3864236

  • 2 Case Reports in Hepatology

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    Figure 1: Linear graphs representing the trend of transaminases, INR, and direct bilirubin throughout patient’s hospital course and outpatientfollow-up.

    with AST 20,176 IU/L, ALT 5,076 IU/L, and INR 3.1 (Figures1(a), 1(b), and 1(c)).Thepatient did not exhibit signs of hepaticencephalopathy, but was transferred to the intensive care unitfor closer monitoring. By the third day of NAC treatment,transaminases started to improve. A complete evaluationfor causes of acute liver injury, including viral hepatitis(hepatitis A, B, C, and E), workup for other viruses (includ-ing EBV, CMV, HHV-6, and HIV), autoimmune workup(ANA, ASMA, AMA, A1AT, IgG, and LTK Ab), metabolictesting (ceruloplasmin, 24-hour urine copper, ophthalmo-logic examination for Keyser-Fleischer rings, MRI brain toevaluate for lenticular degeneration, and iron studies), urinetoxicology, and SPEP/UPEP, was all normal and did notreveal an alternative etiology of the patient’s acute liverinjury. Abdominal ultrasound demonstrated a 17.4 cm liverwith smooth contour and normal echogenicity with patenthepatic and portal vasculature. He underwent a transjugularbiopsy which revealed centrilobular and bridging necrosisaccompanied by portal and lobular inflammation, favoringdrug-induced liver injury (Figures 2(a) and 2(b)). Rhodaninestain for copper and quantitative copper analysis were bothnegative, ruling out Wilson’s disease. Iron staining was not

    consistent with hemochromatosis. The patient ultimatelyrecovered completely from acute liver injury and was dis-charged home. Upon the 6-month outpatient follow-up,patient was asymptomatic and reported feeling well, andrepeat liver function tests did not show any evidence of liverinjury.

    3. Discussion

    Acute liver injury can be attributed to a wide array of causes,with viral and drug etiologies being the most common inadults. In the United States, acetaminophen toxicity andidiosyncratic drugs reaction are the leading causes of acuteliver failure while viral hepatitis is the leading cause in Asiaand Europe [4, 5].

    Drug-induced liver injury remains one of the mostchallenging diagnoses to make but must be considered inthe differential diagnosis of any liver injury [6, 7]. Patientsshould undergo careful evaluation to exclude other causesof liver disease, including viral hepatitides (hepatitis A, B,C, and E), EBV, CMV, HHV-6, autoimmune hepatitis, andWilson’s disease if age is less than 40 [8, 9]. Offending agents

  • Case Reports in Hepatology 3

    (a) Liver biopsy sample at 100x magnification (b) Liver biopsy sample at 400x magnification

    Figure 2: On Hematoxylin and Eosin stain (100x and 400x), there is centrilobular and bridging necrosis accompanied by portal and lobularinflammation including eosinophils and plasma cells. There is evidence of cholestasis and bile duct injury is noted in some portal tracts.Hepatocellular injury, that is, hepatocyte ballooning degeneration, is also present. Fibrosis is absent on Trichrome staining. There is noevidence of steatosis, glycogenic nuclei, Mallory’s hyaline, or copper deposition. Overall, these findings favor a diagnosis of drug-inducedliver injury.

    can include prescription and over-the-counter medications,such as antibiotics (nitrofurantoin, isoniazid, and trimetho-prim/sulfamethoxazole), immunomodulatory agents (suchas infliximab), analgesics (especially those that containacetaminophen), antineoplastic agents, antiepileptics, andstatins [10, 11]. Additionally, DILI can result from herbalingestions or dietary supplements [12, 13]. Manifestationsof liver injury can range from asymptomatic transaminaseelevation and/or jaundice (depending on a hepatocellularor cholestatic pattern of injury, resp.) to development ofacute liver failure marked by encephalopathy and syntheticdysfunction [13, 14].

    Drug-induced liver injury can be divided into two classesof medication-related hepatotoxicity: intrinsic and idiosyn-cratic. The former, which includes acetaminophen, is oftendose-dependent with predictable liver injury at hepatotoxicdoses [11, 15]. Idiosyncratic DILI is not dose-dependent andthus is harder to predict. It is thought to mainly affectindividuals with underlying susceptibility or predispositionand therefore, may have variable latency [11, 16].

    In the presented case, multiple etiologies for the liverinjury were considered and excluded. The liver biopsy wasconsistent with DILI and after ascertainment of an exhaus-tive mediation history diphenhydramine was identified asthe only possible culprit. Although there are reports ofdiphenhydramine and acetaminophen causing liver injurywhen ingested together, there are no prior cases in theliterature of diphenhydramine alone causing DILI. Althoughconsidered to have minimal to no hepatotoxic effects, thiscase suggests that diphenhydramine may be hepatotoxicat high doses with chronic use (as the patient had beentaking at least 400mg per day for over four months). It hasbeen reported that compounds with more than 50% hepaticmetabolism given at doses higher than 50mg/day were athighest risk of hepatotoxicity [13, 17]. Diphenhydramineundergoes extensive first-pass metabolism, whereby 50–60%of ingested medication is metabolized by the liver beforereaching the systemic circulation. Nearly all the availabledrug is metabolized by the liver within 24–48 hours, thusincreasing risk for liver injury. It is unclear if a predispositionfor hepatotoxicity was present in this patient given his history

    of a balanced chromosomal translocation. However, certaingenetic predispositions have been noted to play a role in riskfor DILI. For example, theHLA-1 andHLA-II genotypes havebeen shown to confer an increased susceptibility to DILI forpatients taking amoxicillin-clavulanate [7, 17, 18].

    In summary, we present a case of diphenhydramine-induced liver injury, without the concomitant use ofacetaminophen. Although not previously thought to causeliver injury, this case highlights that any medication metab-olized by the liver has potential to lead to liver injury wheningested at high enough doses and for long enough durationin susceptible individuals.

    Consent

    Patient consent was obtained for publication of case detailsincluding images.

    Competing Interests

    There is no financial support or competing interests.

    Authors’ Contributions

    Yunseok Namn is the main author of manuscript andarticle guarantor; Yecheskel Schneider is the 2nd authorof manuscript; Isabelle H. Cui attained and analyzed thehistological slide; Arun Jesudian is the advisor.

    References

    [1] H. J. Zimmerman, “Drug-induced liver disease,” Clinical LiverDisease, vol. 4, no. 1, pp. 73–96, 2000.

    [2] G. Ostapowicz, “Results of a prospective study of acute liverfailure at 17 tertiary care centers in the United States,” Annalsof Internal Medicine, vol. 137, no. 12, pp. 947–954, 2002.

    [3] A. M. Larson, J. Polson, R. J. Fontana et al., “Acetaminophen-induced acute liver failure: results of aUnited Statesmulticenter,prospective study,” Hepatology, vol. 42, no. 6, pp. 1364–1372,2005.

    [4] D. Gotthardt, C. Riediger, K. H. Weiss et al., “Fulminant hep-atic failure: etiology and indications for liver transplantation,”

  • 4 Case Reports in Hepatology

    Nephrology Dialysis Transplantation, vol. 22, supplement 8, pp.viii5–viii8, 2007.

    [5] C. Stephens, R. J. Andrade, and M. I. Lucena, “Mechanismsof drug-induced liver injury,” Current Opinion in Allergy andClinical Immunology, vol. 14, no. 4, pp. 286–292, 2014.

    [6] R. Marudanayagam, V. Shanmugam, B. Gunson et al., “Aetiol-ogy and outcomeof acute liver failure,”HPB:TheOfficial Journalof the International Hepato Pancreato Biliary Association, vol. 11,no. 5, pp. 429–434, 2009.

    [7] M. Ghabril, N. Chalasani, and E. Björnsson, “Drug-inducedliver injury: a clinical update,”Current Opinion inGastroenterol-ogy, vol. 26, no. 3, pp. 222–226, 2010.

    [8] M. D. Leise, J. J. Poterucha, and J. A. Talwalkar, “Drug-inducedliver injury,”Mayo Clinic Proceedings, vol. 89, no. 1, pp. 95–106,2014.

    [9] N. Kaplowitz, “Drug-induced liver injury,” Clinical InfectiousDiseases, vol. 38, no. 2, pp. S44–S48, 2004.

    [10] P. Sarges, J. M. Steinberg, and J. H. Lewis, “Drug-induced liverinjury: highlights from a review of the 2015 literature,” DrugSafety, vol. 39, no. 9, pp. 801–821, 2016.

    [11] R. A. Roth and P. E. Ganey, “Intrinsic versus idiosyncraticdrug-induced hepatotoxicity—two villains or one?” Journal ofPharmacology and ExperimentalTherapeutics, vol. 332, no. 3, pp.692–697, 2010.

    [12] A. Reuben, D. G. Koch, and W. M. Lee, “Drug-induced acuteliver failure: results of a U.S. multicenter, prospective study,”Hepatology, vol. 52, no. 6, pp. 2065–2076, 2010.

    [13] C. Lammert, S. Einarsson, C. Saha, A. Niklasson, E. Bjornsson,and N. Chalasani, “Relationship between daily dose of oralmedications and idiosyncratic drug-induced liver injury: searchfor signals,” Hepatology, vol. 47, no. 6, pp. 2003–2009, 2008.

    [14] R. Marudanayagam, V. Shanmugam, B. Gunson et al., “Aetiol-ogy and outcome of acute liver failure,” HPB, vol. 11, no. 5, pp.429–434, 2009.

    [15] N. Chalasani, H. L. Bonkovsky, R. Fontana et al., “Features andoutcomes of 899 patients with drug-induced liver injury: theDILIN prospective study,” Gastroenterology, vol. 148, no. 7, pp.1340–1352.e7, 2015.

    [16] S. R. Knowles, J. Uetrecht, and N. H. Shear, “Idiosyncratic drugreactions: the reactive metabolite syndromes,” The Lancet, vol.356, no. 9241, pp. 1587–1591, 2000.

    [17] B. Fromenty, “Drug-induced liver injury in obesity,” Journal ofHepatology, vol. 58, no. 4, pp. 824–826, 2013.

    [18] N. Chalasani, H. L. Bonkovsky, R. Fontana et al., “Features andoutcomes of 899 patients with drug-induced liver injury: theDILIN prospective study,” Gastroenterology, vol. 148, no. 7, pp.1340.e7–1352.e7, 2015.

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