Case Report

J Sci Discov (2020); 4(2):jsd20020; DOI:10.24262/jsd.4.2.20020; 
Received July 05th, 2020, Revised August 01st, 2020, Accepted August 13rd, 2020, Published Accepted August 19th, 2020.

Acute liver failure in an adolescent with marijuana use: A case report

Mohammed Alkhero¹, Saja Al adhami², Aws Alamer³

¹UHS SOCAL MEC Internal Medicine. Email: mohammed.alkhero@uhsinc.com, 31700 Temecula Pkwy, Temecula, CA 92592.

²Community Regional Medical Center / Fresno, 2823 Fresno St, Fresno, CA 93721

³The University of Texas Health Science Center at San Antonio / Internal Medicine, 7703 Floyd Curl Dr, San Antonio, TX 78229.

* Correspondence: Mohammed Alkhero, UHS SOCAL MEC Internal Medicine, 31700 Temecula Pkwy, Temecula, CA 92592. Email: mohammed.alkhero@uhsinc.com.

Introduction Recreational marijuana has been associated with a variety of health hazards. There is a controversial discussion about the effects of recreational marijuana on the gastrointestinal tract. A few case reports have linked the use of marijuana with fulminant liver failure which is considered a rare occurrence. There is no known literature review explaining how marijuana could play a role in hepatic injury. Many medications and herbs have been identified as causes of drug-induced liver injury. It has not been proven scientifically that the consumption of recreational marijuana could be a cause of acute liver failure. We present an unfortunate but interesting case of acute fulminant liver failure related to marijuana use in a young adolescent.

Background Acute liver failure (ALF) is a rare but life-threatening disease defined as coagulopathy (INR>1.5) and the presence of hepatic encephalopathy of any degree less than 26 weeks duration, in a patient without preexisting liver disease (1). It is affecting around 2,000 patients annually in the United States (2).

It is commonly caused by drug toxicity (50%), viral hepatitis (9%), and autoimmune hepatitis (7%) with 30-40% of cases with an unknown etiology (3). It is vital to be able, when possible, to identify the etiology of ALF for defining the treatment approach and prognosis.

Keywords: acute liver injury, marijuana toxicity, coagulopathy, encephalopathy, hepatic necrosis.

Our patient is a 21 years old female with a history of asthma presented to our hospital for yellow discoloration to her eyes for 4 days associated with nausea, vomiting, diarrhea, and dark-colored urine. Denied abdominal pain, pale stools, fevers, chills, and dysuria. Reported marijuana use for the past 6 months. No drug or alcohol use. Unremarkable family history. Physical examination was positive for yellowish discoloration of the skin and sclera. Initial blood work showed highly elevated liver enzymes alkaline phosphatase at 117 IU/L, aspartate aminotransferase at 745 IU/L, and alanine aminotransferase at 1711 IU/L. Total bilirubin at 7.5 mg/dl with direct bilirubin at 5.2 mg/dl and indirect bilirubin at 2.3 mg/dl. INR at 2 with mildly prolonged prothrombin time but normal partial thromboplastin time. lipase was normal and the pregnancy test was negative. During the course of her hospitalization, the patient was confused and delirious for which she was admitted to the ICU for management of her acute liver failure.

Abdominal imaging was unremarkable. Urine toxicology was positive for cannabinoids. Infectious, autoimmune, metabolic, and other toxic etiologies of liver injury were ruled out. A liver biopsy was obtained which showed active hepatitis pattern, with hepatocellular dropout involving approximately 20% of the biopsy specimen. The patient was managed supportively. Her liver enzymes were back to normal levels, and she was discharged home.

ALF has a common clinical presentation regardless of the etiology that represents the final pathway of acute organ failure. The course of ALF is variable and the mortality rate is high. Our 21-year-old received the diagnosis of ALF after meeting the criteria of coagulopathy of INR > 1.5 and hepatic encephalopathy. An extensive workup that included viral serologies (HAV, HBV, HCV, CMV, and herpes virus), autoimmune, and metabolic studies were unremarkable. Work up for the miscellaneous causes of ALF (Wilson’s disease, malignant infiltration, leptospirosis, hepatic amoebiasis, malaria, rickettsial disease, and mushroom poisoning) were negative as well. Liver biopsy showed findings consistent with an active hepatitis pattern with evidence of hepatocyte injury. A presumptive diagnosis of liver toxicity due to marijuana use was assumed. Tetrahydrocannabinol (THC) is the active compound found in recreational cannabis and is responsible for the cannabis psychoactive effects by acting on cannabinoid receptors type 1 and 2 (CB1 and CB2) (4). THC is well known for the psychological and physiological changes that include alterations of perceptions and mood as well as effects on multiple functional systems in the body including but not limited to neurological, cardiovascular, and gastrointestinal systems. There is no formal literature review as to the exact mechanism behind THC-induced liver injury with very few case reports published in this regard. This was a diagnosis of exclusion after ruling out the most common causes of ALF. The patient was treated supportively and was able to be discharged home. The patient was advised to avoid using recreational marijuana indefinitely.

In conclusion, we report a case of a rare cause of ALF induced by chronic marijuana use. Although rare, physicians must have a high index of suspicion to consider this etiology when approaching a case of ALF in adolescent patients with a history of marijuana or other cannabis use. While overall outcomes have improved since the era before transplants, ALF remains a challenging syndrome with high mortality and a major burden to the medical care system.

Not applicable as this case report does not involve human trials.

Not applicable as this case report does not contain any personal health information.

Not applicable

We declare that we have no competing interests

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1. Popper Hans, and Fenton Schaffner, eds. Progress in Liver Diseases: Volume 2. Vol. 2. Butterworth-Heinemann, 2013.
2. Bower WA, Johns M, Margolis HS, Williams IT, Bell BP. Population based surveillance for acute liver failure. Am J Gastroenterol 2007; 102:2459–
3. Reuben A,Koch DG,LeeWM; Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. multicenter, prospective study. Hepatology 2010; 52:2065–
4. Sharma P, Murthy P, Bharath MM: Chemistry metabolism, and toxicology of cannabis: clinical implications. Iran J Psychiatry. 2012, 7:149-156.

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