S2627 A Case of K2-Induced Hyperbilirubinemia

Abstract

INTRODUCTION: Over the last decade, synthetic cannabinoids (SCB) have been marketed as a natural and safer version of marijuana, leading to an increase in its recreational use. We present a case of isolated hyperbilirubinemia caused by K2 and, to our knowledge, this is the first reported case of K2-induced indirect hyperbilirubinemia. CASE DESCRIPTION/METHODS: An 18-year-old male with no significant medical history presented with behavioral changes. He admitted to using K2 daily. His sibling and paternal uncle had Gilbert's syndrome. On physical exam he was withdrawn and agitated. He had Scleral icterus and jaundice. Slit Lamp exam was equivocal. On labs: Total Bilirubin 11.2 mg/dL, Indirect bilirubin 10.8 mg/dL, Urine toxicology positive for marijuana.Serum ceruloplasmin, serum copper, 24h urinary copper excretion, anti-mitochondrial Ab, anti-Nuclear Ab, anti-LKM, Soluble Liver antigen, ferritin, iron, TIBC, A1AT, A1AT phenotype, IgG, IgM, IgA, hepatitis A, B, C serologies, LDH, haptoglobin, uric acid, Coombs test, and G6PD levels were all within normal limits. His peripheral blood smear was normal. Imaging: MRI brain: unremarkable, Liver biopsy:normal hepatic architecture without severe pathological process (Figures 2a and 2b). He was treated with supportive care and indirect hyperbilirubinemia improved. DISCUSSION: • There is no current literature that correlates indirect hyperbilirubinemia and SCB use. In our otherwise healthy patient, this hyperbilirubinemia was likely a consequence of his K2 ingestion. We hypothesize that K2 may impair hepatic glucuronidation which is the process by which indirect bilirubin is converted to direct bilirubin. • During the time of exacerbation of Gilbert's disease, most often the indirect bilirubin levels remain < 5mg/dL. In the case of our patient, he presented with an indirect bilirubin level of 10.8 mg/dL. His work-up excluded other causes of indirect hyperbilirubinemia. • This leads us to hypothesize that K2 may induce significant isolated indirect hyperbilirubinemia in patients with a predisposition to impaired hepatic glucuronidation. • We believe that removal of the insulting agent is required for resolution of the hyperbilirubinemia. • With the use of SCB increasing recreationally, it is crucial we understand the effects these drugs can have. SCB do not appear on standard hospital drug screens. Therefore, a focused history and exam should be obtained from the patient. Our case serves to increase awareness of SCB use as a cause of indirect hyperbilirubinemia.Figure 1Figure (2a).: Liver biopsy stained with Hematoxylin & Eosin, showing normal hepatic architecture with no periductal or ductular inflammatory infiltration.Figure (2b).: Hepatic tissue stained with Periodid acid-Schiff Diastase and for copper; normal pathology & negative copper staining.