Oral Papers: Addiction, Pain, & Transplant I
Background/Significance: Alcohol abstinence monitoring is important in pre-transplant waitlist candidacy. Incorrect abstinence monitoring interpretation in transplant patients can cause rejection of qualified individuals from the waitlist. Clinical Case: A 61-year old female with poorly controlled T2DM and cirrhosis was declined for liver transplant at two institutions after positive urine ethanol results. Negative plasma ethanol and urine ethanol metabolites (ethyl glucuronide and sulfate)1 were noted corresponding with positive urine ethanol and no symptoms of alcohol intoxication despite urine ethanol >180 mg/dL. Hyperglycosuria ( > 1000 mg/dL) with budding yeast was also noted. These findings and patient denial of drinking led our group to test the hypothesis of ethanol production by fermenting yeast.2 Methods: Freshly voided urine was transported to the lab on ice and read for baseline ethanol (44 mg/dL) using headspace gas chromatography. The specimen was centrifuged into yeast-poor and yeast-rich fractions and incubated at three temperatures (4°C, 25°C, and 37°C) for 24 hours. The yeast-rich fraction was also incubated in the presence of 1% NaF, a fermentation inhibitor. Ethanol increased to 476 mg/mL and 816 mg/mL after incubation at 25°C and 37°C, respectively. In contrast, minimal ethanol was observed in the yeast-poor fraction and NaF and 4°C conditions. Results: Such remarkable urine ethanol production (18 mg/dL/h 25°C, 32 mg/dL/h 37°C), supports positive labs secondary to bladder colonization by fermenting yeast. The organism was identified as candida glabrata, an opportunistic fungi related to “Brewer’s Yeast”, Saccharomyces cerevisiae.3 Discussion: The diagnosis of alcohol-related liver disease is being revisited with this patient’s transplant candidacy. We propose calling this phenomenon urinary auto-brewery syndrome, similar to but distinct from traditional auto-brewery syndrome, whereby alcohol is generated by gastrointestinal fermenters to produce positive plasma ethanol.4 In our case, alcohol is produced in the bladder and collection tube with greater production if specimen processing is delayed. Despite similar descriptions in the literature post-mortem and ex vivo2, we demonstrate proof-of-concept in a living patient. Conclusion/Implications: Since similar cases have possibly been misinterpreted as drinking, it is essential to promote correct interpretation of alcohol abstinence monitoring labs, especially when labs appear contradicting. There is also a need for standardized guidelines for alcohol abstinence monitoring. References: 1.) Hannuksela ML, Liisanantti MK, Nissinen AE, Savolainen MJ. Biochemical markers of alcoholism. Clin Chem Lab Med 2007;45:953-61. 2.) Gruszecki AC, Robinson CA, Kloda S, Brissie RM. High urine ethanol and negative blood and vitreous ethanol in a diabetic woman: a case report, retrospective case survey, and review of the literature. Am J Forensic Med Pathol 2005;26:96-8. 3.) Tam P, Gee K, Piechocinski M, Macreadie I. Candida glabrata, Friend and Foe. J Fungi (Basel) 2015;1:277-92. 4.) Logan BK, Jones AW. Endogenous ethanol 'auto-brewery syndrome' as a drunk-driving defence challenge. Med Sci Law 2000;40:206-15.