Abstract: TH-PO636
Labetalol or Amphetamine? : That Is the Question
Session Information
- Fellows/Residents Case Reports: Genetic Diseases, Pregnancy, Monoclonal Gammopathy
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Mitra, Shimontini, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
- Agrawal, Nikhil, Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
Background
Uncontrolled hypertension is a frequent cause of hospitalizations. Evaluation for causes of accelerated hypertension includes urine analysis for ingested substances like amphetamine. Interpretation of urine amphetamine testing becomes difficult when patients are administered high doses of labetalol. Understanding the chemical structures of amphetamines and their breakdown products can help distinguish true amphetamine use from labetalol effect. In this case, mass spectroscopy proved helpful in interpreting a positive urine amphetamine test.
Methods
A forty-two year old male with ESRD and Type I Diabetes status post pancreas and kidney transplant in October 2015 and hypertension presented with elevated blood pressures and acute kidney injury. The patient was noted to have uncontrolled blood pressures for the past month. His blood pressure on admission was 211/113 and throughout most of his stay ranged 160-190/90-110mm Hg. His admission physical exam was notable for a chronic systolic murmur, no abdominal or carotid bruits, non-tenderness over kidney and pancreatic graft sites, no papilledema, and no edema. His admission creatinine was 1.8 mg/dL from a baseline of 1.4 mg/dL. Cardiac enzymes and EKG were unrevealing. His blood pressure regimen in-house consisted of labetalol 800mg TID, hydralazine 75mg QID and clonidine patch 0.3mg QD. A urine toxicology screen was also performed which returned positive for amphetamine. The patient denied the use of illicit substances prompting further analysis. Mass spectroscopy of the sample was negative for amphetamine but demonstrated a breakdown compound of labetalol, 3-amino-1-phenylbutane (APB). His blood pressures were eventually controlled with the addition of isosorbide mononitrate 120mg QD and furosemide 40mg QD orally. His creatinine returned back to baseline and patient was discharged.
Conclusion
Labetalol breaks down into multiple compounds. One of these metabolites is APB. Urine amphetamine assays work by competitive inhibition between glucose-6-phosphate dehydrogenase (G6PDH)-labeled amphetamine and urinary amphetamine for a fixed number of reagent antibody binding sites. APB is structurally similar to amphetamine and can bind to reagent antibody in this assay resulting in false positivity. Therefore, for patients with uncontrolled hypertension who are also on high doses of labetalol, mass spectroscopy is a means of correctly interpreting a positive test.