ORAL PRESENTATIONS – STUDENTS
WHAT THE BRASH? David Nguyen 1 , Hina Qureshi MD 2 , Michael Olejniczak MD 2 , Ross McCarron MD 2 ; School of Medicine 1 , Department of Medicine 2 , LSU Health New Orleans, New Orleans, LA
Introduction: BRASH syndrome, an underreported condition characterized by bradycardia, renal failure, shock, and hyperkalemia, typically emerges from the chronic use of atrioventricular (AV) nodal blocking agents, particularly affecting elderly individuals with compromised renal function. Despite its clinical significance, BRASH remains inadequately understood. The pathophysiology involves an intricate interplay among AV nodal- blocking agents, resulting in bradycardia, diminished cardiac output, inadequate renal perfusion, kidney damage, and hyperkalemia. This case report presents an instance of BRASH syndrome, shedding light on its clinical manifestation, management, and the importance of timely intervention. Case: A 74-year-old man with a myriad of comorbidities presented with complaints of fatigue, diarrhea, and myalgias over the past 24 hours. His medical history included emphysema, hypertension, irritable bowel syndrome, gastroesophageal reflux disease, and heart failure. Notably, he was on a complex medication regimen, including recently supplemented potassium and Aldactone, along with other medications. Vital signs on admission revealed bradycardia (46 bpm), hypertension, and hyperkalemia (6.9 mmol/L). The diagnosis of BRASH syndrome was swiftly made, prompting
immediate management in the ED, including calcium gluconate, nebulized albuterol, and sodium citrate. During hospitalization, AV nodal blocking agents (Lotrel, Metoprolol, and Aldactone) were discontinued. Targeted interventions successfully addressed hyperkalemia, including insulin, dextrose, Lasix, sodium citrate, and sodium zirconium cyclosilicate. Over four days, the patient's heart rate stabilized, and renal function improved,
culminating in discharge with normalized potassium levels and reduced creatinine.
Discussion: The epidemiology and pathophysiology of BRASH syndrome remain elusive, despite its clinical significance. Originating from the mid-20th- century introduction of AV nodal blocking agents, this condition is marked by bradycardia-induced reduced cardiac output, leading to inadequate renal perfusion, acute kidney injury (AKI), and hyperkalemia. Essential in the therapeutic approach is the discontinuation of AV nodal blocking agents. Our case underscores the necessity of considering BRASH in patients with bradycardia, renal failure, and a history of AV nodal blocking agent use. Timely intervention, involving medication discontinuation and targeted management, is pivotal for a favorable outcome, preventing long- term complications associated with this syndrome.
ADENOSINE ANALOGS HAVE A DUAL IMMUNOMODULATORY AND ANTIVIRAL FUNCTION AND ARE POTENTIAL THERAPEUTIC AGENTS AGAINST SARS-COV-2 Brionna King, Giulia Monticone, Ph.D.; LSU Health Sciences Center School of Medicine; New Orleans, LA.
Introduction: SARS-CoV-2 is a contagious virus that causes COVID-19, a disease that has affected millions of people worldwide and claimed over six million lives. The pandemic has unveiled an urgent need for new antivirals to control emerging infectious diseases and potential future pandemics. Classic antivirals are currently designed to directly interfere with pathogens. However, antivirals are often insufficient to rapidly clear infections in the absence of an effective immune response. Immunotherapy could complement the use of antivirals; however, its application to infectious diseases remains
largely unexplored. Adenosine analogs are antiviral drugs that resemble the structure of adenosine, a metabolite that derives from the breakdown of ATP and can suppress the immune response through activation of the Adenosine A2A Receptor (A2AR) in immune cells. Adenosine is overproduced in some infectious diseases, like COVID-19, where it restricts protective antiviral immune responses. Previous work from our lab showed that adenosine-mediated activation of A2AR causes suppression of CD8+ T-cells effector functions in COVID-19 mouse models. Importantly, our group showed that adenosine 47
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