S4556 Monster Burn: Severe Gastritis Following Acute Mononucleosis in the Setting of Excess Energy Drink Consumption

Introduction: While milder GI symptoms have been independently reported with both infectious mononucleosis (IM) and excessive energy drink consumption, the following is a rare case of severe, biopsy-confirmed gastritis temporally linked to excess energy drink intake, following a recent diagnosis of IM. Case Description/Methods: Twenty-three-year-old man presented with a few weeks onset of emesis, abdominal discomfort. Upon admission, labs are significant for elevated liver function tests, hypocalcemia, severely low vitamin D level, elevated PTH, and hypoalbuminemia. He was also diagnosed with Epstein Barr virus (EBV)+ IM (positive Monospot test and significantly elevated EBV VCA IgG levels). Computed tomography abdomen/pelvis, magnetic resonance cholangiopancreatography were unrevealing. Esophagogastroduodenoscopy (EGD) found severe esophagitis and gastroduodenitis with erosion of many portions of the gastric body lumen. Biopsies confirmed marked reflux-associated changes in esophagus; atypical gastric mucosa with acute erosive changes, focal lamina propria changes suggestive of healing ulcer; acute on chronic erosive duodenitis. No H. pylori. The patient denied alcohol, nonsteroidal anti-inflammatory drugs, smoking, & other illicit drug use. On further laboratory work up: B12, gastrin, HIV, GPC Ab- IgG, LKM-1 Ab IgG, ceruloplasmin, VIP, all other viral/bacterial polymerase chain reactions were normal or negative. The only notable history was the patient's chronic energy drink intake of ∼5 drinks per day. The patient was prescribed proton pump inhibitors and advised energy drink cessation, with plans to repeat EGD with Sydney Protocol. At 4-week follow-up, GI symptoms had resolved, liver function tests normalized. Discussion: The lab findings alone point toward chronic malabsorption, rather than an isolated acute EBV infection. The acute-on-chronic histologic changes on biopsy suggest that the combination of preexisting inflammation—worsened by a systemic viral illness—and repeated irritation from ongoing stimulant consumption likely exacerbated the severity of the gastritis. Energy drinks, which contain high levels of caffeine, taurine, citric acid, are known to stimulate gastric acid secretion, delay emptying, and disrupt mucosa. Atypia on biopsy without lymphocytic infiltration reflects chemical irritation rather than viral effect and posits that stimulant exposure was the primary driver of the clinical presentation. This case highlights the diagnostic challenge of distinguishing between viral and chemically induced gastric injury. It also underscores a shift- to rank energy drink toxicity higher among differentials for severe gastritis—particularly in younger patients, among whom ∼60% may consume energy drinks daily.