P6052 - HSV-1 in the Setting of a Suspected Systemic Lupus Erythematosus Flare as a Cause of Acute Liver Failure and Acute Decompensation

Daniel Bujnowski, MD¹, Omar Martinez-Uribe, MD², Amanda Broderick, MD², Matthew Kappus, MD³
1Duke University Health System, Durham, NC; 2Duke University Medical Center, Durham, NC; 3Division of Gastroenterology, Duke University School of Medicine, Durham, NC

Introduction: HSV-1 infection in immunocompromised individuals can disseminate to systemic illness and progress to hepatitis and acute liver failure. The most common sign of HSV-1 activation is a vesicular mucocutaneous eruption, often in the buccal mucosa and genitals with up to 70% of HSV-1 hepatitis cases presenting with mucocutaneous involvement. Here, we describe the first case of HSV-1 without any mucocutaneous involvement in a patient with systemic lupus erythematosus (SLE) leading to acute liver failure and decompensation.

Case Description/

Methods: The patient is a 22-year-old male with a history of SLE complicated by stage 4 lupus nephritis who presented to a neighboring hospital with two days of nausea and vomiting. During the ensuing 3 days, he was treated with pulse dose steroids, broad-spectrum antibiotics, and his home immunosuppression regimen for treatment of a suspected lupus flare and sepsis of unknown origin. During this time, he developed an acute liver and kidney injury. He pursued a patient-directed discharge and presented to our tertiary care center. The patient’s vital signs were T: 103.6°F, BP: 144/92 mmHg, HR: 120 BPM, RR: 16 BPM, and O2 sat: 100% on admission. Laboratory data revealed a negative toxicology screen, normal acetaminophen and salicylate levels, creatinine of 3.5 mg/dL, WBC count of 13.2 cells/µL with neutrophilic predominance, c-reactive protein of 0.7 mg/L, prothrombin INR of 1.7, ALT of 2,138 U/L, and AST of 2,352 U/L. Empiric treatment for cytomegalovirus and HSV hepatitis was started with ganciclovir. Overnight, he developed acute encephalopathy, lactic acidosis, and worsening synthetic dysfunction which rapidly progressed to intubation. Despite aggressive resuscitation, empiric N-acetylcysteine, bicarbonate infusions, and calcium stabilization, he developed pulseless electrical activity arrest. ACLS was performed, and ROSC was achieved. Over the next hour, the patient’s respiratory acidosis and electrolyte derangements worsened, despite continuous renal replacement therapy, and pulseless electrical activity recurred this time without successful resuscitation.

Discussion: One day after death, serum culture data returned positive for HSV-1, with a concentration greater than 1 x 10^⁸ copies per milliliter. Bacterial and fungal blood cultures, hepatitis panel, and cytomegalovirus labs ultimately all returned negative. This case highlights the swift progression of disseminated HSV-1 without mucocutaneous findings, causing frank liver failure and multiorgan failure.

Disclosures:
Daniel Bujnowski indicated no relevant financial relationships.
Omar Martinez-Uribe indicated no relevant financial relationships.
Amanda Broderick indicated no relevant financial relationships.
Matthew Kappus indicated no relevant financial relationships.

Daniel Bujnowski, MD¹, Omar Martinez-Uribe, MD², Amanda Broderick, MD², Matthew Kappus, MD³. P6052 - HSV-1 in the Setting of a Suspected Systemic Lupus Erythematosus Flare as a Cause of Acute Liver Failure and Acute Decompensation, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.