S5862 HSV-1 in the Setting of a Suspected Systemic Lupus Erythematosus Flare as a Cause of Acute Liver Failure and Acute Decompensation

Introduction: Herpes simplex virus-1 (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: A 22-year-old man with a history of SLE complicated by stage 4 lupus nephritis presented to a neighboring hospital with 2 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, white blood cell count of 13.2 cells/µL with neutrophilic predominance, c-reactive protein of 0.7 mg/L, prothrombin international normalized ratio of 1.7, alanine aminotransferase of 2,138 U/L, and aspartate aminotransferase 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. Advanced Cardiac Life Support was performed, and return of spontaneous circulation 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 × 108 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.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150908.67998.b1
Primary Topic
Cytomegalovirus and herpesvirus research
Type
article
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article

S5862 HSV-1 in the Setting of a Suspected Systemic Lupus Erythematosus Flare as a Cause of Acute Liver Failure and Acute Decompensation

The American Journal of Gastroenterology
Cytomegalovirus and herpesvirus research
article

S5862 HSV-1 in the Setting of a Suspected Systemic Lupus Erythematosus Flare as a Cause of Acute Liver Failure and Acute Decompensation

article en

Abstract

Introduction: Herpes simplex virus-1 (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: A 22-year-old man with a history of SLE complicated by stage 4 lupus nephritis presented to a neighboring hospital with 2 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, white blood cell count of 13.2 cells/µL with neutrophilic predominance, c-reactive protein of 0.7 mg/L, prothrombin international normalized ratio of 1.7, alanine aminotransferase of 2,138 U/L, and aspartate aminotransferase 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. Advanced Cardiac Life Support was performed, and return of spontaneous circulation 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 × 108 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.

The American Journal of GastroenterologyVol. 120(10S2)
Good health and well-being
Openalex Percentile: Top 32%
Cytomegalovirus and herpesvirus research
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