Infectious Mononucleosis Causing Acute Liver Failure and Hemolytic Anemia in a Patient with Underlying Hereditary Hemochromatosis

Infectious mononucleosis is a largely benign disease process that occurs secondary to infection with the Epstein-Barr virus. However, it can also present with more serious complications, including auto-immune hemolytic anemia and acute liver failure. Hereditary hemochromatosis is a genetic disorder that leads to organ damage via increased iron uptake and deposition. This case report describes a 25-year-old man who presented with acute liver failure and severe hemolytic anemia. Workup revealed that not only did he have a rare presentation of Epstein-Barr virus-induced acute liver failure and C<sub>3</sub>-positive IgG-negative hemolytic anemia, he also had previously undiagnosed hereditary hemochromatosis. This combined presentation of these pathologies presents a unique opportunity to study their interaction and possible synergistic pathophysiology. Furthermore, the evolving understanding of the disease mechanisms behind these disease processes is described.

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A RARE CASE OF HETEROPHILE NEGATIVE EBV VCA IGM POSITIVE INFECTIOUS MONONUCLEOSIS COMPLICATED BY COLD AUTOIMMUNE HEMOLYTIC ANEMIA

10.36106/ijar/1301109 ◽

2021 ◽

pp. 26-27

Author(s):

Tony K S ◽

Rakhee joshi ◽

Alok Parekh ◽

Saurabh Atey ◽

Payal Tayade

Keyword(s):

Hemolytic Anemia ◽

Infectious Mononucleosis ◽

Autoimmune Hemolytic Anemia ◽

Rare Case ◽

Epstein Barr Virus ◽

Viral Capsid Antigen ◽

Barr Virus ◽

Symptomatic Management ◽

Biliary Stasis ◽

Epstein Barr

Infectious mononucleosis (IM) is often an uncomplicated self-limited illness resulting from Epstein-Barr virus (EBV) in 90% cases. This is a case report of 21-year-old female whose initial clinical and laboratory presentation suggested Heterophile antibody negative Epstein–Barr Viral capsid Antigen (VCA) IgM positive infectious Mononucleosis. Our case was complicated by biliary stasis, cold autoimmune hemolytic anemia with acrocyanosis, thrombocytopenia and some of the features of hemophagocytic lymphohistiocytosis (HLH). Following symptomatic management patient recovered. Physicians should routinely counsel their patients with IM for these complications and should avoid overzealous treatment

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Acute Liver Failure with Hepatitis E and Epstein-Barr Virus Coinfection

The American Journal of Gastroenterology ◽

10.14309/00000434-201310001-01075 ◽

2013 ◽

Vol 108 ◽

pp. S320-S321

Author(s):

Joshua Peck ◽

Lana Alghothani ◽

Steven Campbell ◽

John Davis ◽

James Hanje

Keyword(s):

Liver Failure ◽

Acute Liver Failure ◽

Epstein Barr Virus ◽

Hepatitis E ◽

Barr Virus ◽

Epstein Barr

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SH2D1A mutations in Japanese males with severe Epstein-Barr virus–associated illnesses

Blood ◽

10.1182/blood.v98.4.1268 ◽

2001 ◽

Vol 98 (4) ◽

pp. 1268-1270 ◽

Cited By ~ 35

Author(s):

Ryo Sumazaki ◽

Hirokazu Kanegane ◽

Maki Osaki ◽

Takashi Fukushima ◽

Masahiro Tsuchida ◽

...

Keyword(s):

Genetic Analysis ◽

Infectious Mononucleosis ◽

Epstein Barr Virus ◽

Genetic Disorder ◽

Lymphoproliferative Disease ◽

Barr Virus ◽

Ebv Infection ◽

Sporadic Cases ◽

Epstein Barr ◽

Acute Infectious Mononucleosis

X-linked lymphoproliferative disease (XLP), a genetic disorder characterized by immunodeficiency to Epstein-Barr virus (EBV) infection, has been linked to mutations in the SH2D1A gene. To search for the occurrence of SH2D1A mutations in Japan, we performed genetic analysis of the SH2D1A gene in 40 males presenting with severe EBV-associated illnesses, including fulminant infectious mononucleosis, EBV-positive lymphoma, and severe chronic active EBV infection. SH2D1A mutations were detected in 10 of these 40 patients. Five of these 10 cases were sporadic. Patients with SH2D1A mutations displayed severe acute infectious mononucleosis with hyperimmunoglobulin M, hypogammaglobulinemia, and B-cell malignant lymphoma. By contrast, chronic active EBV infection was not associated with SH2D1Amutations. XLP survivors exhibited normal levels of circulating EBV-DNA during convalescence, suggesting that SH2D1A protein is not directly responsible for control of EBV replication. Thus, genetic analysis of the SH2D1A gene is particularly useful in the diagnosis of sporadic cases and carriers of XLP.

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Ceftriaxone-Induced Immune Hemolytic Anemia: In Vitro Reversal with Peptide Inhibitor of Complement C1 (PIC1)

Case Reports in Hematology ◽

10.1155/2019/4105653 ◽

2019 ◽

Vol 2019 ◽

pp. 1-3 ◽

Cited By ~ 1

Author(s):

Kenji M. Cunnion ◽

Lisa M. Feagin ◽

Michael F. Chicella ◽

Cortney L. Kaszowski ◽

Pamela S. Hair ◽

...

Keyword(s):

Hemolytic Anemia ◽

Epstein Barr Virus ◽

Virus Disease ◽

Peptide Inhibitor ◽

Classical Complement Pathway ◽

Barr Virus ◽

Immune Hemolytic Anemia ◽

Epstein Barr ◽

Classical Complement

We report a case of ceftriaxone-induced immune hemolytic anemia in a 10-year-old with chronic active Epstein–Barr virus disease and hemophagocytic lymphohistiocytosis. After chemotherapy, she became febrile and received ceftriaxone. She rapidly developed respiratory failure and anemia. Her direct antiglobulin test was positive for IgG and C3. To confirm this was ceftriaxone-induced complement-mediated hemolysis, we adapted the complement hemolysis using human erythrocytes (CHUHE) assay by adding exogenous ceftriaxone to the patient’s serum which enhanced lysis of her erythrocytes. We confirmed that ceftriaxone initiated a classical complement pathway-mediated hemolysis by in vitro reversal with peptide inhibitor of complement C1 (PIC1).

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