IgM and IgG Platelet Antibodies in a Case of Infectious Mononucleosis and Severe Thrombocytopenia

A 19-year-old male intercollegiate football player presented to the athletic training room with symptoms of sore throat, nasal congestion, fatigue, and bleeding, experienced for 3 weeks. His clinical and laboratory evaluation was consistent with infectious mononucleosis and severe thrombocytopenia. The athlete was immediately removed from participation and evaluated by a hematologist who confirmed the diagnosis and started oral glucocorticoid therapy. The athlete’s symptoms improved and thrombocytopenia resolved with therapy. Timely identification of severe thrombocytopenia allows for safe removal from participation. Collaboration among the sports medicine team as well as specialists, when needed, allows for optimal management of these rare complications.

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SEVERE THROMBOCYTOPENIA IN INFECTIOUS MONONUCLEOSIS

The American Journal of the Medical Sciences ◽

10.1097/00000441-196412000-00011 ◽

1964 ◽

Vol 248 (6) ◽

pp. 703-708 ◽

Cited By ~ 23

Author(s):

B. F. Clarke ◽

S. H. Davies

Keyword(s):

Infectious Mononucleosis ◽

Severe Thrombocytopenia

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Acute Immune-Mediated Thrombocytopenia due to Oxaliplatin and Irinotecan Therapy

Case Reports in Oncological Medicine ◽

10.1155/2019/4314797 ◽

2019 ◽

Vol 2019 ◽

pp. 1-5 ◽

Cited By ~ 1

Author(s):

Eric L. Tam ◽

Padma L. Draksharam ◽

Jennifer A. Park ◽

Gurinder S. Sidhu

Keyword(s):

Colon Cancer ◽

Flow Cytometry ◽

Severe Thrombocytopenia ◽

Flow Cytometry Assay ◽

Drug Induced ◽

Advanced Colon Cancer ◽

Platelet Antibodies ◽

Immune Mediated ◽

Drug Dependent ◽

Underlying Mechanisms

We describe a case of a 63-year-old woman with advanced colon cancer and liver metastases who was treated with fluorouracil, leucovorin, and oxaliplatin (FOLFOX) and cetuximab chemotherapy. She tolerated 13 cycles of chemotherapy without any significant hematological side effects, but after the 14th cycle, she developed melena and was admitted for severe thrombocytopenia. After supportive care, the platelet counts rapidly improved to 76,000/μL. Upon initiation of FOLFIRI and cetuximab chemotherapy, she again developed rectal bleeding and severe thrombocytopenia with a platelet count of 6000/μL. Lab testing was positive for oxaliplatin and irinotecan drug-dependent platelet antibodies on flow cytometry assay. Drug-induced thrombocytopenia (DITP) is associated with several classes of drugs with several proposed underlying mechanisms. Prospective studies are needed to further address different mechanisms of drug-induced thrombocytopenia.

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Megakaryocyte Abnormalities Occur In The Absence Of Cell-Mediated Immunity In a Murine Model Of Passive Immune Thrombocytopenia (ITP)

Blood ◽

10.1182/blood.v122.21.3537.3537 ◽

2013 ◽

Vol 122 (21) ◽

pp. 3537-3537

Author(s):

John W. Semple ◽

Kristin Hunt ◽

Yu Hou ◽

Rukhsana Aslam ◽

Edwin R. Speck ◽

...

Keyword(s):

Bone Marrow ◽

Immune Thrombocytopenia ◽

Conflicts Of Interest ◽

In Vivo Model ◽

Cell Mediated Immunity ◽

Severe Thrombocytopenia ◽

Platelet Destruction ◽

Platelet Counts ◽

Antiplatelet Antibodies ◽

Platelet Antibodies

Abstract Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by increased peripheral immune platelet destruction and megakaryocyte defects in the bone marrow. Although ITP was originally thought to be primarily due to humoral mediated autoimmunity it is now evident that T cells can also play a contributing role to the thrombocytopenia. In fact, the exact interplay between platelet destruction, megakaryocyte dysfunction, and the elements of both the humoral and cell mediated immune systems still remain incompletely defined. In murine passive models of ITP, the direct administration of anti-platelet antibodies can result in severe thrombocytopenia which is evident within 24 hours of injection. While most studies have focused on immune platelet destruction in the spleen, an additional possibility is that the anti-platelet antibody also has an effect on megakaryocytes. To unequivocally determine if antiplatelet antibodies have an effect on megakaryocytes in an in vivo model, BALB/c mice were intravenously administered 2 ug of an anti-GPIIbIIIa antibody (MReg30) or 50 uL of a high tittered anti-GPIIIa (anti-β3) serum from BALB/c GPIIIa (CD61) knockout mice immunized with wild type platelets. Platelet counts were assessed over time and the bone marrow and spleens were harvested for histological examination of megakaryocytes. Both preparations of antiplatelet antibodies significantly reduced platelet numbers within 1 day of antibody or serum administration. This thrombocytopenia could be rescued by administration of 2 g/kg of IVIg ip. Compared with naïve control mice, histological (H&E staining) examination of the bone marrow and spleens revealed that megakaryocytes were significantly increased in number and all exhibited abnormalities consistent with apoptosis e.g. pyknotic nuclei. IVIg administration completely prevented these megakaryocyte abnormalities. These results show that passively administered anti-platelet antibodies not only affect platelet counts but also significantly affect megakaryocyte physiology in the absence of cell mediated immunity. Disclosures: No relevant conflicts of interest to declare.

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Infectious Mononucleosis Sepsis with Severe Thrombocytopenia and ARDS.

Southern Medical Journal ◽

10.1097/00007611-200311001-00026 ◽

2003 ◽

Vol 96 (Supplement) ◽

pp. S13-S14

Author(s):

Antonio E. Muñiz

Keyword(s):

Infectious Mononucleosis ◽

Severe Thrombocytopenia

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Adalimumab-induced platelet antibodies resulting in severe thrombocytopenia

10.22541/au.161031083.39787297/v1 ◽

2021 ◽

Author(s):

Henk-Jan Boiten ◽

Sufia Amini ◽

Frank Wolfhagen ◽

Peter Westerweel

Keyword(s):

Crohn’S Disease ◽

Crohn's Disease ◽

Laboratory Tests ◽

Tumor Necrosis ◽

Bone Marrow Suppression ◽

Severe Thrombocytopenia ◽

Necrosis Factor Alpha ◽

Platelet Antibodies ◽

Factor Alpha ◽

Necrosis Factor

Anti-tumor necrosis factor alpha (TNFα) agents are effective in diseases including Crohn’s disease (CD) but may cause cytopenias. The mechanisms involved in anti-TNFα agents induced thrombocytopenia are scarce. We report a 73-year-old male with Crohn’s disease for which he currently used adalimumab, an anti-TNFα agent. He had received mesalazine and infliximab before the treatment of adalimumab. No comorbidities were present. Routine laboratory tests revealed a deep thrombocytopenia (thrombocytes 24x10*9/L) after which adalimumab was discontinued. Bleeding symptoms included cutaneous hematomas and mild epistaxis. Direct monoclonal antibody-specific immobilization of platelet antigens (MAIPA assay) revealed autoantibodies specific to glycoprotein IIb/IIIa (GPIIb/IIIa) and glycoprotein V (GPV) platelet receptors. There was no bone marrow suppression. Other causes of the thrombocytopenia were ruled out. The platelet count normalized after adalimumab discontinuation. No further interventions were required. Monitoring thrombocyte levels after initiating anti-TNFα agents is recommended, which could lead to prevention of this potential fatal phenomenon.

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Infectious Mononucleosis Presenting with Severe Thrombocytopenia, Positive Anti-Platelets Antibodies, and Peripheral Blood Blasts.

Blood ◽

10.1182/blood.v108.11.3976.3976 ◽

2006 ◽

Vol 108 (11) ◽

pp. 3976-3976

Author(s):

Rami Y. Haddad ◽

Rami S. Komrokji

Keyword(s):

Infectious Mononucleosis ◽

Peripheral Blood ◽

Normal Limit ◽

Cervical Lymphadenopathy ◽

Differential Count ◽

Severe Thrombocytopenia ◽

Peripheral Smear ◽

History Of ◽

Immature Myeloid Cells ◽

Reactive Lymphocytes

Abstract Case Report: 18 year old male presents with 2 weeks history of sore throat, fever, and hemoptysis. Physical examination revealed exudative and hemorrhagic tonsillo-pharyngitis, posterior cervical lymphadenopathy, mild splenomegaly, and petechieal rash involving the extremeties and the trunk. On presentation, CBC showed Hgb of 15.5gm/dl, WBCs of 11.8 K/uL, Platelets count of 4 K/uL. Differential count showed lymphocytes of 56%, reactive lymphocytes 1%. Monospot test was positive. CT abdomen confirmed the physical finding of splenomegaly, and showed mild hepatomegaly. Treatment was initiated with pulse methylprednisone 1g/d, and IVIG 1g/kg/day. Both were given for 2 days. One unit of SDP was transfused on days 2, 4, 5. On day 4 platelets count was 6 K/uL. 2–3% blasts were detected on the peripheral smear on days 4 and 5. Bone marrow biopsy and aspiration were done on day 5. They revealed reactive marrow changes with no increase in blasts. Flow cytometry revealed reactive marrow lymphocyte subpopulations and no inrease in immature myeloid cells. Subsequently, EBV serology was reported; EBV capsid IgM and IgG were both positive at >4-fold higher than upper normal limit. In addition, Platelets antibodies were reported positive for IIB/IIIA, IB/IX, and IA/IIA. Platelets count on day 7 was 58 K/uL without platelets transfusion in the previous 24 hours. Conclusion: Literature review reveals rare cases of Infectious Mononucleosis presenting with severe thrombocytopenia. Most of these cases were treated successfully with steroids and /or IVIG, similarly to ITP. However, no previous association with peripheral blood blasts has been described. Moreover, only two previous reports have described the association between Infectious Mononucleosis and the presence of platelets antibodies but without details of the receptors involved.

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