Epstein Barr virus causes megaloblastic anemia (methylation related)

gbells

Improved ME from 2 to 6
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I was troublesheeting a high MCV on CBC labs and learned that Epstein Barr virus causes it (megaloblastic anemia). It is a deficiency of activated folic acid and activated B12. I am heterozygous for MTHFR deficiency but never had a problem with it before EBV infection in 2008. Post infection I have slightly abnormal MCV on CBC labs for years. I found this report of it from 2006 but it has not been integrated into the medical guidelines for EBV. People concerned about methylation need to be aware that if they have MTHFR deficiency they MUST use activated folate and activated B12 for this or it will not work.

Was the viral syndrome causally related to the megaloblastic anemia or was a preexisting megaloblastic anemia being brought to the attention of the clinician by the acute viral syndrome? This puzzling question was solved when a patient who had a normal complete blood count in March 2005 at our institute, developed severe pancytopenia after a febrile illness in October 2005. Another patient in the series had normal hemoglobin and had actually donated a unit of blood one month prior to his admission with diarrhea and severe pancytopenia.

The next question that we faced was regarding the identity of the virus. We initially performed a lymphadenitis panel (Euro Immune) consisting of 16 common viral markers. Epstein Barr virus (EBV) was positive in the initial case. An EBV Immunofluorescence panel (Euro Immune) was done in all the subsequent patients. This test was positive in 6 out of the10 patients, they were positive for EBV Capsid IgG, EBV Capsid IgM, and EBV early antigen Ig G (acute infection markers). EBV nuclear antigen IG G (chronic infection marker) was negative.

It should be noted that none of the patients had neurological deficits despite having diagnostically low cobalamine levels and this we presume is due to the acute onset of illness not allowing enough time for the development of neurological symptoms. There were quite a few patients seen in this period of time with typical EBV infection without any megaloblastic changes and similarly there were patients with overt megaloblastic anemia without any features of EBV infection. Hence there must be a patient specific characteristic that predisposes them to acute megaloblastic anemia on developing the viral infection. Since only two of these ten patients are pure vegans and since none were malnourished we have to look for a non nutritional cause for this predisposition. An acute coombs negative hemolytic anemia due to the viral infection can explain the cytpenias but the low B12 levels and the prompt response to B12 supplementation are unexplained.

We feel that this is a new syndrome of reversible viral induced acute onset megaloblastic anemia. There exists a possibility that this is a new strain of EBV virus, and we have stored the sera of all the patients for future epidemiological purposes. We are recommending that physicians should consider B12/folate supplementation in acute EBV syndromes and obtain follow-up CBC one month after the illness. We believe that further work has to be done before a definite association between EBV and megaloblastic anemia can be established.
(Suresh Nukala, C.R.R.M. Reddy, P. Shrikant, Jhansi Vani, Shanti Naidu, Sarat Talluri, K. Vijaya; Viral Infection Induced Acute Megaloblastic Anemia: A Case Series.. Blood 2006; 108 (11): 3757. doi: https://doi.org/10.1182/blood.V108.11.3757.3757 )