An infant with refractory cytomegalovirus‐induced thrombocyt
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Most cases of cytomegalovirus (CMV) infection are asymptomatic or self‐limited in immunocompetent patients. However, CMV infection occasionally induces severe thrombocytopenia.1-6 Immune thrombocytopenia (ITP) is an autoimmune disease characterized by isolated thrombocytopenia due to the inhibition of platelet production and the destruction of existing platelets.1 Moreover, it is the most common cause of pediatric thrombocytopenia.

A 38‐day‐old boy was admitted to hospital because of the presence of petechiae from trunk to legs and oral wet purpura. His mother was a 35‐year‐old woman her pregnancy course was uncomplicated, and her platelet count was also normal during pregnancy. There were no hemorrhagic episodes during the perinatal period of the boy, and he was born at full term via aspiration delivery. His weight at birth was 3304 g. At admission, he was afebrile with a blood pressure of 98/60 mm Hg, the pulse of 142/min, respiratory rate of 36/min, and O2 saturation of 100% on room air. He had neither hepatomegaly nor splenomegaly.

A laboratory examination showed a white blood cell count of 23 600/µL with 11.0% atypical lymphocytes, CD4‐positive cell count of 1044/µL, a hemoglobin level of 11.9 g/dL, and platelet count of 4000/µL. The aspartate aminotransferase and alanine aminotransferase levels were 59 IU/L and 55 IU/L, respectively. Immunoglobulin G (IgG), IgA, and IgM were 773, 21, and 50 mg/dL, respectively.

Platelet transfusion was performed after admission because ITP was not suspected due to his age. However, his platelet count was only 12 000/µL after platelet transfusion. IVIG (1 g/kg) was subsequently administered because of the refractoriness to transfusion, which was suspected to be due to ITP. Despite IVIG administration, his platelet count decreased to 2000/µL. Although another platelet transfusion was performed, his platelet count increased only to 9000/µL. A subsequent bone marrow examination showed a nuclear cell count of 105 000/µL without morphologically abnormal cells and megakaryocyte count of 8/µL. After the exclusion of malignant diseases, prednisolone (PSL; 1 mg/kg) was administered as second‐line therapy for ITP with another platelet transfusion. After the initiation of PSL therapy, his platelet count increased to 31 000/µL, but decreased to 18 000/µL after 2 days. CMV infection was diagnosed based on the presence of CMV IgM and IgG, and the results of a CMV antigenemia assay using monoclonal antibodies C10/C11 at admission. IVIG were re‐administered, and PSL dose was increased to 2 mg/kg.

Thereafter, his platelet count gradually normalized. Thrombocytopenia has not recurred after the discontinuation of PSL. The patient has been normal development, without recurrence, for more than 6 months after onset. Using quantitative PCR analysis, CMV‐DNA was detected in his urine after treatment but not in his dried umbilical cord. Based on these results, thrombocytopenia was associated with acquired CMV infection. Auditory brainstem responses revealed normal waves from I to V at 90 dB and V wave was detected at 30dB. These clinical findings indicate that the patient was infected with CMV after birth, excluding a congenitally acquired infection.

In conclusion, CMV should be evaluated in suspected cases of refractory thrombocytopenia because CMV infection occasionally induces severe and refractory thrombocytopenia, requiring antiviral therapy