Trombocitopenie imună secundară la un pacient pediatric prezentând coinfecţie virală – prezentare de caz

Introduction

Immune thrombocytopenia (ITP) is defined as an acquired thrombocytopenia with antibodies detected against platelet surface antigens, being the most common form of thrombocytopenia in otherwise asymptomatic children. Secondary thrombocytopenia caused by cytomegalovirus (CMV) is common, CMV being one of the major infectious etiologies that induce a variety of hematological changes (hemolytic anemia, neutropenia, lymphopenia and thrombocytopenia)⁽¹⁾.

Case report

We report the case of a 5-year-old boy admitted to our hospital for petechiae, ecchymoses and a few short episodes of epistaxis accompanied by symptoms of acute upper respiratory tract infection (nasal congestion and productive cough). Both the family medical history and the patient’s history were unremarkable. The physical examination revealed a relatively good general appearance, with normal weight, disseminated petechiae, ecchymoses on the left arm and chest, bilateral cervical lymphadenopathy, congested pharynx with petechiae on the soft palate; the liver was palpable 3 cm below the right costal border, without splenomegaly, and with no signs of active bleeding.

The laboratory investigations revealed a mild normocytic normochromic anemia (Hb=10.8 mg/dl), normal white blood cell count and severe thrombocytopenia (7000/microL); the additional tests revealed a mild hepatic cytolysis (with both AST and ALT of 54 U/L), and a positive antigen test for respiratory syncytial virus – RSV (that would account for the respiratory tract infection symptoms). Based on the presence of macrothrombocytes on the peripheral blood smear and the reticulocytosis, we excluded a possible impaired medullary hematopoiesis. The absence of schistocytes, normal bilirubin, urea and creatinine levels ruled out the possibility of a non-immune peripheral destruction (disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome). Most viral screens we did were negative (influenzae virus, human immunodeficiency virus, Ebstein-Barr virus, hepatitis B and C viruses) with the exception of cytomegalovirus (positive IgM and IgG), thus we established the final diagnosis: CMV-related immune thrombocytopenia.

We started the patient on a five-day course of dexamethasone (0.6 mg/kg/day) during which the platelet number increased progressively (from 7000/microL to 155,000/microL). A month after discharge, the platelet number was 298,000/microL, and no other signs of bleeding appeared.

Discussion

Acute respiratory infections are a major cause of hospital admission in young children, and in most cases, viruses are the etiological agents involved. Up until recently, infection by two or more viral agents concomitantly was considered a rare event. However, the latest studies show that there is a much higher prevalence of viral respiratory coinfections, ranging from 10% to 30% in pediatric patients⁽²⁾. At the moment, it is not very clear whether the outcome of the children with coinfections is worse than that of the children with one etiology. A 2016 meta-analysis concluded that the risk of fever and intensive care unit admission increased in children with coinfections but remained nonsignificant, thus further investigations by pathogen pairs are warranted⁽³⁾.

Thrombocytopenia, which signifies a platelet count below 150,000/microL, is a common finding following or during many viral infections. This phenomenon is clas­si­cally attributed to platelet consumption due to in­flam­mation-induced coagulation, impaired platelet production due to defective megakaryopoiesis or cyto­kine-induced myelosuppression and, in some cases, antibody-mediated destruction (secondary immune thrombocytopenia). Interestingly though, thrombocytosis rather than thrombocytopenia appears to be a common phenomenon found during acute RSV disease, in contrast to most respiratory infections⁽⁴⁾. Typically, the cytomegalovirus leads to a low platelet count either by directly infecting the megakaryocytes and interfering with the platelet production, or by splenic destruction of antibody-covered platelets⁽⁵⁾. In our case, the fact that the bone marrow showed signs of increased function, we concluded that the mechanism responsible for the thrombocytopenia was a peripheral one. Also, the patient was minimally symptomatic respiratory wise, and in the absence of the hemorrhagic stigmata, the two etiologies may have never been determined. So, we raise the following question: did the presence of both viral agents lead to the development of the hematological complication, or was it just a mere coincidence?

Conclusions

Thrombocytopenia is a common hematological finding in CMV infection in children. Most cases resolve without treatment⁽⁶⁾, but certain laboratory or clinical findings demand the initiation of treatment⁽⁷⁾. We presented the case of a 5-year-old boy with CMV-related immune thrombocytopenia, with 7000 platelets/microL, who responded favorably and quickly to a short course of corticosteroids.

Autor corespondent: Eugenia Buzoianu E-mail: eugenia.buzoianu@yahoo.com

CONFLICT OF INTEREST: none declared.

FINANCIAL SUPPORT: none declared.

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