Pseudothrombocytopenia in Case of Acute Viral Hepatitis A

Pseudothrombocytopenia is a laboratory-based iatrogenic phenomenon. Pseudothrombocytopenia is not important in terms of bleeding and does not require transfusion of thrombocytopenia. If not identified at the early stages, pseudothrombocytopenia can lead to patients undergoing unnecessary investigations and overtreatment. Here we present a childhood case of pseudothrombocytopenia caused by hepatitis A virus (HAV) infection. A 9-year-old male was referred to our department for thrombocytopenia (thrombocyte count 70x109/L). The liver was palpable 3-4 cm below the costal margin. Leukocyte count was 6.52x109/L, hemoglobin 14.7 g/L, hematocrit 46.6%, thrombocyte count 58x109/L. Aspartate transaminase 79.8 U/L, alanine transaminase 116.9 U/L, gamma-glutamyl transferase 156 U/L, alkaline phosphatase 1114 U/L, total bilirubin 0.98 mg/dL, and direct bilirubin 0.6 mg/dL. Other biochemistry values were normal. Anti HAV immunoglobulin M and immunoglobulin G were positive. The patient was diagnosed with hepatitis A. A peripheral smear revealed many thrombocyte clusters composed of 10-20 cells. HAV infection was thought to be the reason for pseudothrombocytopenia. The pseudocytopenia started to recover as the HAV infection got better and the thrombocyte count increased to over 150x109/L at the end of a year. Peripheral smear evaluation is critical for accurate detection of thrombocytopenia and should be considered the initial step in cases with a familial or medical history of thrombocytopenia.

Akut Hepatit A Virüs Enfeksiyonu Olgusunda Psödotrombositopeni

Psödotrombositopeni iyatrojenik bir laboratuvar fenomendir. Psödotrombositopeni kanama bakımından (riski) önemli değildir ve trombosit verilmesini gerektirmez. Bu fenomenin erken evrede tanınmaması, hastaların gereksiz tetkiklere ve gereksiz tedavilere maruz kalmasına neden olmaktadır. Biz burada, hepatit A virüs (HAV) enfeksiyonunun neden olduğu psödotrombositopenili bir çocuk olgusu sunuyoruz. Dokuz yaşındaki erkek hasta, trombositopeni (trombosit 70x109/L) nedeni ile bölümümüze yollandı. Karaciğer kot altında 3-4 cm ele geliyordu. Hastada, lökosit 6,52x109/L, hemoglobin 147 g/L, hematokrit %46,6, trombosit 58x109/L. Aspartat aminotransferaz 79,8 U/L, alanin aminotransferaz 116,9 U/L, gama-glutamil transferaz 156 U/L, alkalen fosfataz 1114 U/L, total bilirubin 0,98 mg/dL, direkt bilirubin 0,6 mg/dL ve diğer biyokimya değerleri normal idi. Anti HAV immünoglobulin M ve immünoglobulin G pozitif bulundu. Hepatit A kabul edilen hastanın periferik yaymasında çok sayıda 10-20’li trombosit kümeleri görüldü. Pseudotrombositopeni nedeninin HAV enfeksiyonu olduğu düşünüldü. Nitekim HAV enfeksiyonu geriledikçe, psödotrombositopeni de düzelmeye başladı ve trombosit sayısı, bir yılın sonunda 150x109/L’nin üzerine çıktı. Tıbbi ve aile öyküsünde trombositopeni olan olgularda periferik yayma değerlendirilmesi çok önemlidir ve ilk adım olmalıdır.

Kaynakça

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