A previously healthy 3-year-old boy, with physical growth and psychomotor development normal for age, was referred to our institution due to severe anaemia. There was no family history of haematological… Click to show full abstract
A previously healthy 3-year-old boy, with physical growth and psychomotor development normal for age, was referred to our institution due to severe anaemia. There was no family history of haematological disorders. He presented with a history of progressive pallor and lethargy of a duration of 1 week. Two weeks before presentation, he suffered from febrile upper respiratory tract infection. There was no history of toxin exposure or acute blood loss. There was no previous complete blood count. Upon admission, he was pale, afebrile and tachycardic (138 bpm) with normal blood pressure and had a grade II/VI systolic flow murmur. No rash, lymphadenopathy or hepatosplenomegaly was noted, and his physical examination was otherwise unremarkable. A complete blood count demonstrated severe normocytic normochromic anaemia – haemoglobin (Hb) 3.6 g/dL, mean corpuscular volume (MCV) 77.9 fL, mean corpuscular haemoglobin 24.8 pg, with reticulocytopenia (28 300/mm). White blood cell (WBC) and platelet counts were normal (WBC 7520/mm, neutrophils 3400/ mm, lymphocytes 3360/mm and platelets 559 000/mm). The peripheral blood smear was non-specific. Direct antiglobulin test was negative, and the biochemical markers of haemolysis were absent (total bilirubin 0.34 mg/dL, lactate dehydrogenase 228 U/L and aspartate transaminase 25 U/L). Fetal Hb level (HbF) was normal (0.4%), and serum erythropoietin was increased up to 3250 U/L (<29 U/L). Serum ferritin value was normal (52 ng/mL). No laboratory evidence of occult blood loss in the stool was found. Serology for parvovirus B19, cytomegalovirus (CMV) and Epstein– Barr virus (EBV) showed no evidence of acute infection. He received a red blood cell transfusion on admission (day 1), increasing the Hb concentration to 6.4 g/dL on day 2. On day 4, absolute reticulocyte count increased significantly (245 000/ mm), with the improvement of Hb (7.1 g/dL). He was discharged on day 6 with Hb of 7.8 g/dL and reticulocyte count of 618 300/mm. Spontaneous recovery was observed 3 weeks later, with normalisation of haematological findings (Hb 12 g/dL, reticulocyte count 56 900/mm). One year later, he maintained stable haematological parameters. In this case, the findings of severe normocytic normochromic anaemia with low reticulocyte count for the degree of anaemia, otherwise normal blood count and no morphological abnormalities in peripheral blood smear, together with normal HbF, high erythropoietin and negative serology for parvovirus B19, in a child in the characteristic age range allowed the suggestion of a diagnosis of transient erythroblastopenia of childhood (TEC). Subsequent normalisation of haematological findings confirmed this diagnosis.
               
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