Acute Hepatitis-A Infection Induced Anemia in Concurrence of Glucose-6-Phosphate Dehydrogenase Deficiency and Thalassemia Trait: A Case Report

Glukoz-6-Fosfat Dehidrogenaz Eksikliği ve Talasemi Ta?ıyıcılığı Birlikteliğinde, Akut Hepatit-A Enfeksiyonunun Tetiklediği Anemi: Bir Olgu Sunumu

Özet

Talasemi ve glukoz-6-fosfat dehidrogenaz (G6PD) eksikliği hemolitik anemiye neden olan genetik bozukluklardır. Her iki hematolojik bozukluğun yüksek sıklıkta görüldüğü bölgelerde talasemi ile G6PD eksikliğinin birlikte kalıtımı bulunabilir. Bununla beraber

Abstract

Thalassemia and glucose-6-phosphate dehydrogenase (G6PD) deŞ ciency are genetic disorders causing hemolytic anemia. Coinheritance of thalassemia and G6PD deŞ ciency can be present in regions where both hematological disorders have a high incidence. Infections may trigger hemolysis in both thalassemia and G6PD deŞ ciency. My aim is to present a patient with both G6PD deŞ ciency and thalassemia trait where I believe the hemolysis was triggered by acute hepatitis A virus (HAV) infection. Pallor, jaundice, growth-development retardation and hepatosplenomegaly were found in a three-year-old male patient. Laboratory tests revealed anemia, reticulocyte elevation (6%), target cells in the peripheral smear, (+++) hemoglobin in the urine and no erythrocyte on urine microscopy. The patient's HbA2, HbA and HbF2 ratios were 4.20%, 76.10% and 19.7%, respectively. The father's HbA2 was high (5.03%) while the mother's HbA2 was normal (2.65%). A heterozygous codon 15G/A mutation was found in the patient's beta-globulin gene DNA sequence analysis.In conclusion, intravascular hemolysis and coinheritance of different disorders must be considered and peripheral smear (erythrocyte morphology) and urine microscopy should not be neglected if anemia and signiŞ cant hyperbilirubinemia are present in patients with hepatitis A infection