<![CDATA[Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme in erythrocytes that functions to maintain glycolysis, form an erythrocyte membrane, and protect hemoglobin from oxidative denaturation. Clinical manifestations of anemia and severe jaundice are risk factors for acute hyperbilirubinemia encephalopathy, which can progress to kernicterus. G6PD deficiency is X-linked. The incidence is most common in males with an incidence in Indonesia of 1-14%. A 3-day-old male baby appeared yellowish and had a history of being pale since 1 day of age. There was a history of phototherapy and packed red blood cell transfusion from a previous hospital. The baby was born via caesarean section, term baby, with a birth weight of 2700 grams. The Physical examination revealed Kramer V, tachypnea, but no hepatosplenomegaly. A previous laboratory examination at AM Hospital showed total bilirubin of 23.3 mg/dL, indirect bilirubin 23 mg/dL, and pre-transfusion hemoglobin 9.8 g/dL. Chest X-rays revealed grade I–II hyaline membrane disease. Meanwhile, the laboratory test results at the Dr Wahidin Sudirohusodo Hospital showed a total bilirubin of 38.5 mg/dL, indirect bilirubin 37.17 mg/dL, reticulocytes 9.95%, hemoglobin 11.8 g/dL, CRP 5.2 mg/L, Procalcitonin 0.5 ng/mL, and a negative Coombs test. The peripheral blood smear showed fragmented cells of erythrocytes. The G6PD level was 17.2 U/dL (reference value >20.5 U/dL). The patient received low-flow oxygenation, antibiotics, and 72 hours of intensive phototherapy. On the 7th day of treatment, the condition improved, and the baby was discharged. Therefore, Rapid diagnosis and treatment of G6PD deficiency are important to prevent other potential complication such as acute hyperbilirubinemia encephalopathy.]]>
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