Early transient neonatal cyanosis related to interatrial right-to-left shunting at an altitude of 1890 meters: a report of five cases

We report five term neonates born at an altitude of 1890 meters with transient early neonatal cyanosis due to right-to-left shunting at atrial level through patent foramen ovale. The five neonates with no clinical sign or symptom other than marked cyanosis were examined in two neonatal units of Erzurum city. Hematologic and radiologic examinations were normal. Partial oxygen pressure [PO[2]] in the arterial blood samples was lower than 45 mmHg in all of the patients, and did not increase more than 15 mmHg in any of the patients after inhalation of 100% oxygen. Echocardiography revealed normal intracardiac structure. The right-to-left interatrial shunt at diastole was detected through a patent foramen ovale in all of these infants. By only observation with no treatment, diastolic right-to-left shunt disappeared in 40.15 +/- 9.52 hours. Oxygen saturation was increased from 69.80 +/- 9.55 percent to 90.40 +/- 8.80 percent. The patients were discharged from the hospital at 5.6 +/- 0.4 days of life. Follow up for 6 months revealed no clinical problem in any of the cases. Transient cyanosis can be seen in the very early neonatal period because of interatrial right-to-left shunting in some healthy term neonates born at an altitude of 1890 meters. Decreased right atrial compliance due to relative hypoxia at that altitude can be speculated to be the causative mechanism

Hereditary spherocytosis with immunoglobulin a nephropathy

Hereditary spherocytosis is a familial hemolytic anemia. Immunoglobulin A [IgA] nephropathy associated with hereditary spherocytosis has not been reported in children. Here, we report a case of a 17-year-old boy with IgA nephropathy and hereditary spherocytosis. The patient was diagnosed with hereditary spherocytosis at the age of 12 years and splenectomy was done at the age of 15 years. Later, the patient presented with macroscopic hematuria and proteinuria. Kidney biopsy of the boy was consistent with IgA nephropathy. Treatment with angiotensin-converting enzyme inhibitor was started. The patient became free of proteinuria after the 6th month of therapy