Complications in children and adolescents with Chuvash polycythemia

To the editor: In the Chuvash form of congenital polycythemia,[1][1] a homozygous germ-line VHL R200W mutation leads to impaired degradation of the α subunits of the hypoxia inducible transcription factors (HIF-1α and HIF-2α) and augmented hypoxic responses during normoxia including