Cautions

Some hemoglobin disorders and variants, including common alpha-thalassemia conditions, are not detected by screening methods and require further reflex testing to identify. If there is a family history of a known hemoglobin disorder, prior therapy for a hemoglobin disorder, or otherwise unexplained lifelong/familial symptoms, such as hemolysis, microcytosis, erythrocytosis/polycythemia, cyanosis, or hypoxia are present, this should be clearly communicated to the laboratory so appropriate reflex testing can be added.

Recent transfusion may mask protein results, including hemoglobin electrophoresis, hereditary persistence of fetal hemoglobin by flow cytometry, stability studies, and sickle solubility studies depending on percentage of transfused cells present. Some hemoglobin variants can originate from the donor blood product and not from the tested recipient. These are typically found in low percentages.

If the patient has undergone a bone marrow transplant, the results may be atypical and should be interpreted in the context of clinical information.

Some therapies cause artefactual effects in protein studies, including hydroxyurea and decitabine (increased hemoglobin F levels), voxelotor (artefactual peaks), and gene therapy (alternate protein detection, beta T87Q, by mass spectrometry). Clear communication of prior therapy is strongly recommended.