Hohl R J, Sherburne A R, Feeley J E, Huisman T H, Burns C P
Department of Internal Medicine, The University of Iowa, Iowa City 52242, USA.
Am J Hematol. 1998 Nov;59(3):181-4. doi: 10.1002/(sici)1096-8652(199811)59:3<181::aid-ajh1>3.0.co;2-i.
Unexpectedly low hemoglobin oxygen saturation as determined by pulse-oximeter analysis was observed in a patient who underwent an elective surgical procedure. Specific hemoglobin derivatives such as carboxyhemoglobin, methemoglobin, and reduced hemoglobin that have been described to lower pulse-oximetry determination of oxygenation were not detected. Absorbance spectra revealed the patient's hemoglobin to be different than that obtained from two normal volunteers. High-pressure liquid chromatographic analysis of the hemoglobin showed an unknown band that comprised 15% of the patient's hemoglobin. DNA sequence analysis showed a point mutation in the second nucleotide of the 45th codon of the beta-globin chain. This mutation encodes for an abnormal beta-chain (beta-45 Phe-->Ser) that has been described as hemoglobin Cheverly. Hemoglobin Cheverly is an unstable hemoglobin that has a similar mutation as the beta-42 Phe-->Ser mutation seen in hemoglobin Hammersmith. Hemoglobin Hammersmith and another unstable hemoglobin, hemoglobin Köln, have previously been described to have unexpectedly low pulse-oximeter-determined oxyhemoglobin levels. That we find hemoglobin Cheverly to result in a similar phenomenon suggests that pulse-oximeter monitoring of oxygenation status may not be appropriate for the unstable hemoglobins. Low pulse-oximeter oxygenation determinations for these hemoglobins do not appear to predict clinical hypoxemia.
