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Ralph E. Bernstein, MB, FRCPath
Johannesburg, South Africa

Arch Intern Med. 1980;140(3):442.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—In the February ARCHIVES (139:225-230, 1979), Colwell and colleagues rightly consider impaired transport of oxygen a causative factor for microvascular disease in diabetics. However, the role they attribute to glycosylated hemoglobin (Hb A_1c) calls for comment. While normal (nondiabetic) children and adults of both sexes have 2% to 6% Hb A_1c, glycosylated hemoglobin formed 4% to 16% of total hemoglobin in newly diagnosed (untreated) diabetics,¹ with similar values in uncontrolled diabetes and cases of ketoacidosis. Thus, although Hb A_1c per se does have a somewhat higher oxygen affinity than adult hemoglobin,² the overall effect in unloading oxygen in vivo to the tissues is slight. Compared to the normal blood oxygen Po_, at 50% oxygen saturation (P₅₀) of 26 to 27 mm Hg, maturity-onset diabetics without ketoacidosis have a P₅₀ of 24 to 26 mm Hg. Similarly, Ditzel³ found that 42 diabetic children had a mean . . . [Full Text PDF of this Article]

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