The
deoxyuridine (dU) suppression test evolved out of investigations into the biochemical basis of the megaloblastic changes seen in
vitamin B12 and
folate deficiency. Although the abnormality in dU suppression which occurs in
vitamin B12- or
folate-deficient states is assumed to reflect impaired methylation of deoxyuridylate, there is still no direct demonstration that this is so. Furthermore, there is evidence that reactions other than the methylation of deoxyuridylate are involved in the phenomenon of dU suppression. Nevertheless, in clinical practice abnormal dU suppression serves as a sensitive index of the presence of megaloblastosis due to
vitamin B12 or
folate deficiency. dU suppression is also abnormal in a number of conditions other than
vitamin B12 or
folate deficiency, but its overall specificity in detecting tissue dysfunction due to these two deficiency states is considerably higher than that of the serum
vitamin B12 or red cell
folate levels. Consequently, the test enables us simply and rapidly to define those patients in whom macrocytosis is unrelated to a deficiency of
vitamin B12 or
folate. For these reasons, the dU suppression test has been adopted by several laboratories across the world for investigating patients with (a) possible
vitamin B12 or
folate deficiency, (b) macrocytosis, and (c) megaloblastic erythropoiesis. Since the dU suppression test is abnormal in
transcobalamin II deficiency and in some
congenital disorders of
vitamin B12 and
folate metabolism, it is very useful in the investigation of obscure anaemias in infancy and childhood. In addition, it has contributed to our understanding of the mechanisms underlying the myelotoxicity of certain drugs, and particularly of
nitrous oxide.