The cause of
sudden infant death syndrome (
SIDS) is unknown, although deficits in cardiopulmonary function and central respiratory control have been suggested as possible mechanisms of the disorder. In this study, we tested the hypothesis that
SIDS is associated with a delay in the maturation of hematopoiesis. Prolonged elevation in the levels of
fetal hemoglobin (
hemoglobin F) in infants with
SIDS could denote a compromised delivery of
oxygen to sensitive tissue sites. Normally,
hemoglobin F (alpha 2 gamma 2) is largely replaced by adult
hemoglobin,
hemoglobin A (alpha 2 beta 2), during the first six months after birth. Using an isoelectric-focusing procedure for measuring stable
hemoglobin subunits, we quantitated the levels of
hemoglobin F in blood samples from 59 patients with
SIDS and 40 controls (32 living and 8 dead) matched for postconceptional age. The level of
hemoglobin F in the population with
SIDS was significantly higher than that in the controls in the age range tested (39 to 75 weeks); the mean (+/- SEM) proportion of
hemoglobin F was 63.2 +/- 3.6 percent in the group with
SIDS, as compared with 48.1 +/- 5.0 percent in the controls (P less than 0.025). The difference in
hemoglobin F levels was most pronounced 50 weeks after conception: the proportion of
hemoglobin F in the 37 patients with
SIDS with a postconceptional age of more than 50 weeks was 47.4 +/- 3.6 percent, as compared with 18.8 +/- 3.1 percent in the 19 controls of that age (P less than 0.0005). We conclude that
hemoglobin F is a useful postmortem marker for the population with
SIDS that we studied and that it may have value as a prospective marker for some infants at risk for
SIDS.