FIGURE 7-11 Platelet counts by gestational age obtained the first day of life. Mean values and 5th and 95th percentiles are shown. (Data from Christensen RD, Henry E, Antonio DV: Thrombocytosis and thrombocytopenia in the NICU: incidence, mechanisms and treatments, J Matern Fetal Neonatal Med 2012 Oct;25 SuppIo4:15-17) • •• • •••• • • • •• •• •• • Moderateanemia • • ,• •• Mildanemia • Severeanemia•• • • 1.16 :JA12 0.84 ) 0.65 0.55 ) :;)I S
FIGURE 7-10 Relationship between fetal hemoglobin across gestational age. Blue dots indicate fetuses with hydrops. (Reproduced with permission from Mari G, Deter RL, Carpenter RL, et al: Noninvasive diagnosis by Doppler ultrasonography offetal anemia due to maternal red-cell alloimmunization. Collaborative Group for Doppler Assessment ofthe Blood Velocity in Anemic Fetuses (Level II-I), N Engl J Med 2000 Jan 6;342(1 ):9-14.)
The timing ofproduction ofeach ofthese earlyhemoglobins corresponds to the site of hemoglobin production. Fetal blood is first produced in the yolk sac, where hemoglobins Gower 1, Gower 2, and Portland are made. Erythropoiesis then moves to the liver, where fetal hemoglobin F is produced. When hemopoiesis finally moves to the bone marrow, adult-type hemoglobin A appears in fetal red blood cells and is present in progressively greater amounts as the fetus matures (Pataryas, 1972).
he final adult version of the . chain is produced exclusively by 6 weeks. Mter this, there are no functional alternative 400,000 /95th :J:LD 300,000 200,000 ::D)5 ) 100,000 24262830323436384042 versions. Ifan a-gene mutation or deletion occurs, no alternate a-type chain can be substituted to form functional hemoglobin. In contrast, at least two versions of the � chain-6 and ,-remain in production throughout fetal life and beyond. In the case ofa �-gene mutation or deletion, these two other versions of the � chain often continue to be produced, resulting in hemoglobin A2 or hemoglobin F, which substitute for the abnormal or missing hemoglobin.
Genes are turned of by methylation of their control region, which is discussed in Chapter 13 (p. 267). In some situations, methylation does not occur. For example, in newborns ofdiabetic women, hemoglobin F may persist due to hypomethylation of thei, gene (Perrine, 1988). With sickle cell anemia, thei, gene remains unmethylated, and large quantities of fetal hemoglobin continue to be produced. s discussed in Chapter 56 (p. 1081), elevated hemoglobin F levels are associated with fewer sickle-cell disease symptoms, and pharmacological modiication ofthese levels by hemoglobin F-inducing drugs is one approach to treatment.