Introduction
Fetal red blood cells include fetal hemoglobin, which is crucial in carrying oxygen from the mother's bloodstream to the fetus' organs and tissues. It begins to be created at around six weeks of pregnancy, and its levels continue to be high until the baby is between two and four months old. Because hemoglobin F is made differently from adult hemoglobin, it can bind (or adhere to) oxygen more firmly. Through the placenta, which is located in the mother's uterus, in this manner, the developing fetus is able to absorb oxygen from the mother's bloodstream in this manner.
Fetal hemoglobin levels in the newborn rapidly decline over the first year as adult forms of hemoglobin start to be produced, eventually reaching adult levels (less than 1 percent of total hemoglobin) in the infant. Fetal hemoglobin levels can rise above normal levels due to diseases such as beta thalassemias, disrupting adult hemoglobin components and postponing this process. One method for treating some of the symptoms of sickle cell anemia is to increase fetal hemoglobin synthesis.
How Does Fetal Hemoglobin Have High Oxygen Affinity Compared to Adult Hemoglobin?
The four heme, or oxygen-binding components of hemoglobin, are the same in fetal hemoglobin and other forms of hemoglobin, including adult hemoglobin. Thus, the crucial property is the presence of gamma subunits that enables fetal hemoglobin to bind to oxygen more strongly. In contrast, several naturally occurring chemicals in our bodies can attach to hemoglobin and modify its affinity for oxygen. 2,3-bisphosphoglycerate (2,3-BPG) is a chemical that improves hemoglobin's ability to release oxygen. 2,3-bisphosphoglycerate interacts with adult hemoglobin significantly more than fetal hemoglobin. The adult subunit has more positive charges than the fetal subunit, attracting negative charges from 2,3-bisphosphoglycerate. Because 2,3-bisphosphoglycerate preferentially binds to adult hemoglobin, fetal hemoglobin binds to oxygen with greater affinity in general.
How Is Oxygen Exchanged Between Mother and Fetus in the Womb?
During pregnancy, the mother's circulatory system supplies oxygen and nutrients to the fetus even while transporting nutrient-depleted blood laden with carbon dioxide. The maternal and fetal blood circulations are separate, and molecular exchange occurs through the placenta in an area known as the intervillous space that is located between the maternal and fetal blood vessels.
In the oxygen exchange process, there are three critical factors that allow it to flow from the maternal circulation into the fetal circulation that is as follows:
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For instance, the existence of fetal hemoglobin in the fetus allows for better oxygen binding than maternal hemoglobin.
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The mother's bloodstream contains more oxygen than the fetus's. Oxygen spontaneously diffuses into the fetal circulation.
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As the maternal blood absorbs more carbon dioxide, it becomes more acidic, which promotes oxygen release by the maternal hemoglobin. At the same time, the drop in carbon dioxide in fetal blood makes it more alkaline, which promotes oxygen intake.
What Pathophysiology Lies Behind Hemoglobinopathies?
In the pathogenesis of hemoglobinopathies, fetal hemoglobin plays a significant role. When one or more of the four alpha-chain genes on chromosome 16 are removed, it causes alpha thalassemia, which can result in aberrant beta or gamma-chain production or decreased adult hemoglobin production. The number of missing genes affects the severity. A single gene can be deleted without causing many symptoms. Still, the deletion of three genes causes chronic microcytic anemia and hemolysis that can cause symptoms including weariness, hepatosplenomegaly (it is a condition in which the spleen and liver both are enlarged), and pigmented gallstones.
Hemoglobin barts is a type of hemoglobin that is abnormally synthesized in hemoglobin Bart's syndrome, also known as alpha-thalassemia major, the most severe form of alpha-thalassemia. Alpha-thalassemia is a genetic blood illness that affects the generation of hemoglobin components. It is one of the most frequent hemoglobin-related diseases. Hemoglobin barts is produced when all four genes are lost. The gamma chains in hemoglobin barts have a high affinity for oxygen, adversely affecting oxygen transport and making it incompatible with life. Hydrops fetalis, a disorder that results in fluid build-ups throughout the body, causes ascites (it is a disorder where fluid builds up in the abdomen's cavities), pleural effusions (It is a disorder where fluid builds up in the space between the parietal and visceral pleura), pericardial effusions (it is a disorder where excess fluid build up around the heart in the pericardiac sac), and scalp edema in affected fetuses. Nearly always, this disease causes spontaneous abortion.
What Is the Clinical Significance of Fetal Hemoglobin?
In the treatment of sickle cell anemia, fetal hemoglobin medicinal benefits are used. Due to fetal hemoglobin's higher oxygen affinity, which makes it less likely to deoxygenate, sickle, or trigger pain crises in sickle cell disease patients, depending on a variety of patient-dependent parameters, fetal hemoglobin makes up between 2 percent to 20 percent of hemoglobin at baseline. Infants with sickle cell disease do not exhibit symptoms since their fetal hemoglobin levels are high, but when fetal hemoglobin levels fall, patients may experience symptoms. Due to hemolysis brought on by vaso-occlusive crises that take place during sickling and hypoxia, adult hemoglobin has a shorter half-life in sickle cell disease. The pharmacologic medication Hydroxyurea raises the fraction of fetal hemoglobin present in adults through an unidentified mechanism. Patients that are suffering from severe anemia, acute chest syndrome, or recurrent pain crises should receive treatment with hydroxyurea. Hydroxyurea decreases sickle cell anemia patients' need for blood transfusions by raising fetal hemoglobin.
Conclusion
Fetal hemoglobin (HbF) is the primary type of hemoglobin found in the fetus throughout pregnancy. Fetal hemoglobin is produced by erythroid precursor cells from ten to twelve weeks of pregnancy through the first six months of postnatal life. After birth, fetal hemoglobin is replaced by adult hemoglobin in red cells, a process that represents a developmental switch in the beta-globin locus that favors the expression of beta-globin and the suppression of gamma-globin. Therapies to disrupt this switch have long been sought, based on observations that the persistence of fetal-hemoglobin synthesis after birth ameliorates the phenotypes of sickle cell disease and beta-thalassemia major, as well as the absence of indications of either disease when fetal hemoglobin levels are high in pregnancy or after birth. To know more about the condition, consult the doctor online.
