Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
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Hematology
Hematology is the branch of biology. Hematology is the medical field that deals with the treatment of blood disorders and cancers, such as hemophilia, leukemia, lymphoma, and sickle-cell anemia. Hematologists and hematopathologists are medical profession…
Question

When an RH-negative woman is ABO- compatible with her husband, as Mr. and Mrs Waymarsh are, the risk of Rh alloimmunization is 16 percent. When they are ABO incompatible the risk falls to 7 percent. How do you explain this difference?

248 Case 44: Hemolytic Disease of the Newborn Fig. 44.1 Hemagglutination is used to type blood and match compatible donors and recipients for blood transfusion. Common gut bacteria bear antigens that are similar or identical to blood group antigens, and these stimulate the formation of antibodies against these antigens in individuals who do not bear the corresponding antigen on their own red blood cells (left column); thus, type O individuals, who lack A and B antigens, have both anti-A and anti-B antibodies, whereas type AB individuals have neither. The pattern of agglutination of the red blood cells of a transfusion donor or recipient with anti-A and anti-B antibodies reveals the individual's ABO blood group. Before transfusion, the serum of the recipient is also tested for antibodies that agglutinate the red blood cells of the donor, and vice versa, a procedure called a cross-match, which may detect potentially harmful antibodies against other blood groups that are not part of the ABO system. 30.5 weeks: hematocrit up to 16.3% Further transfusion requested. Serum from individuals of type Anti-A and anti-B antibodies Anti-B antibodies B Anti-A antibodies AB No antibodies against A or B R-GlcNAc-Gal Fue no agglutination no agglutination no agglutination no agglutination Red blood cells from individuals of type Express the carbohydrate structures R-GlcNAc-Gal-GalNAc R-GlcNAc-Gal-Gal Fúc Ric agglutination no agglutination agglutination no agglutination agglutination agglutination no agglutination no agglutination R-GlcNAc-Gal-GaNAC 3-2.3-2 R-GNA-Gal-Gal agglutination agglutination agglutination no agglutination The Rh antigenic determinants are spaced very far apart on the red cell surface. As a consequence, IgG antibodies against the Rh antigen do not fix complement and therefore do not hemolyze red blood cells in vitro. For reasons that are less well understood, IgG antibodies against the Rh antigen do not agglutinate Rh-positive red blood cells. Because of this it was very difficult to detect Rh antibodies until Robin Coombs at the University of Cambridge devised a solution to the prob- lem by developing antibodies against human immunoglobulin. He showed that Rh-positive red blood cells coated with IgG anti-Rh antibodies could be taken from a fetus and agglutinated by antibodies against IgG. Furthermore, he showed that when the serum of an alloimmunized woman was incubated with Rh-positive red blood cells, these red blood cells could then be agglutinated by antibody against IgG (Fig. 44.2). The former is called the direct Coombs test and the latter the indi- rect Coombs test. This application of immunology to a vexing clinical problem led ultimately to treatment and prevention of the problem. The case of Cynthia Waymarsh: a fetus in immunological distress. Mrs Waymarsh was 31 years old when she became pregnant for the third time. She was known to have blood group A, Rh-negative red cells. Her husband was also type A but Rh-positive. Their first-born child, a male, was healthy. During her second pregnancy Mrs Waymarsh was noted to have an indirect Coombs titer at a 1:16 dilu- tion of her serum. The fetus was followed closely, and the delivery of a healthy baby girl was induced at 36 weeks of gestation. Five years later, Mrs Waymarsh became pregnant again. At 14 weeks of gestation her indirect Coombs titer was 1:8, and at 18 weeks it was 1:16. Amniotic fluid was obtained at 22, 24, 27, and 29 weeks of gestation and was found to have increasing
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Transcribed Image Text:248 Case 44: Hemolytic Disease of the Newborn Fig. 44.1 Hemagglutination is used to type blood and match compatible donors and recipients for blood transfusion. Common gut bacteria bear antigens that are similar or identical to blood group antigens, and these stimulate the formation of antibodies against these antigens in individuals who do not bear the corresponding antigen on their own red blood cells (left column); thus, type O individuals, who lack A and B antigens, have both anti-A and anti-B antibodies, whereas type AB individuals have neither. The pattern of agglutination of the red blood cells of a transfusion donor or recipient with anti-A and anti-B antibodies reveals the individual's ABO blood group. Before transfusion, the serum of the recipient is also tested for antibodies that agglutinate the red blood cells of the donor, and vice versa, a procedure called a cross-match, which may detect potentially harmful antibodies against other blood groups that are not part of the ABO system. 30.5 weeks: hematocrit up to 16.3% Further transfusion requested. Serum from individuals of type Anti-A and anti-B antibodies Anti-B antibodies B Anti-A antibodies AB No antibodies against A or B R-GlcNAc-Gal Fue no agglutination no agglutination no agglutination no agglutination Red blood cells from individuals of type Express the carbohydrate structures R-GlcNAc-Gal-GalNAc R-GlcNAc-Gal-Gal Fúc Ric agglutination no agglutination agglutination no agglutination agglutination agglutination no agglutination no agglutination R-GlcNAc-Gal-GaNAC 3-2.3-2 R-GNA-Gal-Gal agglutination agglutination agglutination no agglutination The Rh antigenic determinants are spaced very far apart on the red cell surface. As a consequence, IgG antibodies against the Rh antigen do not fix complement and therefore do not hemolyze red blood cells in vitro. For reasons that are less well understood, IgG antibodies against the Rh antigen do not agglutinate Rh-positive red blood cells. Because of this it was very difficult to detect Rh antibodies until Robin Coombs at the University of Cambridge devised a solution to the prob- lem by developing antibodies against human immunoglobulin. He showed that Rh-positive red blood cells coated with IgG anti-Rh antibodies could be taken from a fetus and agglutinated by antibodies against IgG. Furthermore, he showed that when the serum of an alloimmunized woman was incubated with Rh-positive red blood cells, these red blood cells could then be agglutinated by antibody against IgG (Fig. 44.2). The former is called the direct Coombs test and the latter the indi- rect Coombs test. This application of immunology to a vexing clinical problem led ultimately to treatment and prevention of the problem. The case of Cynthia Waymarsh: a fetus in immunological distress. Mrs Waymarsh was 31 years old when she became pregnant for the third time. She was known to have blood group A, Rh-negative red cells. Her husband was also type A but Rh-positive. Their first-born child, a male, was healthy. During her second pregnancy Mrs Waymarsh was noted to have an indirect Coombs titer at a 1:16 dilu- tion of her serum. The fetus was followed closely, and the delivery of a healthy baby girl was induced at 36 weeks of gestation. Five years later, Mrs Waymarsh became pregnant again. At 14 weeks of gestation her indirect Coombs titer was 1:8, and at 18 weeks it was 1:16. Amniotic fluid was obtained at 22, 24, 27, and 29 weeks of gestation and was found to have increasing
Case 44: Hemolytic Disease of the Newborn Fig. 44.2 The Coombs direct and indirect anti-globulin tests for antibody to red blood cell antigens. An Rh-negative (Rh-) mother of an Rh-positive (Rh+) fetus can become immunized to fetal red blood cells that enter the maternal circulation at the time of delivery. In a subsequent pregnancy with an Rh+ fetus, IgG anti-Rh antibodies can cross the placenta and damage the fetal red blood cells. In contrast to anti-Rh antibodies, anti-ABO antibodies are of the IgM isotype; they cannot cross the placenta, and so do not cause harm. Anti-Rh antibodies do not agglutinate red blood cells, but their presence can be shown by washing the fetal red blood cells and then adding antibody against human immunoglobulin, which agglutinates the antibody-coated cells. The washing removes unrelated immunoglobulins that would otherwise react with the anti-human immunoglobulin antibody. Anti-Rh antibodies can be detected in the mother's serum in an indirect Coombs test; the serum is incubated with Rh+ red blood cells, and once the antibody has bound, the red cells are treated as in the direct Coombs test. amounts of bilirubin (a pigment derived from the breakdown of heme, indicating that the fetus's red blood cells were being hemolyzed). At 29 weeks of gestation a blood sample was obtained from the umbilical vein and found to have a hematocrit of 6.2% (normal 45%). (The hematocrit is the proportion of blood that is composed of red cells, and because the volume of white cells is comparatively negligible, this is simply ascertained by centrifuging whole unclotted blood in a tube.) On finding that the fetus was profoundly anemic, 85 ml of type 0, Rh-negative packed red blood cells were transfused into the umbilical vein. At 30.5 weeks of gestation another sample of blood from the umbilical vein was obtained; the hematocrit was 16.3%. The etus was transfused with 75 ml of type 0, Rh-negative packed red blood cells. The fetus was examined at weekly intervals for the appearance of hydrops (see below), and none was observed. At 33.5 weeks of gestation, the hematocrit of a blood sample from the umbilical vein was 21%, so 80 ml of type 0, Rh-negative packed red blood cells were again transfused into the umbilical vein. At 34.5 weeks of gestation it was determined that the fetus was sufficiently mature to sustain extrauterine life without difficulty; labor was induced and a normal female infant was born. The hematocrit in the umbilical vein blood was 29%. The baby did well and no further therapeutic measures were undertaken. Hemolytic disease of the newborn. Although hemolytic disease of the newborn is most commonly the result of alloim- munization with Rh antigen, other red blood cell alloantigens, such as Lewis, Kell, Duffy, Kidd, and Lutheran, may cause alloimmunization. In each case, the mater- nal IgG antibodies cross the placenta in increasing amounts during the second tri- mester of pregnancy and hemolyze the fetal red blood cells. The resulting anemia may become so severe that, if untreated, the fetus goes into heart failure and devel- ops massive edema; this is called hydrops fetalis and results in fetal death. The risk of fetal development of hydrops rises from 10% when the indirect Coombs titer of the mother is 1:16 to 75% when the maternal titer is 1:128. If the anemia is not so severe as to cause hydrops, the affected infant at birth is still massively hemolyz- ing red blood cells. The newborn must dispose of the heme breakdown pigments rapidly, because an excessive accumulation of bilirubin results in the deposition of this pigment in the brain and severe neurological impairments. In response to the profound anemia, the number of red blood cell precursors (erythroblasts) in the spleen, liver, and bone marrow expands rapidly; for this reason, hemolytic disease of the newborn has also been called erythroblastosis fetalis. As we have seen in this case, the extent of hemolysis can be determined easily by obtaining amniotic fluid, into which the fetus begins to urinate by 20 weeks of Direct Coombs test Indirect Coombs test Rh- mother pregnant with Rh+ child (Rh* Washed fetal red cells coated with maternal antibody Add rabbit anti-human antibody Rh Maternal serum Add Rh+ red cells and wash out unbound antibody Agglutination Add rabbit anti-human antibody 33.5 weeks: hematocrit up to 21%. Further transfusion requested. 249
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Transcribed Image Text:Case 44: Hemolytic Disease of the Newborn Fig. 44.2 The Coombs direct and indirect anti-globulin tests for antibody to red blood cell antigens. An Rh-negative (Rh-) mother of an Rh-positive (Rh+) fetus can become immunized to fetal red blood cells that enter the maternal circulation at the time of delivery. In a subsequent pregnancy with an Rh+ fetus, IgG anti-Rh antibodies can cross the placenta and damage the fetal red blood cells. In contrast to anti-Rh antibodies, anti-ABO antibodies are of the IgM isotype; they cannot cross the placenta, and so do not cause harm. Anti-Rh antibodies do not agglutinate red blood cells, but their presence can be shown by washing the fetal red blood cells and then adding antibody against human immunoglobulin, which agglutinates the antibody-coated cells. The washing removes unrelated immunoglobulins that would otherwise react with the anti-human immunoglobulin antibody. Anti-Rh antibodies can be detected in the mother's serum in an indirect Coombs test; the serum is incubated with Rh+ red blood cells, and once the antibody has bound, the red cells are treated as in the direct Coombs test. amounts of bilirubin (a pigment derived from the breakdown of heme, indicating that the fetus's red blood cells were being hemolyzed). At 29 weeks of gestation a blood sample was obtained from the umbilical vein and found to have a hematocrit of 6.2% (normal 45%). (The hematocrit is the proportion of blood that is composed of red cells, and because the volume of white cells is comparatively negligible, this is simply ascertained by centrifuging whole unclotted blood in a tube.) On finding that the fetus was profoundly anemic, 85 ml of type 0, Rh-negative packed red blood cells were transfused into the umbilical vein. At 30.5 weeks of gestation another sample of blood from the umbilical vein was obtained; the hematocrit was 16.3%. The etus was transfused with 75 ml of type 0, Rh-negative packed red blood cells. The fetus was examined at weekly intervals for the appearance of hydrops (see below), and none was observed. At 33.5 weeks of gestation, the hematocrit of a blood sample from the umbilical vein was 21%, so 80 ml of type 0, Rh-negative packed red blood cells were again transfused into the umbilical vein. At 34.5 weeks of gestation it was determined that the fetus was sufficiently mature to sustain extrauterine life without difficulty; labor was induced and a normal female infant was born. The hematocrit in the umbilical vein blood was 29%. The baby did well and no further therapeutic measures were undertaken. Hemolytic disease of the newborn. Although hemolytic disease of the newborn is most commonly the result of alloim- munization with Rh antigen, other red blood cell alloantigens, such as Lewis, Kell, Duffy, Kidd, and Lutheran, may cause alloimmunization. In each case, the mater- nal IgG antibodies cross the placenta in increasing amounts during the second tri- mester of pregnancy and hemolyze the fetal red blood cells. The resulting anemia may become so severe that, if untreated, the fetus goes into heart failure and devel- ops massive edema; this is called hydrops fetalis and results in fetal death. The risk of fetal development of hydrops rises from 10% when the indirect Coombs titer of the mother is 1:16 to 75% when the maternal titer is 1:128. If the anemia is not so severe as to cause hydrops, the affected infant at birth is still massively hemolyz- ing red blood cells. The newborn must dispose of the heme breakdown pigments rapidly, because an excessive accumulation of bilirubin results in the deposition of this pigment in the brain and severe neurological impairments. In response to the profound anemia, the number of red blood cell precursors (erythroblasts) in the spleen, liver, and bone marrow expands rapidly; for this reason, hemolytic disease of the newborn has also been called erythroblastosis fetalis. As we have seen in this case, the extent of hemolysis can be determined easily by obtaining amniotic fluid, into which the fetus begins to urinate by 20 weeks of Direct Coombs test Indirect Coombs test Rh- mother pregnant with Rh+ child (Rh* Washed fetal red cells coated with maternal antibody Add rabbit anti-human antibody Rh Maternal serum Add Rh+ red cells and wash out unbound antibody Agglutination Add rabbit anti-human antibody 33.5 weeks: hematocrit up to 21%. Further transfusion requested. 249
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