Anti-C alloantibodies are the most probable antibody present in the patient’s sample. Reagent screening cells 2 and 3 were not reactive at immediate spin, 37°C, or in the AHG phase. The screen ruled out antibodies to D, c, E, e, k, Kpb, Jsb, Fyb, Jka, Jkb, Lea, Leb, P1, M, N, S, s, Lub, and Xg*a antigens. In all positive screening cells, reactions occurred at immediate spin, 37°C, and AHG phases; however, screening cells with positive reactions did not react with same strength.
The panel ruled out antigens V*, Cw, K, Fya, and Lua. In panel cells, reactions occurred at immediate spin, 37°C, and AHG phases. This indicates the presence of IgG class antibodies, as IgM class antibodies only react at immediate spin. The C antigen was expressed in …show more content…
HDFN is caused when the immune system of an Rh negative mother mounts a response against the red blood cells of an Rh positive fetus. It is typically caused by anti-D but can be caused by other antibodies to the Rh blood group system. The development of anti-C makes the patient susceptibility to HDFN. This patient has been pregnant three times, with no previous transfusions or transfusion reactions. Since she has never been transfused with any blood product, she likely become sensitized to the C antigen in either her first or second pregnancy. In the first sensitization, HDFN has no clinical manifestations because the IgM class antibodies produced by the mother cannot cross the placenta and cause harm to the fetus. In the second or current pregnancy IgM antibodies class switches to IgG, which can cross the placenta, leading to hemolysis of fetal red blood cells, which can be fatal if not treated. It is known that this patient has IgG class antibodies because the phases of reaction (immediate spin, 37°C, and after the addition of AHG) are characteristic of IgG reactions. IgM class antibodies only react at immediate spin under 22°C.
An indirect antiglobulin test would be performed on the mother’s serum to detect anti-C. A direct antiglobulin test would be performed on the fetus to detect the presence of antibodies coating the fetus’s red blood cells in vivo. …show more content…
None of QC reagents were expired, which is important because expression of antigens may decrease during storage. Quality control passed for QC1, QC2, and QC3. Positive controls, QC1 and QC2, demonstrated hemagglutination while the negative control, QC3 did not demonstrate hemagglutination. Additionally, check cells added to non-reactive demonstrated agglutination, indicating that AHG was added to the tubes. This means that the non-reactive tubes are not false negatives caused by the lack of AHG. Patient cell auto control as not performed in student lab. Auto control is running the patient’s own red blood cells with their serum for the antibody screen and identification. It is presumed that auto control for this patient was non-reactive, indicating alloantibodies. A reactive auto control indicates the presence autoantibodies and in vitro hemolysis of patient red cells by their own antibodies in the form of a pinkish-red supernatant would be
The panel ruled out antigens V*, Cw, K, Fya, and Lua. In panel cells, reactions occurred at immediate spin, 37°C, and AHG phases. This indicates the presence of IgG class antibodies, as IgM class antibodies only react at immediate spin. The C antigen was expressed in …show more content…
HDFN is caused when the immune system of an Rh negative mother mounts a response against the red blood cells of an Rh positive fetus. It is typically caused by anti-D but can be caused by other antibodies to the Rh blood group system. The development of anti-C makes the patient susceptibility to HDFN. This patient has been pregnant three times, with no previous transfusions or transfusion reactions. Since she has never been transfused with any blood product, she likely become sensitized to the C antigen in either her first or second pregnancy. In the first sensitization, HDFN has no clinical manifestations because the IgM class antibodies produced by the mother cannot cross the placenta and cause harm to the fetus. In the second or current pregnancy IgM antibodies class switches to IgG, which can cross the placenta, leading to hemolysis of fetal red blood cells, which can be fatal if not treated. It is known that this patient has IgG class antibodies because the phases of reaction (immediate spin, 37°C, and after the addition of AHG) are characteristic of IgG reactions. IgM class antibodies only react at immediate spin under 22°C.
An indirect antiglobulin test would be performed on the mother’s serum to detect anti-C. A direct antiglobulin test would be performed on the fetus to detect the presence of antibodies coating the fetus’s red blood cells in vivo. …show more content…
None of QC reagents were expired, which is important because expression of antigens may decrease during storage. Quality control passed for QC1, QC2, and QC3. Positive controls, QC1 and QC2, demonstrated hemagglutination while the negative control, QC3 did not demonstrate hemagglutination. Additionally, check cells added to non-reactive demonstrated agglutination, indicating that AHG was added to the tubes. This means that the non-reactive tubes are not false negatives caused by the lack of AHG. Patient cell auto control as not performed in student lab. Auto control is running the patient’s own red blood cells with their serum for the antibody screen and identification. It is presumed that auto control for this patient was non-reactive, indicating alloantibodies. A reactive auto control indicates the presence autoantibodies and in vitro hemolysis of patient red cells by their own antibodies in the form of a pinkish-red supernatant would be