Resolving Blocked Antigen Phenomenon in Hemolytic Disease of the Fetus and Newborn Due to Anti-K

Moosavi, Mitchell; Ma, Yao; Baez, Janet; Jeffreys, Rebecca; Ward, Dawn; Ziman, Alyssa; McGonigle, Andrea M.

doi:10.1016/j.tmrv.2020.02.002

Cited by 3 publications

(4 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Complement cascade proteins were found on RBCs in only one of these cases. 11 We discuss a blocking phenomenon of anti-K at a titer of 32, which is much lower than previously reported. The findings presented in our case are consistent with the blocking of K antigen sites by a potent anti-K bound on the surface of neonatal RBCs.…”

Section: Discussionmentioning

confidence: 69%

“…In the case report of Manfroi and Velati 13 in which the titer of anti-K was 256, the fetus had severe anemia and received three intrauterine RBC transfusions. The most recent case report, a pre-proof article from Moosavi et al 11 discussing the blocked K phenomenon, claims that high-titer antibodies are the cause of a false-negative phenotype. The neonate had severe HDFN, anemia, and hyperbilirubinemia treated with exchange transfusion, intravenous immune globulin therapy, and phototherapy.…”

Section: Discussionmentioning

confidence: 99%

“…So far, there have been four case reports that describe false-negative K phenotyping due to blocking by maternal anti-K. [10][11][12][13] We present a case report of a potent anti-K with a titer of 32 that caused this blocking phenomenon.…”

mentioning

confidence: 99%

See 2 more Smart Citations

K antigens on neonatal red blood cells blocked by anti-K with titer of 32

et al. 2020

View full text Add to dashboard Cite

The blocking of red blood cell (RBC) antigens occurs when potent maternal antibodies bind to antigens on fetal or neonatal RBCs, causing them to be negative when typed with human IgM antisera. This phenomenon is rare; when it does occur, the antibody is usually of a high titer. This reported finding is typically due to anti-D, with rare reports describing false-negative K phenotyping due to blocking by maternal anti-K. We report a case of a potent anti-K with a titer of 32 that blocked K antigens on neonatal RBCs, causing them to phenotype as K–. The neonate also had clinically significant anemia (i.e., hemolytic disease of the newborn) due to the anti-K.

show abstract

Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

K antigens on neonatal red blood cells blocked by anti-K with titer of 32

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The main clinical manifestations of HDN are anemia and hyperbilirubinemia ( 18 , 19 , 24 ). The allo-immune blood group antibodies that can cause severe HDN mainly include anti-D, anti-c and anti-E of the Rh blood group system ( 18 , 19 , 24 ), anti-K of the Kell blood group system ( 24 – 27 ), anti-Di a and anti-Di b of the Diego blood group system ( 28 , 29 ), anti-M and anti-Mur of the MNSs blood group system ( 30 – 33 ), etc. While, HDN caused by ABO blood group antibodies is the most common among Asian populations, and the incidence and severity are much higher than those of Caucasian populations.…”

Section: Discussionmentioning

confidence: 99%

Case Report: First Case of Cefotaxime-Sulbactam-Induced Acute Intravascular Hemolysis in a Newborn With ABO Blood Type Incompatibility by the Mechanism of Non-Immunologic Protein Adsorption

Wu²,

Bao-chan³

et al. 2021

Front. Immunol.

View full text Add to dashboard Cite

BackgroundABO blood type incompatibility hemolytic disease of newborn (ABO-HDN) and drug-induced immune hemolytic anemia (DIIHA) due to non-immunologic protein adsorption (NIPA) mainly cause extravascular hemolysis. All the reported severe DIIHA were caused by drug-induced antibodies, and rare report of acute intravascular hemolysis was caused by the NIPA mechanism or ABO-HDN.Case presentationWe report the first case of acute intravascular hemolysis induced by cefotaxime sodium - sulbactam sodium (CTX - SBT) in a case of ABO-HDN which resulted in death at 55 h after birth. The mother’s blood type was O and RhD-positive, and the newborn’s blood type was B and RhD-positive. No irregular red blood cell (RBC) antibodies or drug-dependent antibodies related to CTX or SBT was detected in the mother’s plasma and the plasma or the RBC acid eluent of the newborn. Before the newborn received CTX - SBT treatment, the result of direct antiglobulin test (DAT) was negative while anti-B was positive (2 +) in both plasma and acid eluent. After the newborn received CTX - SBT treatment, the results of DAT for anti-IgG and anti-C3d were both positive, while anti-B was not detected in plasma, but stronger anti-B (3 +) was detected in acid eluent. In vitro experiments confirmed that NIPA of SBT promoted the specific binding of maternal-derived IgG anti-B to B antigen on RBCs of the newborn, thereby inducing acute intravascular hemolysis.ConclusionThe NIPA effect of SBT promoted the specific binding of mother-derived IgG anti-B in newborn’s plasma to the newborn’s RBC B antigens and formed an immune complex, and then activated complement, which led to acute intravascular hemolysis. Drugs such as SBT with NIPA effect should not be used for newborns with HDN.

show abstract

Immunohematological testing and transfusion management of the prenatal patient

Quraishy,

Sapatnekar

2023

Advances in Clinical Chemistry

View full text Add to dashboard Cite

Resolving Blocked Antigen Phenomenon in Hemolytic Disease of the Fetus and Newborn Due to Anti-K

Cited by 3 publications

References 10 publications

K antigens on neonatal red blood cells blocked by anti-K with titer of 32

K antigens on neonatal red blood cells blocked by anti-K with titer of 32

Case Report: First Case of Cefotaxime-Sulbactam-Induced Acute Intravascular Hemolysis in a Newborn With ABO Blood Type Incompatibility by the Mechanism of Non-Immunologic Protein Adsorption

Immunohematological testing and transfusion management of the prenatal patient

Contact Info

Product

Resources

About