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      Hemolytic Disease of Fetus and Newborn in a Primigravida with Multiple Alloantibodies Involving Anti-Jk a and Anti-E: A Case Report

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          Abstract

          The majority of hemolytic disease of the fetus and newborn (HDFN) reported in the literature is due to ABO and rhesus incompatibility. However, there are also other minor blood groups that have been identified as a cause of HDFN, although the occurrence is much rarer. The antibody screening program for D negative mother and the anti-D immunoglobulin treatment showed a significant reduction of the occurrence of HDFN secondary to anti-D. In a developed country, the screening for red blood cell antibody in the pregnant mother other than anti-D reduced the possibility of HDFN occurrence hence reduced the fetal morbidity and subsequently increased the fetal well being during pregnancy and after the postnatal period. In this case report, we discuss HDFN in a primigravida patient secondary to multiple alloantibodies (anti-Jk a and anti-E). The baby developed jaundice with bilirubin levels approaching the exchange transfusion level. However, with extensive phototherapy and immunoglobulin treatment, the child did not require exchange transfusion. We also included the importance of the routine antenatal antibody screening program. This practice will help the transfusion center to find the antigen negative blood in a timely manner and reduce the morbidities and mortalities of HDFN among the newborns.

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          Effect of screening for red cell antibodies, other than anti-D, to detect hemolytic disease of the fetus and newborn: a population study in the Netherlands.

          Hemolytic disease of the fetus and newborn (HDFN) is a severe disease, resulting from maternal red cell (RBC) alloantibodies directed against fetal RBCs. The effect of a first-trimester antibody screening program on the timely detection of HDFN caused by antibodies other than anti-D was evaluated. Nationwide, all women (1,002 in 305,000 consecutive pregnancies during 18 months) with alloantibodies other than anti-D, detected by a first-trimester antibody screen, were included in a prospective index-cohort study. In a parallel-coverage validation study, patients with HDFN caused by antibodies other than anti-D, that were missed by the screening program, were retrospectively identified. The prevalence of positive antibody screens at first-trimester screening was 1,232 in 100,000; the prevalence of alloantibodies other than anti-D was 328 in 100,000, of which 191 of 100,000 implied a risk for occurrence of HDFN because the father carried the antigen. Overall, severe HDFN, requiring intrauterine or postnatal (exchange) transfusions, occurred in 3.7 percent of fetuses at risk: for anti-K in 11.6 percent; anti-c in 8.5 percent; anti-E in 1.1 percent; Rh antibodies other than anti-c, anti-D, or anti-E in 3.8 percent; and for antibodies other than Rh antibodies or anti-K, in none of the fetuses at risk. All affected children, where antibodies were detected, were promptly treated and healthy at the age of 1 year. The coverage validation study showed a sensitivity of the screening program of 75 percent. Five of 8 missed cases were caused by anti-c, with delay-induced permanent damage in at least 1. First-trimester screening enables timely treatment of HDFN caused by antibodies other than anti-D, however, with a sensitivity of only 75 percent. A second screening at Week 30 of c- women will enhance the screening program. Severe HDFN, caused by antibodies other than anti-D, is associated with anti-K, anti-c, and to a lesser extent with other Rh-alloantibodies.
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            Hemolytic disease of the fetus and newborn: managing the mother, fetus, and newborn

            Hemolytic disease of the fetus and newborn (HDFN) affects 3/100 000 to 80/100 000 patients per year. It is due to maternal blood group antibodies that cause fetal red cell destruction and in some cases, marrow suppression. This process leads to fetal anemia, and in severe cases can progress to edema, ascites, heart failure, and death. Infants affected with HDFN can have hyperbilirubinemia in the acute phase and hyporegenerative anemia for weeks to months after birth. The diagnosis and management of pregnant women with HDFN is based on laboratory and radiographic monitoring. Fetuses with marked anemia may require intervention with intrauterine transfusion. HDFN due to RhD can be prevented by RhIg administration. Prevention for other causal blood group specificities is less studied.
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              The MHC class I-related receptor, FcRn, plays an essential role in the maternofetal transfer of γ-globulin in humans

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                Author and article information

                Journal
                Oman Med J
                Oman Med J
                OMJ
                Oman Medical Journal
                OMJ
                1999-768X
                2070-5204
                30 November 2020
                November 2020
                : 35
                : 6
                : e206
                Affiliations
                [1 ]School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia
                [2 ]Hospital Universiti Sains Malaysia, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia
                Author notes
                [* ]Corresponding author: salfarina@ 123456usm.my
                Article
                OMJ-35-06-1900139
                10.5001/omj.2020.135
                7736633
                33335745
                01f0afa7-aee1-4dec-b99c-13a903ab52db
                The OMJ is Published Bimonthly and Copyrighted 2020 by the OMSB.

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial (CC BY-NC) 4.0 License. http://creativecommons.org/licenses/by-nc/4.0/

                History
                : 29 August 2019
                : 01 February 2020
                Categories
                Case Report
                Case Report

                hemolytic disease of newborn,infant, newborn,rho(d) antibody,blood group antigens,phototherapy

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