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      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

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          Abstract

          Background

          ABO 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 presentation

          We 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.

          Conclusion

          The 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.

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          Most cited references50

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          Immune hemolytic anemia associated with drug therapy.

          Drug-induced immune hemolytic anemia (DIIHA) is rare; it can be mild or associated with acute severe hemolytic anemia (HA) and death. About 125 drugs have been implicated as the cause. The HA can be caused by drug-independent antibodies that are indistinguishable, in vitro and in vivo, from autoantibodies causing idiopathic warm type autoimmune hemolytic anemia (AIHA). More commonly, the antibodies are drug-dependent (i.e., will only react in vitro in the presence of the drug). The most common drugs to cause DIIHA are anti-microbials (e.g., cefotetan, ceftriaxone and piperacillin), which are associated with drug-dependent antibodies. The most common drug to cause AIHA is fludarabine. Finding out which drug is causing the problem and stopping that drug is the first approach to therapy. It is not easy to identify the drug interactions accurately in vitro; laboratories specializing in this area can be of great help. Copyright 2010 Elsevier Ltd. All rights reserved.
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            Haemolytic disease of the fetus and newborn.

            Haemolytic Disease of the Fetus and Newborn (HDFN) is caused by maternal alloimmunization against red blood cell antigens. In severe cases, HDFN may lead to fetal anaemia with a risk for fetal death and to severe forms of neonatal hyperbilirubinaemia with a risk for kernicterus. Most severe cases are caused by anti-D, despite the introduction of antental and postnatal anti-D immunoglobulin prophylaxis. In general, red blood cell antibody screening programmes are aimed to detect maternal alloimmunization early in pregnancy to facilitate the identification of high-risk cases to timely start antenatal and postnatal treatment. In this review, an overview of the clinical relevance of red cell alloantibodies in relation to occurrence of HDFN and recent views on prevention, screening and treatment options of HDFN are provided.
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              A systematic evaluation of laboratory testing for drug-induced immune thrombocytopenia.

              Drug-induced immune thrombocytopenia (DITP) can be confirmed by the demonstration of drug-dependent platelet antibodies in vitro; however, laboratory testing is not readily accessible and test methods are not standardized. To identify drugs with the strongest evidence for causing DITP based on clinical and laboratory criteria. We developed a grading system to evaluate the quality of DITP laboratory testing. The 'DITP criteria' were: (i) Drug (or metabolite) was required for the reaction in vitro; (ii) Immunoglobulin binding was demonstrated; (iii) Two or more laboratories obtained positive results; and (iv) Platelets were the target of immunoglobulin binding. Laboratory diagnosis of DITP was considered definite when all criteria were met and probable when positive results were reported by only one laboratory. Two authors applied the DITP criteria to published reports of each drug identified by systematic review. Discrepancies were independently adjudicated. Of 153 drugs that were clinically implicated in thrombocytopenic reactions, 72 (47%) were associated with positive laboratory testing. Of those, 16 drugs met criteria for a definite laboratory diagnosis of DITP and thus had the highest probability of causing DITP. Definite drugs were: quinine, quinidine, trimethoprim/sulfamethoxazole, vancomycin, penicillin, rifampin, carbamazepine, ceftriaxone, ibuprofen, mirtazapine, oxaliplatin and suramin; the glycoprotein IIbIIIa inhibitors abciximab, tirofiban and eptifibatide; and heparin. We identified drugs with the strongest evidence for an association with immune thrombocytopenia. This list may be helpful for ranking potential causes of thrombocytopenia in a given patient. © 2012 International Society on Thrombosis and Haemostasis.
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                Author and article information

                Contributors
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                22 December 2021
                2021
                : 12
                : 698541
                Affiliations
                [1] 1 Department of Blood Transfusion, Dongguan Maternal and Child Health Hospital , Dongguan, China
                [2] 2 Department of Blood Transfusion, Dongguan Tungwah Hospital , Dongguan, China
                [3] 3 Department of Neonatology, Dongguan Maternal and Child Health Hospital , Dongguan, China
                [4] 4 Department of Medical Genetics, School of Basic Medical Sciences, Southern Medical University , Guangzhou, China
                [5] 5 Key Laboratory of Single Cell Technology and Application in Guangdong , Guangzhou, China
                Author notes

                Edited by: Chack-Yung Yu, The Research Institute at Nationwide Children’s Hospital, United States

                Reviewed by: Beate Mayer, Charité University Medicine Berlin, Germany; Danlei Zhou, Nationwide Children’s Hospital, United States

                *Correspondence: Yuanjun Wu, wuyuanjun199@ 123456126.com ; Fu Xiong, xiongfu@ 123456smu.edu.cn

                †These authors share first authorship

                This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology

                Article
                10.3389/fimmu.2021.698541
                8727536
                35003054
                66a849cd-a486-4cd9-bb72-badd917db084
                Copyright © 2021 Wu, Wu, Yang, Chen, Li, Guo and Xiong

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 07 May 2021
                : 06 December 2021
                Page count
                Figures: 2, Tables: 2, Equations: 0, References: 52, Pages: 9, Words: 4336
                Funding
                Funded by: Foundation for Innovative Research Groups of the National Natural Science Foundation of China , doi 10.13039/501100012659;
                Award ID: 31970558
                Funded by: Natural Science Foundation of Guangdong Province , doi 10.13039/501100003453;
                Categories
                Immunology
                Case Report

                Immunology
                hemolytic disease of newborn (hdn),cefotaxime,sulbactam,drug-induced immune hemolytic anemia (diiha),non-immunologic protein adsorption (nipa),acute intravascular hemolysis

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