Alloimmune Neonatal Neutropenia

Cartron, J; Tchernia, Gil; Celton, J.L.; Damay, M.; Chéron, Guy; Farrokhi, P; Badoual, J

doi:10.1097/00043426-199121000-00005

Cited by 33 publications

(18 citation statements)

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“…Whereas neonates with an ANC >1,000/µL are unlikely to be at significantly increased risk of secondary infections, an ANC<500/µL may be more likely to increase the risk, particularly if neutropenia persists for more than a few days (18–20). An ANC between 500–1,000/µL may indicate some intermediate risk (21).…”

Section: Normal Blood Neutrophil Concentrations In Neonatesmentioning

confidence: 99%

Evaluation of neutropenia and neutrophilia in preterm infants

Nittala

Subbarao

Maheshwari³

2012

The Journal of Maternal-Fetal & Neonatal Medicine

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Section: Normal Blood Neutrophil Concentrations In Neonatesmentioning

confidence: 99%

Evaluation of neutropenia and neutrophilia in preterm infants

Nittala

Subbarao

Maheshwari³

2012

The Journal of Maternal-Fetal & Neonatal Medicine

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“…6,10,14 These data are to be expected if one examines human alloimmune neutropenia in which maternal antibodies cross the placenta and immunodeplete the PMNs in the fetus or following transfusion of donor antibodies that bind to the PMNs of the recipient and cause immunodepletion, termed transfusion-related alloimmune neutropenia (TRAIN). [53][54][55] Alloimmune neutropenia is dependent upon the type of the antibody or the antigen recognized. Antibodies that prime PMNs through antigen recognition (eg, induce a proinflammatory change) may lead to TRALI and not antibody-mediated clearance, as shown in the presented model.…”

mentioning

confidence: 99%

Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model

Kelher

Masuno

Moore

et al. 2009

Blood

141

276

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Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion death. We hypothesize that TRALI requires 2 events: (1) the clinical condition of the patient and (2) the infusion of antibodies against MHC class I antigens or the plasma from stored blood. A 2-event rat model was developed with saline (NS) or endotoxin (LPS) as the first event and the infusion of plasma from packed red blood cells (PRBCs) or antibodies (OX18 and OX27) against MHC class I antigens as the second event. ALI was determined by Evans blue dye leak from the plasma to the bronchoalveolar lavage fluid (BALF), protein and CINC-1 concentrations in the BALF, and the lung histology. NS-treated rats did not evidence ALI with any second events, and LPS did not cause ALI. LPS-treated animals demonstrated ALI in response to plasma from stored PRBCs, both prestorage leukoreduced and unmodified, and to OX18 and OX27, all in a concentration-dependent fashion. ALI was neutrophil (PMN) dependent, and OX18/OX27 localized to the PMN surface in vivo and primed the oxidase of rat PMNs. We conclude that TRALI is the result of 2 events with the second events consisting of the plasma from stored blood and antibodies that prime PMNs. IntroductionTransfusion-related acute lung injury (TRALI) is the leading cause of transfusion mortality in the United States. 1,2 TRALI is the acute onset of noncardiogenic pulmonary edema as documented by chest radiograph and profound hypoxemia, in accordance with the definition of acute lung injury (ALI), that occurs within 6 hours of transfusion. 3,4 TRALI may occur with or without conditions that predispose the patient to ALI, and may be the worsening of pulmonary function in patients with preexisting ALI. 3,4 All blood products have been implicated in TRALI, but components that contain large amounts of plasma are mainly responsible. 5,6 The current incidence of TRALI has been estimated as 1/7900 to 1/1330 in the United Kingdom and the United States with lesser incidences in Europe. [5][6][7][8] Current mortality rates vary from 5% to 35% with the lesser mortality rates predominating. [5][6][7][8] The pathophysiology of TRALI has not been elucidated despite numerous studies. [9][10][11][12][13][14] The first mechanism proposed was the infusion of donor antibodies directed against the HLA class I or granulocyte-specific antigens on the recipient's leukocytes with animal models composed of an in vivo murine model and an isolated, perfused rabbit lung that provided physiologic relevance. [9][10][11][12]14 In addition, the neutrophil (PMN) was proposed to be the effector cell, identical to other forms of ALI and the acute respiratory distress syndrome (ARDS). [9][10][11][12]14 However, look-back studies of donors with specific antibodies directed against HLA or granulocyte antigens demonstrated that the infusion of donor antibodies into a recipient that expressed the cognate antigen resulted in TRALI in a minority of these patients, implying that the clinical condition of the recipient may be important for the d...

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“…[1][2][3][4][5][6][7][8][9][10][11] During the period of neutropenia, antibiotic treatment is somewhat controversial. Prophylactic antibiotics may be used until the results of 12 rhG-CSF administration is generally very effective in NAN, rapidly increasing the ANC to levels considered safe.…”

Section: Discussionmentioning

confidence: 99%

Resistance to Recombinant Human Granulocyte Colony-Stimulating Factor in Neonatal Alloimmune Neutropenia Associated With Anti-Human Neutrophil Antigen-2a (NB1) Antibodies

2002

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ABSTRACT. Neonatal alloimmune neutropenia is the neutrophil counterpart of the erythrocyte disorder of hemolytic disease of the newborn. Fetal neutrophil antigens, which are inherited from the father but foreign to the pregnant mother, provoke the formation of maternal antibodies, which, on transplacental passage, cause fetal/ neonatal neutropenia. Because infants with this disorder are at a higher risk of infection, recombinant hematopoietic growth factors, such as recombinant human granulocyte colony-stimulating factor, have been tried, with generally good results, to treat those with severe and prolonged neutropenia. We report a neonate who had neonatal alloimmune neutropenia associated with antibodies directed against human neutrophil antigen-2a (NB1) and initially failed to respond to even very high doses of recombinant human granulocyte colony-stimulating factor but eventually had a therapeutic response.

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Alloimmune Neonatal Neutropenia

Cited by 33 publications

References 0 publications

Evaluation of neutropenia and neutrophilia in preterm infants

Evaluation of neutropenia and neutrophilia in preterm infants

Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model

Resistance to Recombinant Human Granulocyte Colony-Stimulating Factor in Neonatal Alloimmune Neutropenia Associated With Anti-Human Neutrophil Antigen-2a (NB1) Antibodies

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