Fiona A. M. Regan
Imperial College London
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Featured researches published by Fiona A. M. Regan.
BMJ | 2005
Sailesh Kumar; Fiona A. M. Regan
Pregnancies complicated by red cell alloimmunisation may result in fetal anaemia secondary to transplacental passage of maternal immunoglobulin G, which causes progressive fetal haemolysis. In severe cases the anaemic fetus develops ascites, subcutaneous oedema, and pleural and pericardial effusions (hydrops fetalis) and dies in the womb. Many different antibodies (anti-D, anti-Kell, anti-c, anti-E, etc) can cause haemolytic disease of the fetus and newborn. This review covers the management of pregnancies affected with RhD alloimmunisation. The principles of management are similar regardless of the type of antibody involved, although care needs to be taken with pregnancies complicated by Kell alloimmunisation, where antibody concentrations do not always correlate with disease severity. We searched PubMed for up to date references on current advances in the treatment of RhD alloimmunisation. In addition, we used guidelines on antenatal care and prophylaxis from the websites of the National Institute for Clinical Excellence (NICE, http://www.nice.org.uk/) and the Royal College of Obstetricians and Gynaecologists (http://www.rcog.org.uk/). Hydrops fetalis was first described in 1609 by a French midwife, Louise Borgeois,1 after the birth of twins one of whom was oedematous and the other deeply jaundiced; both died soon after the birth. However, it was not until 1940 that Landsteiner and Weiner, using rhesus monkeys, discovered the RhD antigen.2 The RhD polypeptide is an integral membrane protein expressed exclusively on erythrocytes. Some 16% of white people are RhD negative because of deletion of the gene. During pregnancy, small volumes of fetal red cells continually get into the mothers circulation. This trafficking of red cells increases as gestation progresses. Bowman et al showed at least 0.01 ml of fetal cells in 3%, 12%, and 46% of women in each trimester.3 In most women, this load of RhD antigen on fetal erythrocytes and erythrocyte precursors does not stimulate the …
Journal of Maternal-fetal & Neonatal Medicine | 2011
Eko G. Zhang; Fiona A. M. Regan; Mark Layton; G. Paramasivam; Jo Wyatt-ashmead; Irene Roberts; Sailesh Kumar
Objectives. To describe a series of complex fetal anemia cases, detail the appropriate investigations and management, and review the literature. Methods. Four cases of non-red cell alloimmunization or infective cases of fetal anemia are presented. Results. Of the four cases presented, one was a neonatal death, one pregnancy was terminated, one case was diagnosed with Diamond Blackfan anemia, and one case was due to recurrent feto-maternal hemorrhages despite negative Kleihauer tests. Conclusions. Non-alloimmune causes of fetal anemia can be difficult to manage. Some cases require repeated and frequent intrauterine transfusions. The perinatal mortality and preterm delivery rates are increased, and some cases require considerable long-term treatment including regular transfusions. We present our experience of a series of non-immune fetal anemia managed in a tertiary unit, review the literature, and suggest appropriate management.
Archive | 2008
John A. J. Barbara; Roger P Eglin; Fiona A. M. Regan; Marcela Contreras
Archive | 2009
Fiona A. M. Regan; Sailesh Kumar; Marcela Contreras
Archive | 2008
John A. J. Barbara; Fiona A. M. Regan; Marcela Contreras
Archive | 2008
John A. J. Barbara; Fiona A. M. Regan; Marcela Contreras
Archive | 2008
John A. J. Barbara; Fiona A. M. Regan; Marcela Contreras
Archive | 2008
John A. J. Barbara; Fiona A. M. Regan; Marcela Contreras
Archive | 2008
John A. J. Barbara; Fiona A. M. Regan; Marcela Contreras
Archive | 2008
John A. J. Barbara; Fiona A. M. Regan; Marcela Contreras