alexa Severe Thromboembolism and Systemic Lupus Erythematosus Developing after Ovarian Hyperstimulation in a Persistent Carrier of Antiphospholipid Antibodies
ISSN: 2329-8790

Journal of Hematology & Thromboembolic Diseases
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Case Report

Severe Thromboembolism and Systemic Lupus Erythematosus Developing after Ovarian Hyperstimulation in a Persistent Carrier of Antiphospholipid Antibodies

Grandone Elvira1, Orefice Giuseppe2, Jose Delgado Alves3 and Ames Paul RJ4*
1Department of Atherosclerosis & Thrombosis Unit, I.R.C.C.S. "Casa Sollievo della Sofferenza", S. Giovanni Rotondo, Italy
2Department of Neurological Sciences, Università degli Studi di Napoli Federico II, Naples, Italy
3Internal Medicine Department, New University of Lisbon, Lisbon, Portugal
4Queen Mary University Hospital London and St George’s Hospital NHS Trust, London, UK
Corresponding Author : Ames Paul RJ
Queen Mary University Hospital London and
St George’s Hospital NHS Trust, London, UK
Tel: +44-0-20 8223
E-mail: [email protected]
Received June 27, 2014; Accepted July 08, 2014; Published July 15, 2014
Citation: Elvira G, Giuseppe O, Alves JD, Ames Paul RJ (2014) Severe Thromboembolism and Systemic Lupus Erythematosus Developing after Ovarian Hyperstimulation in a Persistent Carrier of Antiphospholipid Antibodies. J Hematol Thrombo Dis 2:150. doi:10.4172/2329-8790.1000150
Copyright: © 2014, Ames Paul RJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Ovarian hyperstimulation (OH) is not a contraindication in selected women with antiphospholipid syndrome and/or systemic lupus erythematosus (SLE). A young woman who was persistently positive antiphospholipid antibodies, low protein free S and homozygous for the paraoxonase G192A mutation underwent three courses of OH; after the fourth course she developed severe thromboembolism and clinical features of SLE despite the use of a gonadotropin-releasing hormone agonist alongside aspirin that should have minimised the risk of OH syndrome. We provide a pathogenetic interpretation of these events in the light of the patient’s investigations.

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