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3 results

  • Chapter 19 - Myeloproliferative disorders

  • from Section 7 - Malignant conditions
  • Edited by Sue Pavord, Beverley Hunt
  • Book:
    The Obstetric Hematology Manual
    Published online:
    06 December 2010
    Print publication:
    15 April 2010, pp 229-242

  • Summary

    Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by vascular thrombosis and/or obstetric morbidity in the presence of persistent antiphospholipid antibodies (aPL) namely, lupus anticoagulant antibodies (LAC), anti-cardiolipin antibodies (aCL) and/or anti-β2-glycoprotein I antibodies. The syndrome produces a spectrum of disease, both in terms of clinical manifestations and the presence of other autoimmune conditions. The disease is classified as primary antiphospholipid syndrome (PAPS) when it occurs in the absence of any features of other autoimmune disease, and secondary where other autoimmune disease is present secondary antiphospholipid syndrome (SAPS). Upto 30% of patients with APS have minor valvular abnormalities, which usually do not cause hemodynamic disturbance. Individual treatment strategies for the management of the APS in pregnancy in part depend on the assessment of a number of different factors. The first treatment used and studied for pregnant patients with APS, was a combination of corticosteroids and low dose aspirin.

  • 18 - Recurrent miscarriage – the role of prothrombotic disorders

  • from SECTION 4 - CLINICAL SEQUELAE
  • Edited by Hilary Critchley, University of Edinburgh, Iain Cameron, University of Southampton, Stephen Smith
  • Book:
    Implantation and Early Development
    Published online:
    05 June 2014
    Print publication:
    01 June 2005, pp 229-239

  • Summary

    This chapter develops the hypothesis that some women with a history of recurrent miscarriage (RM) are in a prothrombotic state outside of pregnancy. The causes of RM have been grouped into six main categories: genetic, anatomical, infective, endocrinological, immunological and unexplained. The thrombophilic disorders play a part in the aetiology of recurrent pregnancy loss at various gestations. Haemostasis in vivo is a balancing act between the coagulation and fibrinolytic pathways, and plays a vital role in the establishment and maintenance of pregnancy. Prospective studies have shown an increased prevalence of acquired thrombophilic disorders in women with a history of RM. Women with a history of RM are at greater risk of later pregnancy complications such as pre-eclampsia, fetal growth restriction and intrauterine death. Revised criteria for the diagnosis of Primary antiphospholipid syndrome (PAPS) recognise the obstetric manifestations of antiphospholipid antibodies (aPL), such as a history of pre-eclampsia and preterm labour.

  • The relationship of antiphospholipid antibodies to cognitive function in patients with systemic lupus erythematosus

  • SUSAN D. DENBURG, RAMONA M. CARBOTTE, JEFFREY S. GINSBERG, JUDAH A. DENBURG
  • Journal:
    Journal of the International Neuropsychological Society / Volume 3 / Issue 4 / July 1997
    Published online by Cambridge University Press:
    01 July 1997, pp. 377-386

  • Objective: To examine the relationship between antiphospholipid antibody positivity (expressed as the lupus anticoagulant) and cognitive dysfunction in patients with systemic lupus erythematosus (SLE). Methods: Cross-sectional comparisons of lupus anticoagulant (LA) positive (N = 39) and negative (N = 79) patients and controls (N = 35) on a cognitive test battery; 22 LA-positive and 53 LA-negative patients who had never experienced neuropsychiatric events (never-NP–SLE) were also compared separately. Results: LA-positive patients were 2 to 3 times more likely than were LA-negative patients to be designated as cognitively impaired. As a group, LA-positive patients, particularly those in the never-NP–SLE group, demonstrated lower performance primarily on tasks of verbal memory, cognitive flexibility, and psychomotor speed. Conclusions: LA positivity is associated with subclinical nervous system compromise, and a pattern of deficits compatible with subcortical involvement, possibly on the basis of ongoing LA-related microthrombotic events or vasculopathy. (JINS, 1997, 3, 377–386.)