Objective: to provide an overview of the clinical significance of antiphospholipid antibodies (APLA) in pregnancy, dealing mainly with the diagnosis and management of patients with this disorder.Data Sources: sources were identified from a MEDLINE search of English language articles published from 1985 to 1995 (Keywords: lupus anticoagulant, anticardiolipin antibodies, antiphospholipid antibodies, and antiphospholipid antibody syndrome). Additional sources were identified from references cited in relevant research articles.Methods of Study Selection: thirty-six articles where selected, including publications that recorded the prevalence of commonly described antiphospholipid antibodies, clinical significance, laboratory testing, and management of pregnant women with this disorder. Almost all articles were based on case series, meta-analysis, and prospective trial. Management protocol was based on the findings and recommendations of prospective trials and clinical reviews.Results: lupus anticoagulant (LA) and anticardiolipin (ACL) antibodies belong to a heterogeneous group of antibodies directed against protein epitopes that form complexes with negatively charged phospholipids. The selected studies were reviewed critically and their conclusions were evaluated; the available literature indicates that these antiphospholipid antibodies are frequently found at low levels in otherwise healthy people. At higher levels, the presence of these antibodies is closely associated with the occurrence of arterial and venous thromboembolism, thrombocytopaenia, fetal loss, and a variety of other conditions in patients with and without systemic lupus erythematosus (SLE). This combination of significant antiphospholipid antibody levels with certain clinical sequelae defines the presence of antiphospholipid antibody syndrome (APLAS).Conclusions: screening for antiphospholipid antibodies in the prenatal population seems unwarranted. If investigations of women at risk for APLAS are positive, close maternal and fetal surveillance are required. Prophylactic treatment might be used in this select group of patients, although optimal therapy has yet to be defined. Even though knowledge of APLAS pathophysiology is limited, it is currently the guide to treatment options. All prenatal patients with APLAS should receive low dose acetylsalicylic acid (ASA) and either heparin or steroids. Heparin is suggested if there is a history of thrombosis or placental infarction, while steroids should be considered if APLAS is secondary to SLE, or if there is previous evidence of inflammation and complement activation. Defining optimal therapy will require a large multicentre prospective trial. A detailed management protocol is proposed.