Ethnicity and APS

Wilson, William S.

doi:10.1006/jaut.2000.0411

Cited by 9 publications

(10 citation statements)

References 20 publications

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“…We use both terms together as a phrase, as in “race and ethnicity,” unless specifically discussing one of them. Although many have argued for replacing race with ethnicity [Harrison, 1995; Wilson, 2000; Kalow, 2001; Schwartz, 2001; Wood, 2001] and have provided distinct definitions of the two terms, proponents themselves have not agreed on these definitions. In practice, the definitions and the conceptual distinctions they are intended to embody are not upheld, and the two terms are often used as synonyms.…”

Section: Methodsmentioning

confidence: 99%

Race and ethnicity in genetic research

Sankar¹,

Cho²,

Mountain³

2007

American J of Med Genetics Pt A

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Use of race and ethnicity terms in genetic research continues to generate controversy. Despite differing opinions about their basis or relevance, there is some agreement that investigators using these terms should: explain why the terms or categories were used, define them carefully, and apply them consistently. An important question is whether these recommendations are reflected in practice. Here we addressed this question based on 330 randomly selected articles published between 2001 and 2004 that reported on genetic research and used one or more words from a defined list of race, ethnicity, or population terms. The recommendation that authors using race or ethnicity terms explain the basis for assigning them to study populations was met infrequently (9.1%), and articles that used race and ethnicity as variables were no more likely than those that used them only to label a sample to provide these details. No article defined or discussed the concepts of race or ethnicity. With limited exceptions, current practice does not reflect repeated recommendations for using race or ethnicity terms in genetic research. This study provides a baseline against which to measure future trends.

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Section: Methodsmentioning

confidence: 99%

Race and ethnicity in genetic research

Sankar¹,

Cho²,

Mountain³

2007

American J of Med Genetics Pt A

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“…There are reports of isolated IgM aCL, and occasionally isolated IgA aCL antibodies, associated with clinical manifestations of APS [25][26][27]. aCL antibody isotype distributions may vary in different ethinic groups [24,[28][29][30]. Many individuals have aCL antibodies that are elevated in response to microbial infections and are not associated with risk for thrombotic complications.…”

Section: Anticardiolipin (Acl) Antibodymentioning

confidence: 98%

Recent advances in the diagnosis of antiphospholipid syndrome

Chi

2002

Int J Hematol

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Antiphospholipid antibodies are autoantibodies directed against anionic phospholipids or protein-phospholipid complexes measured in solid-phase immunoassays such as anticardiolipin (aCL) antibody or detected in phospholipid-dependent clotting tests as lupus anticoagulant (LA). The term "antiphospholipid syndrome (APS)" was first coined to denote the clinical association between antiphospholipid antibodies and a syndrome of episodes of thrombosis in arteries and/or veins, pregnancy loss, and thrombocytopenia. The diagnosis of APS is based on the finding of "moderate-to-high" aCL antibody titer and/or an LA test with any one of the characteristic clinical features presented. Recently, the diagnostic criteria of APS was revised and several newer assays that use phosphatidylserine, a mixture of negatively charged phospholipids or beta2-glycoprotein 1 (beta2-GP1) have been proposed for more specific measurements of antibodies present in APS. In this section, recent progress in the laboratory diagnosis of antiphopholipid syndrome will be discussed.

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“…Investigation of the clinical epidemiology of APS is in its early stages. During the past 20 years, studies of aPL and APS have been made in many countries [1][2][3][4][5][6][7][8][9][10][11]. aPL appear to occur in all populations studied, with some variations noted in their frequency and in the clinical complications [1,9,10,12,13].…”

Section: Introductionmentioning

confidence: 99%

“…aPL appear to occur in all populations studied, with some variations noted in their frequency and in the clinical complications [1,9,10,12,13]. Environmental and genetic factors contribute to ethnic variation and susceptibility to APS and thus interethnic differences in disease patterns may be due to environmental or genetic factors, or both [1,14]. A genetic basis for aPL antibodies was suggested for the first time when a familial clustering of chronic false-positive syphilis test individuals were detected [15].…”

Section: Introductionmentioning

confidence: 99%

Genetics of Antiphospholipid Syndrome

Hancer¹

2011

Human Genet Embryol

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Antiphospholipid syndrome (APS) is defined as recurrent arterial and/or venous thrombosis and obstetric complications in the presence of antiphospholipid antibodies (aPL). The possibility of a genetic predisposition to develop antiphospholipid syndrome (APS) and to produce anticardiolipin antibodies and lupus anticoagulant has been examined by family studies and population studies. Similar to many other polygenic autoimmune diseases, human leukocyte antigen associations have been reported. The genetics of β2-glycoprotein I, one of the most representative target antigens of aPL, has been extensively studied. Additional genetic risk factors for the development of thrombosis in patients with aPL have also been discussed. Although the mechanisms and pathophysiology of thrombosis in APS are highly heterogeneous and multifactorial, different genes seem to be involved.The term "antiphospholipid syndrome" has been proposed to describe the association of arterial and venous thrombosis, recurrent fetal loss, and immune thrombocytopenia with a spectrum of autoantibodies directed against cellular phospholipid components. Because of the antigen spesifity of antiphospholipid antibodies (aPL) and the pathophysiology of thrombosis in antiphospholipid syndrome (APS) are heterogeneous and multifactorial, a single scenario can not explain the mechanisms of thrombophilia or pregnancy morbidity in pateints. Investigation of the clinical epidemiology of APS is in its early stages. During the past 20 years, studies of aPL and APS have been made in many countries [1][2][3][4][5][6][7][8][9][10][11]. aPL appear to occur in all populations studied, with some variations noted in their frequency and in the clinical complications [1,9,10,12,13]. Environmental and genetic factors contribute to ethnic variation and susceptibility to APS and thus interethnic differences in disease patterns may be due to environmental or genetic factors, or both [1,14]. A genetic basis for aPL antibodies was suggested for the first time when a familial clustering of chronic false-positive syphilis test individuals were detected [15]. The first description about aPL showed two pairs of siblings with lupus anticoagulant (LA) [16]. Subsequently, primary APS was described [17] and Cevallos et al. [18] reported the development of primary APS in one woman whose identical twin sister was an asymptomatic carrier of aPL. Relatives of patients with sistemic lupus erythematosus (SLE) or primary APS had a higher incidence of anticardiolipin antibodies (aCL) [19,20] suggesting that a genetic factor may relevant with aPL. Mackie et al. [21] reported three families having more than one member with LA and called familial lupus anticoagulants. The identification of several pedigrees with an increased frequency of aPL antibodies and the associated clinical manifestations further support the familial form of APS. In one of these studies, a large kindred in which nine individuals had aPL antibodies was described. Associated clinical manifestations included stroke, deep ve...

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Ethnicity and APS

Cited by 9 publications

References 20 publications

Race and ethnicity in genetic research

Race and ethnicity in genetic research

Recent advances in the diagnosis of antiphospholipid syndrome

Genetics of Antiphospholipid Syndrome

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