A comprehensive screening analysis of antiphospholipid antibodies in Indian women with fetal loss

Author(s):  
Sonal Vora ◽  
Shrimati Shetty ◽  
Vinita salvi ◽  
Purnima Satoskar ◽  
Kanjaksha Ghosh
2015 ◽  
Vol 32 (S1) ◽  
pp. 249-250
Author(s):  
Meera Sikka ◽  
Akanksha Rawat ◽  
Usha Rusia ◽  
Kiran Guleria

1990 ◽  
Vol 163 (1) ◽  
pp. 210-216 ◽  
Author(s):  
D. Ware Branch ◽  
Donald J. Dudley ◽  
Murray D. Mitchell ◽  
Kathryn A. Creighton ◽  
Thomas M. Abbott ◽  
...  

PEDIATRICS ◽  
1993 ◽  
Vol 92 (6) ◽  
pp. 849-853
Author(s):  
Charles Molta ◽  
Olivier Meyer ◽  
Christine Dosquet ◽  
Marcela Montes de Oca ◽  
Marie-Claude Babron ◽  
...  

Objective. Antiphospholipid antibodies (aPL) are noted with increased frequency in patients with systemic lupus erythematosus (SLE). The main manifestations found to be associated with aPL are arterial and venous thrombotic events, thrombocytopenia, and recurrent pregnancy loss This study is an attempt to define the incidence of aPL in patients with childhood-onset SLE and in their relatives and to correlate their presence with clinical manifestations, and especially, to evaluate the risk of thrombosis in aPL-positive subjects. Methodology. We studied 37 unrelated patients and 107 of their first-degree relatives. VDRL, IgG and IgM anticardiolipin, and IgG antiphosphatidylethanolamine antibodies were studied in all probands during periods of clinical remission and in first-degree relatives at the time of interview. Lupus anticoagulant had only been studied in probands during an SLE flare-up. Results. Thirty-eight percent of probands and 19% of relatives were positive for at least one aPL, with little over-lap between the different aPL studied. -No aPL-negative proband developed thrombosis. Two of the aPL-positive probands had thrombotic events before testing, and a third one showed thrombosis after testing. Only two probands had high levels of IgG aCL and showed thrombosis. The occurrence of aPL positivity in relatives was not always related to its presence in probands. None of the aPL-positive relatives had hadthrombosis, but recurrent fetal loss was noted in one aPL-positive mother with SLE. Although there was a high frequency of SLE, SLE-like disease, auto-immune disorders or positive serological findings for lupus in first-degree relatives, many of these relativew did not test positive for aPL. Conclusion. The high levels of IgG aCL may be considered a risk factor for thrombosis. Findings in relatives suggest a multifactorial origin for autoimmune disease and antibody production.


1998 ◽  
Vol 79 (02) ◽  
pp. 282-285 ◽  
Author(s):  
Josep Ordi-Ros ◽  
Francesc Monegal-Ferran ◽  
Nuria Martinez ◽  
Fina Cortes-Hernandez ◽  
Miquel Vilardell-Tarres ◽  
...  

SummaryObjective: To evaluate the usefulness of IgA antiphospholipid antibodies as markers of thrombosis and/or antiphospholipid antibody syndrome. Patients and Methods: A cross-sectional study design in a tertiary, university-based, autoimmune reference hospital. Seven-hundred ninety-five patients classified into five different groups – autoimmune diseases (255), deep vein thrombosis (153), transitory ischemic attacks (108), obstetric complications (196), infectious diseases (83) and controls (81) – were tested for IgA, IgG and IgM aPL, and lupus anticoagulant. Plasma and serum samples were drawn for detection of aPL using an internationally standardized ELISA method and LA was carried out using coagulometric assays. Results: True IgA aPL were found only in two patients with systemic lupus erythematosus; these patients were also positive to IgG aPL. Conclusion: The incidence of true positivity to IgA anticardiolipin antibodies is extremely low. Their determination was not helpful in diagnosing the antiphospholipid syndrome or in explaining thrombotic events or aPL related manifestations – fetal loss – in the groups studied.


2001 ◽  
Vol 7 (4) ◽  
pp. 281-285 ◽  
Author(s):  
L. Heilmann ◽  
G.-F. v. Tempelhoff ◽  
S. Kuse

Several therapeutic regimens have been proposed for women with recurrent spontaneous abortion (RSA) and antiphospholipid antibodies (APA). Conflicting results have been reported about women with history of RSA, positive APA, and failure of standard therapy. To evaluate the use of intravenous immunoglobulin in RSA patients with APA and history of treatment failure, we initiated a study with standard therapy (aspirin and low-molecular- weight heparin) and intravenous immunoglobulin. We used an enzyme-linked immunosorbent assay (ELISA)test to screen IgG and IgM anticardiolipin antibodies, and a diluted Russel viper venom time assay for the lupus anticoagulant activity. Altogether. 66 pregnant women with positive APAs at the first visit could be included. Patients with hereditable thrainbaghilic factors were excluded. After confirmation of the pregnancy, women received a basis immunization of 0.3 g/kg immunoglobulin in a 4-week cycle until the 28th to 32nd week of gestation. All patients received 100 mg/d aspirin and 3,000 anti-Xa U/d certoparin. Among the 66 pregnant women, 17 were persistently autoantibody positive (25.8%), of whom 11 (16.7%) were ACA positive alone, 2 (3%) were lupus anticoagulant positive, and 4 (6.4%) had both antibody types. A total of 49 patients had positive APAs at the initial test, but were negative for ACA and lupus anticoagulant at the second test administered approximately 5 weeks after the start of therapy. We described this group in our following observation as "antibody negative." Sixteen of the 17 autoantibody-positive patients (94.1 %) were delivered of live infants compared with 40 patients (81.6%) in the antibody-negative group (odds ratio [OR]: 1.2; 95% CI: 0.98 to 1.4). The overall miscarriage rate was 12.1% and the fetal loss rate was 15.2%. Four patients (25%) in the antibody-positive group developed symptoms of preeclampsia and fetal growth retardation compared with four patients (9.8%) in the antibody-negative group. In conclusion. we see a reduction of the fetal loss rate in patients with RSA and positive APA (5.8%) compared with APAnegative (18.4%) women with the same therapy (OR: 0.3; 95% CI: 0.04 to 2.3).


1991 ◽  
Vol 50 (8) ◽  
pp. 553-557 ◽  
Author(s):  
H J Out ◽  
H W Bruinse ◽  
G C Christiaens ◽  
M van Vliet ◽  
J F Meilof ◽  
...  

1999 ◽  
Vol 14 (Suppl_3) ◽  
pp. 73-74
Author(s):  
G. Properzi ◽  
S. Francavilla ◽  
Cesare S. Di ◽  
N. Concordia ◽  
S. Colangeli ◽  
...  

2020 ◽  
Vol 21 (21) ◽  
pp. 8411
Author(s):  
Roberta Misasi ◽  
Agostina Longo ◽  
Serena Recalchi ◽  
Daniela Caissutti ◽  
Gloria Riitano ◽  
...  

Antiphospholipid Syndrome (APS) is an autoimmune disease characterized by arterial and/or venous thrombosis and/or pregnancy morbidity, associated with circulating antiphospholipid antibodies (aPL). In some cases, patients with a clinical profile indicative of APS (thrombosis, recurrent miscarriages or fetal loss), who are persistently negative for conventional laboratory diagnostic criteria, are classified as “seronegative” APS patients (SN-APS). Several findings suggest that aPL, which target phospholipids and/or phospholipid binding proteins, mainly β-glycoprotein I (β-GPI), may contribute to thrombotic diathesis by interfering with hemostasis. Despite the strong association between aPL and thrombosis, the exact pathogenic mechanisms underlying thrombotic events and pregnancy morbidity in APS have not yet been fully elucidated and multiple mechanisms may be involved. Furthermore, in many SN-APS patients, it is possible to demonstrate the presence of unconventional aPL (“non-criteria” aPL) or to detect aPL with alternative laboratory methods. These findings allowed the scientists to study the pathogenic mechanism of SN-APS. This review is focused on the evidence showing that these antibodies may play a functional role in the signal transduction pathway(s) leading to thrombosis and pregnancy morbidity in SN-APS. A better comprehension of the molecular mechanisms triggered by aPL may drive development of potential therapeutic strategies in APS patients.


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