***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVE To evaluate the prevalence in normal pregnancies of anti-32 glycoprotein I ( anti-beta2GPI ) antibodies , and their association with obstetrical complications . STUDY DESIGN Prospect i ve study of anti-beta2GPI and anticardiolipin ( CL ) antibodies in 510 healthy pregnant women at 15 - 18 weeks . According to the results , women were categorized into three groups : group I , negative for both antibodies ; group II , positive for anti-beta2GPI antibodies ; group III , positive for aCL only . The rates of fetal loss , abruptio placentae , preeclampsia-eclampsia , and fetal growth retardation were compared in the three groups . RESULTS  Anti-beta2GPI antibodies  were found in 20 women ( 3.9 % ) and aCL in 8 patients ( 1.6 % ) . Obstetrical complications were more frequent , even if not significantly different , in group II , 15 % , than in group I , 4.1 % ( difference 10.9 % ; 95 % confidence interval ( CI ) : 1.6 - 20.2 % ; p=0.0575 ) , while no complications were seen in group III . Preeclampsia-eclampsia were significantly more frequent in group II ( 10 % ) than in group I ( 0.8 % ; difference 9.2 % ; 95 % CI : 4.4 - 14 % ; p=0.021 ) . The prevalence of fetal growth retardation was not significantly different in the two groups ( 5 % vs. 2 % , respectively ) . COMMENT Our findings indicate that anti-beta2GPI antibodies are associated with some obstetrical complications , mainly preeclampsia-eclampsia , even if more conventional antiphospholipid antibodies are not present . This observation suggests that these antibodies should be investigated in such cases , in order to improve the outcome of subsequent pregnancies , as well as in women with a history of early and /or recurrent severe preeclampsia in order to start a prophylactic treatment ( i.e. low-dose aspirin or heparin ) Objective To investigate the association of anticardiolipin antibody with the genesis of spontaneous abortion , fetal growth restriction ( FGR ) , and preeclampsia . Methods Eight hundred sixty pregnant women constituted the study population .  Anticardiolipin antibody was screened by enzyme-linked immunosorbent assay during the first trimester of pregnancy . The outcome of pregnancy in these women was analyzed prospect ively , and the rate of occurrence of spontaneous abortion , preeclampsia , and FGR was compared in the anticardiolipin antibody-positive and -negative groups . Results  Anticardiolipin antibody  was positive in 60 of the 860 women ( 7.0 % ) and negative in 800 ( 93.0 % ) . The rate of spontaneous abortions in the anticardiolipin antibody-positive group , 25.0 % , was significantly higher than that in the anticardiolipin antibody-negative group , at 9.8 % ( P < .001 ; relative risk [ RR ] 2.56 , 95 % confidence interval ( CI ) 1.37–4.81 ) . The rates of preeclampsia ( 11.7 % ) and FGR ( 11.7 % ) in the anticardiolipin antibody-positive group were also significantly higher than those in the -negative group ( 1.9 and 1.9 % , respectively ; for preeclampsia , P < .001 ; RR 6.22 , 95 % CI 2.43–16.0 and for FGR , P < .001 ; RR 6.22 , 95 % CI 2.43–16.0 ) . Conclusion Anticardiolipin antibody is associated with adverse outcomes of pregnancy such as spontaneous abortion , preeclampsia , and FGR OBJECTIVE To estimate whether antiphospholipid antibodies , specifically anticardiolipin and anti – β2-glycoprotein-Iantibodies , are associated with preeclampsia . METHODS Plasma was prospect ively obtained from four groups of pregnant women : those with 1 ) mild preeclampsia ( n = 109 ) ; 2 ) severe preeclampsia ( n = 134 ) ; 3 ) hemolysis , elevated liver enzymes , low platelets ( HELLP ) syndrome ( n = 57 ) ; and 4 ) normotensive controls ( n = 100 ) .  Anticardiolipin and anti – β2-glycoprotein-I levels  were determined by enzyme-linked immunoassay . RESULTS Subjects with mild preeclampsia , severe preeclampsia , and HELLP syndrome did not have significantly elevated levels of immunoglobulin G ( IgG ) and IgM anticardiolipin and anti – β2-glycoprotein-I antibodies compared with normotensive controls ( P > .05 , Kruskal – Wallis ) . Similarly , subjects with mild preeclampsia , severe preeclampsia , and HELLP syndrome did not have a significantly higher proportion of women testing positive for each autoantibody compared with normotensive controls ( χ2 ) . The proportion of patients testing positive for anticardiolipin and anti – β2-glycoprotein-I antibodies were similar in patients with preeclampsia developing before and after 34 weeks ' gestation ( χ2 ) . CONCLUSION Circulating levels of both anticardiolipin and anti – β2-glycoprotein-I antibodies were not increased in patients with mild preeclampsia , severe preeclampsia , or HELLP syndrome compared with normotensive controls . Our data do not support routine testing for anticardiolipin and anti – β2-glycoprotein-I antibodies in women with preeclampsia OBJECTIVE To evaluate in preterm infants the role of intrauterine growth retardation and infant body proportionality on subsequent childhood growth . METHODS Preterm infants ( 818 ) prospect ively enrolled in the Infant Health and Development Program were studied from birth to 36 months of corrected age .  Weights and lengths were recorded at eight intervals . Growth parameters were compared in preterm infants with differing body symmetry at birth , defined by length-for-age and weight-for-age . Infants with both low length-for-age and low weight-for-age at birth were categorized as symmetrically growth retarded , and infants with normal length-for-age and low weight-for-age were categorized as asymmetrically growth retarded . RESULTS Infants born with low length-for-age demonstrated increased growth velocity until 8 months of corrected age ( p < 0.001 ) . However , infants born with low weight-for-age demonstrated decreased weight-gain velocity compared with preterm infants with appropriate weight for gestational age ( AGA ) until 40 weeks of corrected age ( p < 0.001 ) . Heights and weights of infants with either symmetric or asymmetric intrauterine growth retardation remained significantly retarded compared with AGA preterm patients and the National Child Health Survey ( NCHS ) reference population ( p < 0.001 ) . Infants born short but with normal weight did not significantly differ from AGA preterm infants in either weight or length at 36 months of corrected age . Preterm infants with both symmetric and asymmetric growth retardation demonstrated limited catch-up growth in weight until age 4 months and then paralleled the AGA preterm patients and the NCHS reference population . Very low birth weight ( < or = 1250 gm ) , gestational age , and a broad-based day-care intervention did not influence growth outcome after control for the presence of intrauterine growth retardation . CONCLUSIONS Preterm infants with both symmetric and asymmetric intrauterine growth retardation demonstrate limited catch-up growth . Intrauterine growth deficits persist into early childhood Objective To assess the association between the occurrence first of preeclampsia and antiphospholipid antibodies . Methods We conducted a prospect i ve case-control study of 180 pregnant women with their first incidents of preeclampsia and no histories of thrombosis or systemic autoimmune diseases . Preeclampsia ( n = 180 ) was defined as blood pressure ( BP ) at least 140/90 mmHg after 20 weeks ' gestation and proteinuria at least 0.3 g per 24 hours . Two control subjects were matched to each case ( n = 360 ) . They were pregnant women without hypertension or proteinuria and without histories of thrombosis or systemic autoimmune disease .  Lupus anticoagulant ( activated partial thromboplastin time , diluted thromboplastin time , platelet neutralization procedure ) and anticardiolipin antibodies ( immunoenzymatic assays ) were assessed in both groups , and the coagulation state ( levels of thrombin-antithrombin III complexes , fragments 1 + 2 of prothrombin ) was also evaluated . The analysis design was a sequential plan with 5 % type I error and 95 % power . Results There was no association between antiphospholipid antibodies and preeclampsia . The odds ratio for the association was 0.95 ( 95 % confidence interval 0.45 , 2.61 ) . Antiphospholipid antibodies were detected in eight of 180 preeclamptic women and in 19 of 360 controls . In contrast , there was a clear , confirmed activation of coagulation during preeclampsia . Conclusion Despite evidence of a prothrombotic state during preeclampsia , it is unlikely that antiphospholipid antibodies ( lupus anticoagulant and anticardiolipin antibodies ) represent risk factors for preeclampsia among women with no previous preeclampsia and no histories of thrombosis or systemic autoimmune In an attempt to reduce the incidence of  pregnancy associated venous thromboembolism ( PA-VTE ) , some research ers have advocated screening of all women for the factor V(Leiden ) mutation during early pregnancy . We have conducted a large retrospective study ( over 72,000 deliveries ) to determine if this would be useful . Sixty-two objective ly confirmed venous thrombotic events ( 51 DVT , 11 PE ) were recorded at two maternity units in the UK . The incidence of DVT was 0.71 per 1000 deliveries ( 95 % CI 0.5 - 0.9 ) with 0.50 occurring in the antenatal period ( 95 % CI 0.34 - 0.66 ) and 0.21 in the puerperium ( 95 % CI 0.11 - 0.31 ) . The incidence of PE was 0.15 per 1000 deliveries ( 95 % CI 0.06 - 0.24 ) , 0.07 antenatal ( 95 % CI 0.01 - 0.13 ) and 0.08 in the puerperium ( 95 % CI 0.02 - 0.14 ) . Of these 62 , 50 attended for follow-up and thrombophilia screening . 28 % of all episodes of PA-VTE had no clinical risk factor for thrombosis or an identifiable thrombophilic abnormality . Deficiency of antithrombin was identified in 12 % of individuals ( 95 % CI 3 - 21 ) and the factor V(Leiden ) mutation in 8 % ( 95 % CI 0.5 - 15.5 ) . Based on estimates of the prevalence of the factor V(Leiden ) mutation in the population , we estimate that the thrombotic risk for a woman during pregnancy or the puerperium with the defect is approximately 1 in 400 - 500 . This figure would not lend support to the idea of r and om screening for the mutation in early pregnancy Antibodies to cardiolipin and the lupus anticoagulant are overlapping subsets of antiphospholipid antibodies ( aPL ) and were originally described in patients with systemic lupus erythematosus [ 1 - 5 ] and subsequently in those with other rheumatic diseases [ 2 , 6 - 8 ] . These antibodies can also occur in nonrheumatologic disorders [ 9 - 12 ] and in healthy persons [ 13 , 14 ] . The presence of these antibodies in patients with systemic lupus erythematosus has been associated with the clinical features of thrombosis , fetal loss , and thrombocytopenia [ 15 - 18 ] . However , in nonautoimmune and healthy persons , the association of aPL with these clinical features has not been proved [ 14 , 19 , 20 ] . In addition , the value of different measures of aPL in predicting clinical symptoms has not been clearly defined . Furthermore , there is a paucity of prospect i ve studies describing the natural history of aPL and identifying the subset of aPL-positive patients who need therapeutic intervention . Recent studies examined the value of aPL in predicting adverse fetal and maternal outcome in healthy pregnant women [ 20 - 24 ] . The correlation of aPL with low birth weight , intrauterine fetal death , and adverse complications of pregnancy was identified by some authors [ 21 , 24 - 26 ] but not by others [ 22 ] . These studies concentrated on the predictive value of aPL as measured by anticardiolipin antibody ( IgG , IgM ) or lupus anticoagulant ( 
    Output:
    
APLAs appear to be associated with late fetal losses .
However , the association between APLAs and other placenta mediated complications is inconsistent .
LA is most strongly and consistently associated with placenta mediated complications .
There are currently insufficient data to support a significant link between anti-B2 GP1 antibodies and pregnancy morbidity