Antiphospholipid Antibodies and Kininogens in Pathologic Pregnancies: A Review

Sugi, Toshitaka; Makino, Tsunehisa

doi:10.1034/j.1600-0897.2002.01103.x

Cited by 20 publications

(10 citation statements)

References 62 publications

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“…APL antibodies are a common finding in patients with recurrent fetal loss(es) [65][66][67][68][69][70][71]. Moreover, data show that the concerning the induction of aCL by sex hormones in normal subjects are scarce.…”

Section: Recurrent Fetal Lossmentioning

confidence: 99%

Some Recent Insights into the Prothrombogenic Mechanisms of Antiphospholipid Antibodies

Todorova¹,

Baleva

2007

CMC

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Antiphospholipid antibodies (aPL) are a heterogeneous group of autoantibodies, detected in the sera of patients with both autoimmune and various non-autoimmune diseases. They are also detected in subjects with no overt underlying disease - the primary antiphosphilipid syndrome (PAPS). High titers of APL are associated with arterial and venous thrombosis, recurrent fetal loss and thrombocytopenia. There have been many suggestions explaining the potential mechanisms of the procoagulant effect of aPL. These include endothelial cell (EC) activation; increased adhesion molecule expression; inhibition of EC prostacyclin release, increased leucocyte adhesion to EC, downregulation of thrombomodulin expression. APL induce the procoagulant activity of monocytes via increased tissue factor expression and directly stimulate platelet hyperactivity with resultant production of enhanced amounts of the proaggregatory molecule of TXA(2). In vitro studies show that prepro-endothelin-1 mRNA is induced by human monoclonal anticardiolipin antibodies and this might contribute to vasospasm, and, ultimately, to arterial occlusion. The hypercoagulable state in APS patients is associated with alterations in the protein C/S pathway. It is suggested that aPL may impair the protein C anticoagulant system. Acquired protein C and protein S deficiency is described in patients with APS. Beta2- glycoprotein I, (Beta2-GPI) a natural anticoagulant, is involved in the regulation of protein S anticoagulant activity by preventing the binding of protein S to C4b-binding protein. APL were shown to inhibit this effect of Beta2- GP I. As the group of aPL is very heterogeneous, it is unlikely that a single mechanism is responsible for the thrombogenic activity of all aPLs associated with thrombosis.

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Section: Recurrent Fetal Lossmentioning

confidence: 99%

Some Recent Insights into the Prothrombogenic Mechanisms of Antiphospholipid Antibodies

Todorova¹,

Baleva

2007

CMC

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“…Earlier studies showed a strong association between recurrent pregnancy losses and other aPL. [30] It is hoped to establish the clinical significance of APS in women with recurrent pregnancy loss because the identification of antibodies to phospholipids other than cardiolipin is most important. This study emphasizes the correlation and the significance of aPL such as aCL and aPS in the occurrence of recurrent abortion.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of anticardiolipin antibodies and antiphosphatidylserine antibodies in women with recurrent abortion

Velayuthaprabhu

Archunan

2005

Indian J Med Sci

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BACKGROUND: Antiphospholipid syndrome (APS) is a major reproductive complication in women, which is characterized by recurrent fetal loss, thrombosis, and thrombocytopenia in association with anticardiolipin antibodies (aCL). AIMS: To analyze the prevalence of aCL and antiphosphatidylserine antibodies (aPS) in relation to pregnancy failures in women with the history of recurrent spontaneous abortion. SETTINGS AND DESIGN: A sequential study of 155 patients, who had three or more recurrent spontaneous abortions, was carried out. METHODS AND MATERIALS: Women with unexplained recurrent pregnancy loss in first trimester were selected for this study. Anticardiolipin antibodies IgG and aPS IgG were detected in the serum by the enzyme linked immunosorbent assay method. STATISTICAL ANALYSIS: Percentage calculation was carried out. Two-tailed t-test was performed to know the significance of aCL and aPS total population. RESULT: The levels of aCL IgG and aPS IgG were detected as 40% (62) and 19% (18), respectively in women with history of recurrent abortion. CONCLUSION: Anticardiolipin antibody is found to be the most important factor for recurrent abortion. In addition, women with negative aCL are having positive for another antiphospholipid antibodies like aPS, which may involve in recurrent abortion.

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“…It has been suggested that the inhibition of KKS may be a risk factor for early gestation losses[144]. The plasma KKS may contribute to the pathogenesis of pregnancy-induced hypertension (preeclampsia).…”

Section: Role Of the Plasma Kks In Cardiovascular Abnormalitiesmentioning

confidence: 99%

Human Plasma Kallikrein-Kinin System: Physiological and Biochemical Parameters

Bryant

Shariat‐Madar²

2009

CHAMC

116

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The plasma kallikrein-kinin system (KKS) plays a critical role in human physiology. The KKS encompasses coagulation factor XII (FXII), the complex of prekallikrein (PK) and high molecular weight kininogen (HK). The conversion of plasma to kallikrein by the activated FXII and in response to numerous different stimuli leads to the generation of bradykinin (BK) and activated HK (HKa, an antiangiogenic peptide). BK is a proinflammatory peptide, a pain mediator and potent vasodilator, leading to robust accumulation of fluid in the interstitium. Systemic production of BK, HKa with the interplay between BK bound-BK receptors and the soluble form of HKa are key to angiogenesis and hemodynamics. KKS has been implicated in the pathogenesis of inflammation, hypertension, endotoxemia, and coagulopathy. In all these cases increased BK levels is the hallmark. In some cases, the persistent production of BK due to the deficiency of the blood protein C1-inhibitor, which controls FXII, is detrimental to the survival of the patients with hereditary angioedema (HAE). In others, the inability of angiotensin converting enzyme (ACE) to degrade BK leads to elevated BK levels and edema in patients on ACE inhibitors. Thus, the mechanisms that interfere with BK liberation or degradation would lead to blood pressure dysfunction. In contrast, anti-kallikrein treatment could have adverse effects in hemodynamic changes induced by vasoconstrictor agents. Genetic models of kallikrein deficiency are needed to evaluate the quantitative role of kallikrein and to validate whether strategies designed to activate or inhibit kallikrein may be important for regulating whole-body BK sensitivity.

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Antiphospholipid Antibodies and Kininogens in Pathologic Pregnancies: A Review

Abstract: Because kallikrein-kinin system may play an important role in pregnancy especially in fetoplacental unit, disruption of this system may be a risk factor for early gestational losses.

Cited by 20 publications

References 62 publications

Some Recent Insights into the Prothrombogenic Mechanisms of Antiphospholipid Antibodies

Some Recent Insights into the Prothrombogenic Mechanisms of Antiphospholipid Antibodies

Evaluation of anticardiolipin antibodies and antiphosphatidylserine antibodies in women with recurrent abortion

Human Plasma Kallikrein-Kinin System: Physiological and Biochemical Parameters

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