Plasma fibronectin levels and pre‐eclampsia

Akgül, Cemil; Salmayenli, Nihal; Ibrahimoglu, L.

doi:10.1016/0020-7292(94)90180-5

Cited by 4 publications

(6 citation statements)

References 3 publications

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“…Also this decline may be related with oxygen species, plasma mitogenic factor(s), or lipoxygenase products. It has been reported that the activity of reactive oxygen species is increased [1], also that plasma mitogen factor(s) [3,4] and lipoxygenase products [17] increase in preeclampsia. Plasma mitogens can generate reactive oxygen species, which probably activate lipoxygenase enzyme and result in increment of lipoxygenase products.…”

Section: Discussionmentioning

confidence: 99%

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Urinary PGE2 and PGF2α Levels and Renal Functions in Preeclampsia

Vural

Akgül²,

Canbaz³

1998

Gynecol Obstet Invest

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The role of prostaglandin E₂ (PGE₂) and prostaglandin F_2α (PGF_2α) in the pathogenesis of hypertension and altered renal functions, which are the main symptoms of preeclampsia, has gained importance. Serum and urine samples of 59 women (24 preeclamptic pregnant (PEP), 20 normotensive pregnant (NTP) and 15 nonpregnant) were investigated by means of prostaglandin levels and urea, creatinine and creatinine clearance values. PEP patients, when compared with NTP patients, show a significant decrease in PGE₂ and PGF_2α levels (p < 0.01 and p < 0.05, respectively) accompanied by changes in some parameters of renal function such as serum urea, creatinine and creatinine clearance. Although disorders in prostaglandin levels may be responsible for some renal pathologic changes, renal functional and morphologic alterations may also result in abnormal prostaglandin activity.

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Section: Discussionmentioning

confidence: 99%

“…The pathologic mechanism that underlies preeclampsia is unknown and it is possible that the rise in blood pressure is a manifestation of more than one pathophysiologic condition [1][2][3][4]. One of these conditions is related with abnormal prostaglandin action [5,6].…”

Section: Introductionmentioning

confidence: 99%

Urinary PGE2 and PGF2α Levels and Renal Functions in Preeclampsia

Vural

Akgül²,

Canbaz³

1998

Gynecol Obstet Invest

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“…These findings include altered endothelial procoagulant expression, 36 increased concentration of the endothelial pressor, endothelin, [37][38][39][40][41][42][43][44][45][46] increased adhesion molecules [47][48][49] in the circulation, and direct markers of endothelial activation. [50][51][52][53][54][55][56][57][58][59][60][61] Most importantly, several of these markers are increased weeks to months before evident preeclampsia. 35,[62][63][64] On the basis of these findings, the concept that many of the pathophysiological changes of preeclampsia are initiated by altered endothelial function seems reasonable ( Fig.…”

Section: Markers Of Endothelial Activation In Preeclampsiamentioning

confidence: 99%

Endothelial Dysfunction in Preeclampsia

Roberts¹

1998

Semin Reprod Med

551

314

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Several years ago the hypothesis was advanced that alterations of endothelial function could explain much of the pathophysiology of preeclampsia. Since that time, extensive data have been generated to support the hypothesis. Markers of endothelial activation can be demonstrated in women with overt preeclampsia. More importantly, many of these markers precede clinically evident disease and disappear with resolution of the disease. The original postulate was that materials produced by the poorly perfused placenta, which is characteristic of preeclampsia, entered the systemic circulation and altered endothelial cell activity. This was proposed to change vascular sensitivity to circulating pressors, activate coagulation, and reduce vascular integrity resulting in the pathophysiological changes of preeclampsia. As data have accumulated it has become increasingly evident that the insult to the endothelium is neither toxicity nor nonspecific injury but rather can better be characterized as endothelial activation. Candidate molecules have been suggested but not established. It seems likely that the responsible agent(s) will not be unique molecules but rather usual molecules present in excessive amounts. The hypothesis has been expanded to invoke involvement of the maternal constitution in the generation of endothelial injury and injurants. This concept is stimulated by the observation that reduced placental perfusion per se is not sufficient to generate the maternal syndrome. Women with growth-restricted fetuses frequently are not preeclamptic. Placental bed biopsies from not only growth-restricted but also prematurely born infants demonstrate failure of the physiological remodeling of decidual vessels responsible for the reduced placental perfusion of preeclampsia. This has led to the concept that preeclampsia is secondary to an interaction of reduced placental perfusion and maternal factors. Interestingly these maternal factors, obesity, insulin resistance, black race, hypertension, and elevated plasma homocysteine concentration are all risk factors for atherosclerosis in later life.

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“…Akgül and associates (28) prospectively observed 30 pregnant women, seven who developed preeclampsia. They found that the sensitivity and specificity values for elevated plasma fibronectin levels were 100% and 96%, respectively.…”

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confidence: 99%

Third Trimester Maternal Plasma Total Fibronectin Levels in Pregnancy-Induced Hypertension: Results of a Tertiary Center

Aydin¹,

Varol

Sayın

2006

Clin Appl Thromb Hemost

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The aim of this study was to evaluate maternal plasma total fibronectin values in pregnancy-associated hypertension in women in the third trimester of pregnancy. A total of 125 pregnant women at the 24th week of gestation participated in this study. Nonpregnant normotensive women were included as control group (n = 30). Plasma samples for fibronectin were obtained at the 24th, 28th, and 32nd weeks of gestation from all pregnant patients. From this cohort, 10 patients met the criteria for the diagnosis of gestational hypertension and 15 women met the stringent requirements of preeclampsia, whereas 100 patients were normotensive later in gestation. Plasma total fibronectin levels were determined by radial immunodiffusion technique. Data were analyzed using the SPSS program. The mean plasma fibronectin levels of the pregnant women in whom gestational hypertension and preeclampsia developed were significantly higher at the 24th, 28th, and 32nd weeks in comparison to normotensive pregnant women (p < 0.001). However, throughout the period from the 24th to 32nd weeks of pregnancy, plasma total fibronectin levels did not exhibit a significant change in normotensive pregnant patients or in patients with preeclampsia and gestational hypertension. There was also no correlation between plasma fibronectin levels and gestational age, mean arterial pressure, birth weight, and 5-minute Apgar scores in all groups (p < 0.05). The elevated maternal plasma fibronectin level over 40 mg/dL is capable of predicting preeclampsia with a sensitivity of 73% and a specificity of 92%. These results suggest that serial plasma fibronectin measurements before 24 weeks' of gestation may be helpful in the early detection of preeclampsia in normotensive gravid women who are destined to become clinically preeclamptic.

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Plasma fibronectin levels and pre‐eclampsia

Cited by 4 publications

References 3 publications

Urinary PGE<sub>2</sub> and PGF<sub>2α</sub> Levels and Renal Functions in Preeclampsia

Urinary PGE<sub>2</sub> and PGF<sub>2α</sub> Levels and Renal Functions in Preeclampsia

Endothelial Dysfunction in Preeclampsia

Third Trimester Maternal Plasma Total Fibronectin Levels in Pregnancy-Induced Hypertension: Results of a Tertiary Center

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