First trimester serum inhibin A in normal pregnant women

Objectives To establish reference ranges for maternal serum inhibin A in normal first trimester pregnant women. Materials and methods This was a cross-sectional study. We measured maternal serum inhibin A in normal pregnant women gestation age between 6⁺⁰ and 14⁺⁶ weeks using the enzyme-linked immunosorbent assay (ELISA) method. Maternal serum inhibin A was analyzed according to gestational ages (GA). Results Serum of 300 pregnancies was analyzed and the outcome demonstrated the median of maternal serum inhibin A according to gestational age. The levels of maternal serum inhibin A during the 6⁰–6⁺⁶ week of gestations are lowest when compared with other gestational age. The levels of maternal serum inhibin A during 9⁰–9⁺⁶ week of gestations are maximal. Maternal serum inhibin A then declined until 14 weeks of gestation. Conclusion Serum inhibin A can be measured during the first trimester of pregnancy by using the recent ELISA technique. Our reference ranges might be useful for further studies, such as prediction of adverse pregnancy outcome in threatened abortion.     

Serum levels of apelin,salusin-alpha and salusin-beta in normal pregnancy and preeclampsia

Objective: The purpose of this study was to investigate the relationship between the serum apelin, salusin-alpha and salusin-beta levels and preeclampsia. Method: Twenty-one healthy pregnant women (control group) and 48 patients with preeclampsia (study group) were included in the study between August 2010 and February 2011. Serum apelin, salusin-alpha and salusin-beta levels of the groups were compared. Results: The patients in the study group were divided into two categories: mild preeclampsia and severe preeclampsia. The mild preeclampsia group consisted of 31 patients, and the severe preeclampsia group consisted of 17 patients. Serum salusin-alpha and salusin-beta levels of the control and study groups were not significantly different (p > 0.05). Apelin levels were statistically significantly higher in the study group. No statistically significant difference was detected between the mild and severe preeclampsia groups in terms of the mean serum apelin levels. Conclusion: The serum levels of apelin were higher in the pregnant women with preeclampsia; however, there was no positive relationship between serum salusin-alpha and salusin-beta levels and the disease. Larger prospective studies are needed to validate our findings.     

Maternal and cord blood cyclophilin A in severe preeclampsia and normal pregnancy and its correlation with vitamin D and zinc

Objective: To investigate maternal and cord blood cyclophilin A level in severe preeclampsia compared with normal pregnancy and its correlation with vitamin D and zinc level.

Methods: We conducted a cross-sectional observational study of pregnant women who gave birth in Cipto Mangunkusumo Hospital between January and April 2014.

Results: Thirty-nine subjects were included. Subjects with severe preeclampsia have higher serum cyclophilin A levels compared with normotensive pregnancy (1299.60 vs. 1039.50; p 0.017). Maternal cyclophilin A, vitamin D, and zinc correlation were not statistically significant (p 0.189 & p 0.853).

Conclusion: Cyclophilin A levels in severe preeclampsia is higher compared to normal pregnancy. There is no correlation between cyclophilin A, zinc, and vitamin D.     

Genetic predisposition to elevated levels of C-reactive protein is associated with a decreased risk for preeclampsia

Objective: To examine the association between genetic predisposition to elevated C-reactive protein (CRP)and risk for preeclampsia using validated genetic loci for C-reactive protein. Methods: Preeclampsia cases (n = 177) and normotensive controls (n = 116) were selected from live birth certificates to nulliparous Iowa women during the period August 2002–May 2005. Disease status was verified by the medical chart review. Genetic predisposition to CRP was estimated by a genetic risk score on the basis of established loci for CRP levels. Logistic regression analyses were used to evaluate the relationships between the genotype score and preeclampsia. Replication analyses were performed in an independent, US population of preeclampsia cases (n = 516) and controls (n = 1,097) of European ancestry. Results: The genetic risk score (GRS) related to higher levels of CRP demonstrated a significantly decreased risk of preeclampsia (OR 0.89, 95% CI 0.82–0.96). When the GRS was analyzed by quartile, an inverse linear trend was observed (p = 0.0006). The results were similar after adjustments for the body mass index (BMI), smoking, and leisure-time physical activity. In the independent replication population, the association with the CRP GRS was also marginally significant (OR 0.97, 95% CI 0.92, 1.02). Meta-analysis of the two studies was statistically significant (OR 0.95, 95% CI 0.90, 0.99). Conclusion: Our data suggest an inverse, counterintuitive association between the genetic predisposition to elevated levels of CRP and a decreased risk of preeclampsia. This suggests that the blood CRP level is a marker of preeclampsia, but it does not appear to be a factor on the causal pathway.     

Toremifene use does not alter serum inhibin A and B levels during mid-luteal phase in women with premenstrual mastalgia

Aims.?To find out if there is any link between the therapeutic effect of toremifene on premenstrual mastalgia and luteal phase serum inhibin A and/or B levels.

Methods.?Forty-eight patients participating in a randomized cross-over trial on toremifene vs. placebo for premenstrual mastalgia gave three blood samples during the luteal phase of the menstrual cycle: the first at baseline, the second during the third toremifene/placebo cycle, and the third during the third placebo/toremifene cycle, respectively. The blood samples were analyzed for inhibin A and B with respective specific two-site enzyme-linked immunosorbent assays. Toremifene (20?mg/d) and placebo were administered during the luteal phase only.

Results.?When all the toremifene-treated cycles were compared with all the placebo cycles and with the baseline, the median inhibin A levels were 42, 38, and 40?pg/ml, respectively (baseline versus toremifene, p?=?0.638; baseline versus placebo, p?=?0.468; and toremifene versus placebo, p?=?0.365). The median inhibin B levels were at baseline 19?ng/l, during placebo 20?ng/l, and during toremifene 17?ng/l (baseline versus toremifene, p?=?0.983; baseline versus placebo, p?=?0.519; and toremifene versus placebo, p?=?0.880).

Conclusion.?A luteal administration of toremifene does not seem to result in any changes in mid-luteal concentrations of inhibin A or B in serum.     

Placental miR-1301 is dysregulated in early-onset preeclampsia and inversely correlated with maternal circulating leptin

Introduction

miRNAs are small non-coding RNAs important for the regulation of mRNA in many organs including placenta. Adipokines and specifically leptin are known to be dysregulated in preeclampsia, but little is known regarding their regulation by miRNAs during pregnancy.

Methods

We performed high-throughput sequencing of small RNAs in placenta from 72 well-defined patients: 23 early-onset preeclampsia (PE), 26 late-onset PE and 23 controls. The regulation of some miRNAs was confirmed on qRT-PCR. Maternal circulating levels and placental mRNA of leptin, resistin and adiponectin were measured using Bio-Plex and qRT-PCR.

Results

We found that miR-1301, miR-223 and miR-224 expression was downregulated in early-onset PE, but not in late-onset PE, compared to controls. In silico analysis predicted the leptin gene (LEP) to be a target for all three miRNAs. Indeed, we found significant correlation between maternal circulating levels of leptin and placental LEP expression. In addition, we found a significant inverse correlation between maternal circulating leptin/placental LEP expression and placental miR-1301 expression levels. Interestingly, placental expression of miR-1301 was also correlated with newborn weight percentile and inversely correlated with both maternal systolic and diastolic blood pressure prior to delivery.

Discussion

Our results confirm that placenta is a major site of LEP expression during pregnancy. It further suggests that miR-1301 could be involved in the regulation of leptin during pregnancy and may play a role in early-onset PE.

Conclusions

miR-1301 is dysregulated in early-onset preeclampsia and could possibly play a role in the regulation of leptin during pregnancy.     

Raised maternal serum inhibin A concentration at 10 to 14 weeks of gestation is associated with pre-eclampsia

Maternal serum inhibin A and free β human chorionic gonadotrophin (β-hCG) were measured in 759 chromosomally normal, pregnant women at 10–14 weeks of gestation. There were nine who subsequently developed pre-eclampsia and in these women the maternal serum inhibin A concentration was significantly higher than in the normotensive controls.     

The reduction of melatonin levels is associated with the development of preeclampsia: a meta-analysis

Objective: The aim of this analysis was to demonstrate the association between melatonin levels and the development of preeclampsia.

Methods: Standardized mean difference (SMD) with 95% confidence interval (CI) was calculated using a random effects model.

Results: The pooled SMD between case and control was 1.40 (95% CI: 0.26, 2.55; P = 0.02). And the pooled SMD between mild PE and severe PE was 5.25 (95% CI: 1.5, 9.01; P = 0.006).

Conclusion: The meta-analysis illustrated that melatonin concentration was significantly lower in women with preeclampsia, and correlated with the severity of the disease.     

Placental perfusion in normal pregnancy and early and late preeclampsia: A magnetic resonance imaging study

Objective

Our primary aim was to investigate if women with early or late preeclampsia have different placental perfusion compared with normal pregnancies. A secondary aim was to investigate if placental perfusion changes with increasing gestational age in normal pregnancy.

Methods

The study population included thirteen women with preeclampsia (five with early and eight with late preeclampsia) and nineteen women with normal pregnancy (ten with early and nine with late pregnancy). Early was defined as <34 weeks and late as ≥34 weeks gestation. All women underwent a magnetic resonance imaging (MRI) examination including a diffusion weighted sequence at 1.5 T. The perfusion fraction was calculated.

Results

Women with early preeclampsia had a smaller placental perfusion fraction (p = 0.001) and women with late preeclampsia had a larger placental perfusion fraction (p = 0.011), compared to women with normal pregnancies at the corresponding gestational age. The placental perfusion fraction decreased with increasing gestational age in normal pregnancies (p = 0.001).

Conclusion

Both early and late preeclampsia differ in placental perfusion from normal pregnant women. Observed differences are however in the opposite direction, suggesting differences in pathophysiology. Placental perfusion decreases with increasing gestational age in normal pregnancy.     

Serum inhibin A, inhibin B, and pro-alphaC levels are altered after surgically or pharmacologically induced menopause

OBJECTIVE: To evaluate the course of changes in serum inhibin A, inhibin B, and pro-alphaC levels in women with surgically or pharmacologically induced menopause. DESIGN: Longitudinal study. SETTING: Academic Health Center of Siena, Siena, Italy. PATIENT(S): Four groups of women were studied: [1] surgical menopause including bilateral oophorectomy (n = 15), [2] amenorrhea induced by GnRH-analogue for treatment of endometriosis (n = 13), [3] amenorrhea induced by antineoplastic chemotherapy before (n = 15) and after chemotherapy (n = 13), and [4] control physiological menopause (n = 67). INTERVENTION(S): Collection of blood specimens. MAIN OUTCOME MEASURE(S): Serum inhibin A, inhibin B, and pro-alphaC concentrations were measured by using specific two-site ELISAs. RESULT(S): Following oophorectomy, serum inhibin A, inhibin B, and pro-alphaC levels were decreased on the first postoperative day; on the fifth postoperative day they were still significantly reduced. Women with amenorrhea induced by GnRH-analogue treatment exhibited serum inhibin A and pro-alphaC levels that were significantly higher than those observed in physiological menopause. Patients undergoing antineoplastic chemotherapy had higher serum inhibin A levels than those in physiological menopause, whereas inhibin B and pro-alphaC levels did not differ. During the course of chemotherapy, median serum inhibin A concentrations were similar to those of patients evaluated after the suspension of treatment. In postmenopause, inhibin A, and inhibin B levels were low, whereas levels of pro-alphaC were still detectable. CONCLUSION(S): Circulating levels of inhibin A, inhibin B, and pro-alphaC are reduced after oophorectomy. Women with amenorrhea induced by GnRH-analogue treatment or by antineoplastic chemotherapy still produce inhibin A and pro-alphaC. This probably reflects a residual ovarian function and hormone synthesis. Therefore, the ovary may be a source of pro-alphaC after menopause; significant amounts of pro-alphaC are present in circulation after natural menopause, but not after oophorectomy.     

Spontaneous liver hematoma in pregnancy not clearly associated with preeclampsia: A case presentation and literature review

Spontaneous liver hemorrhage with formation of subcapsular hematomas and rupture of Glissan's capsule is a rare but often lethal complication of pregnancy. This entity has usually been associated with severe preeclampsia or the HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome. A case of spontaneous subcapsular hematoma of the liver occurring in the third trimester is presented in which the patient probably had neither preeclampsia nor the HELLP syndrome. The literature on liver hematomas in pregnancy published since 1982 when the term HELLP syndrome was coined is reviewed with a focus on the association of liver hematomas with preeclampsia and the HELLP syndrome. Therapy and maternal and neonatal outcomes for this entity are reassessed. (Am J Obstet Gynecol 1997;176:1328-33)     

Early-onset preeclampsia is associated with perinatal mortality and severe neonatal morbidity

Objective: To evaluate neonatal outcomes of pregnancies complicated by early-onset preeclampsia (PE) and compare these outcomes to those of gestational age matched neonates born to mothers whose pregnancy was not complicated by early-onset PE.

Methods: We analyzed the outcome in 97 neonates born to mothers with early-onset PE (24–32 weeks amenorrhea at diagnosis) and compared it to that of 680 gestational age-matched neonates born between 25–36 weeks due to other etiologies and admitted to the Neonatal Intensive Care Unit (NICU) of a tertiary referral hospital in the Netherlands. We used Chi-square test, Wilcoxon test, and logistic regression analyses.

Results: Neonates born to PE mothers had a higher perinatal mortality (13% vs. 7%, p?=?0.03) and infant mortality (16% vs. 9%, p=?0.03), a 20% lower birth weight (1150 vs. 1430?g, p<0.001), were more often SGA (22% vs. 9%, p?Conclusions: Overall adverse perinatal outcome is significantly worse in neonates born to mothers with early-onset PE. The effect of early-onset PE on perinatal mortality seems partially due to SGA. Whether these differences are due to uteroplacental factors or intrinsic neonatal factors remains to be elucidated.