Preeclampsia is a multisystem disorder of pregnancy that remains a leading cause of maternal and foetal morbidity and mortality. It is still an underestimated risk factor for future cardiovascular, cerebrovascular, and kidney disease, developing often in the perimenopausal period of a woman’s life. It remains unclear whether preeclampsia is an individual risk factor for future cardiovascular, cerebrovascular, and renal events or an early marker of women with high-risk profiles for these diseases. Risk factors for cardiovascular disorders and preeclampsia are very similar and include the following: obesity, dyslipidaemia, insulin resistance, pro-inflammatory and hypercoagulable state, and endothelial dysfunction. Thus, the pregnancy can only be a trigger for cardiovascular alterations that manifest in development of preeclampsia. On the other hand, there is strong evidence that changes in cardiovascular, endothelial, and metabolic systems occurring in the course of preeclampsia may not fully recover after delivery and can be a cause of future disease, especially in the presence of other metabolic risk factors regarding, for example, perimenopause. In this review the authors present current knowledge about short- and long-term maternal consequences of preeclampsia, such as: cardiovascular disease, cerebrovascular incidents (posterior reversible encephalopathy and stroke), kidney injury (including the risk of end-stage renal disease), liver failure, and coagulopathy (thrombocytopenia and disseminated intravascular coagulation).

To assess the effect of lead exposure from cigarette smoke on fetal growth, blood lead concentrations were measured using inductively coupled plasma mass spectrometry in 150 healthy pregnant women. Mean lead concentrations in plasma and whole blood were significantly higher in the smoking group compared with the nonsmoking group in each trimester of pregnancy (p < 0.001). Logistic regression analysis showed the highest impact of the number of cigarettes smoked per day for serum lead concentration (β = 0.238; p < 0.05), while in whole blood, it was duration of smoking before conception (β = 0.297; p < 0.001). Birth weight of the smoking mothers' infants was significantly lower (mean ± SEM, 3,192 ± 50.8 and 3,569 ± 49.6 g, respectively; p < 0.001) and negatively correlated with lead levels in plasma (r = −0.38; p < 0.001) and in whole blood (r = −0.27; p < 0.001). Therefore, it is suggested that smoking during pregnancy increases lead concentrations in maternal blood. Fetal exposure to low doses of lead in utero may be a serious risk factor causing lower birth weight.

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Preeclampsia affects about 3–8% of all pregnancies. It represents a complex and multifaceted syndrome with at least several potential pathways leading to the development of disease. The main dogma in preeclampsia is the two-stage model of disease. Stage 1 (placental stage) takes place in early pregnancy and is thought to be impaired placentation due to inadequate trophoblastic invasion of the maternal spiral arteries that leads to reduced placental perfusion and release of numerous biological factors causing endothelial damage and development of acute maternal syndrome with systemic multiorgan failure (stage 2—the onset of maternal clinical symptoms, maternal stage). Recently, in the light of the vast body of evidence, two-stage model of preeclampsia has been updated with a few novel pathways leading to clinical manifestation in the second part of pregnancy. This paper reviews current state of knowledge about pathophysiology of preeclampsia and places particular focus on the recent advances in understanding of uterine artery remodeling alterations, as well as the role of microRNAs in preeclampsia.

Purpose To establish the surgical, demographic and histopathological factors associated with inaccurate sentinel lymph nodes (SLNs) identification using indocyanine green (ICG) and near-infrared (NIR) fluorescence imaging in uterine and cervical neoplasms during both open and laparoscopic surgery. Methods We reviewed patients with atypical endometrial hyperplasia (AEH), clinical stage I and II cervical cancer or uterine malignancies who underwent primary surgery with SLN mapping between September 2015 and January 2018. An analysis of patients’ demographics, tumor factors and surgical approach was conducted. Bilateral and overall detection rates were calculated and univariate analysis was performed to estimate factors associated with failed SLN mapping. Results A total of 32 patients with uterine and cervical neoplasms were included in the study. The overall detection rate of the SLN was 84% and bilateral detection rate was 75%. There were no statistically relevant differences in overall and bilateral SLN detection rates by BMI, surgical approach or age. Regarding endometrial cancer, there were no differences in SLN detection rates when comparing tumor grade, histology nor myometrial invasion. For SLN detection failure, only the presence of metastatic lymph nodes and lack of surgical experience significantly increased the disability to detect SLNs ( p = 0.03, p = 0.04, respectively). Conclusions SLN mapping technique using NIR fluorescence imaging with ICG appears to be accurate method in most of the patients with cervical or endometrial carcinoma, regardless of demographic characteristics, tumor-related features and surgical approach. Surgeons’ expertise in that field allows obtaining excellent detection rates.

To estimate the effect of tobacco smoking on iron homeostasis and the possible association between hepcidin and the neonatal birth weight and length, concentrations of serum hepcidin and selected iron markers were measured in 81 healthy pregnant women (41 smokers and 40 nonsmokers). The smoking mothers had significantly lower concentrations of serum hepcidin (p < 0.001), iron (p < 0.001), and hemoglobin (p < 0.05), but higher erythropoietin (p < 0.05) levels compared with non-smoking pregnant women. Logistic regression analysis showed the highest negative impact of the number of cigarettes smoked per day (β = −0.46; p < 0.01) and positive impact of ferritin level (β = 0.47; p < 0.001) on serum hepcidin concentration. The birth weight and the body length of smoking mothers’ infants were significantly lower than in tobacco abstinent group (p < 0.001). In multiple regression analysis, birth body weight (β = 0.56; p < 0.001) and length (β = 0.50; p < 0.001) were significantly related to maternal hepcidin values. Tobacco smoking affected hepcidin level in serum of pregnant women in a dose-dependent manner. Low concentrations of iron and hemoglobin in maternal serum coexisting with high level of erythropoietin suggest that smoking could lead to subclinical iron deficiency and chronic hypoxia not only in mothers but also in fetus. Low serum hepcidin concentration in smoking pregnant women might be associated with lower fetal birth weight and length.

A tumor growth depends on the potency of the tumor to support itself with nutrients and oxygen. The development of a vascular network within the tumor is key to its survival. The permanent contest between the tumor and its host involves tumor cells on one side and an immunological system and tissue stroma on the other. The angiogenesis is not only a specialty of the tumor, but it also depends on this complex multidirectional interaction. The most common gynecological cancers, cervical, endometrial and ovarian carcinoma are good examples for studying this problem. In this review, we aim to show that an inflammatory response against a tumor can be reverted into an undesirable process leading to the development of a vascular network within the tumor and, subsequently, further growth of the tumor and progression of a disease. Therefore, a key for tumor management should be searched within the immunological system, rather than focused on cell cycle and anti-angiogenic treatment only.

Smoking tobacco can impair proper vascular endothelial functioning. This is exhibited through reduced nitric oxide synthesis as well as activity due to accompanying oxidative stress. We examined the relationship between nitric oxide and markers of oxidative stress/antioxidant defense in serum of smoking and non-smoking pregnant women. Subjects included 99 healthy pregnant women, who were tested for nitric oxide (NO), endothelial (eNOS) and inducible (iNOS) nitric oxide synthase, total oxidant capacity (TOC), and total antioxidant capacity (TAC). NO, eNOS, and TAC serum concentrations were significantly lower (p < 0.005), but iNOS (p < 0.05) and TOC (p < 0.001) were higher in smokers than in non-smokers. Multivariate regression analysis showed associations between NO concentration and eNOS, TAC, and smoking status in the whole group of patients. In the model estimated separately for smokers, the highest impact of eNOS (β = 0.375; p = 0.021) and cotinine (β = −0.323; p = 0.037) was indicated for NO concentration. In the model of non-smokers, eNOS (β = 0.291, p = 0.030) and TAC (β = 0.350; p = 0.015) were important for NO level. Smoking during pregnancy could exacerbate oxidative stress, impair the action of nitric oxide synthases, and adversely affect the balance of oxygen and nitrogen metabolism. Relationships between NO concentrations and TAC in the studied women’s blood can confirm the antioxidant nature of nitric oxide.