Uterine arteriovenous malformations are uncommon but potentially life-threatening conditions. They can be congenital or acquired and should be suspected in cases of severe or persistent uterine bleeding. In recent years, there has been an in­creasing number of reports of acquired vascular lesions of the uterus following pregnancy, abortion, caesarean delivery and curettage. This paper presents the review of the literature considered epidemiology, pathophysiology, diagnostic methods and treatment options. Unexplained uterine bleeding should be always an indication for colour Doppler ultrasonography and the presence of arteriovenous malformation should be always excluded. Uterine arteriovenous malformations are uncommon but potentially life-threatening conditions. They can be congenital or acquired and should be suspected in cases of severe or persistent uterine bleeding. In recent years, there has been an in­creasing number of reports of acquired vascular lesions of the uterus following pregnancy, abortion, caesarean delivery and curettage. This paper presents the review of the literature considered epidemiology, pathophysiology, diagnostic methods and treatment options. Unexplained uterine bleeding should be always an indication for colour Doppler ultrasonography and the presence of arteriovenous malformation should be always excluded.

There are many theories regarding the ultimate cause of pre-eclampsia, and nowadays it is thought that the mechanism of pathogenesis is most likely multifactorial. The pathophysiology probably involves both fetal or placental and maternal factors. The most likely relevant factors in the pathogenesis are the abnormal development of the placenta, systemic endothelial dysfunction or cell activation, and an imbalance between pro-angiogenic and anti-angiogenic proteins with a predominance of antiangiogenic factors. In women with pre-eclampsia, placental tissue overproduces two main anti-angiogenic proteins which enter into the maternal circulation: soluble Fmssuch as tyrosine kinase 1 (sFlt1 or sVEGFR1) and soluble endoglin (sEng). Moreover, these patients have low circulating blood levels of two pro-angiogenic peptides: placental growth factor (PlGF) and vascular endothelial growth factor (VEGF). Adequate levels of CECs (circulating endothelial cells), EPCs (endothelial progenitor cells) and microparticles most likely play an important part in the development and regulation of vascularization in pregnancy but the exact role of these cells and micropatticles in the pathogenesis of pre-eclampsia is unknown. Some imbalances in these levels are associated with endothelial insufficiency.

Purpose The diminished function of 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) was found in placentae from preeclamptic pregnancies. Here, we examine the overall maternal glucocorticoid balance in pregnancy-related hypertension. We aim to answer the question if the functions of primary enzymes involved in cortisol metabolism: 11β-HSD1 and 11β-HSD2 and 5-reductases (both 5α- and 5β) are altered in the course of hypertensive pregnancy. Methods We determined plasma and urinary cortisol and cortisone as well as their urinary tetrahydro- and allo-tetrahydrometabolites, both in free and conjugated forms in samples obtained from 181 Polish women in the third trimester of pregnancy. We compared steroid profiles in women with preeclampsia (PE), gestational hypertension (GH), chronic hypertension (CH) and in normotensives (controls). Results We found significant differences in glucocorticoid balance in pregnancy-related hypertension. Plasma cortisol to cortisone was significantly lower in PE than in controls (3.00 vs. 4.79; p < 0.001). Increased function of renal 11β-HSD2 in PE and GH was manifested by significantly lower urinary free cortisol to cortisone ratio (0.169 and 0.206 vs. 0.277 in controls; p < 0.005). Markedly enhanced metabolism of cortisol was observed in pregnancy-related hypertension, with no significant alterations in CH, and the changes were more clearly expressed in PE than in GH. Conclusions The glucocorticoid balance in PE and GH is shifted towards decreasing cortisol concentration either due to intensified conversion to cortisone or enhanced production of tetrahydro and allo-tetrahydrometabolites.

Background: The analysis of steroids in biological matrices is challenging. One can apply immunoassay as well as gas and liquid chromatography with various types of detection, depending on the available equipment and the experience of the analyst. The question is how the methods are interchangeable between themselves. Doubts were reported having compared immunoassays and chromatography-mass spectrometry, but there are scarce data on chromatographic methods with detection types other than mass spectrometry. Methods: Here, we present the detailed comparison of two liquid chromatographic methods for the determination of free urinary cortisol and cortisone: one with fluorescence detection (high-performance liquid chromatography [HPLC-FLD]) and the other with tandem mass spectrometry (HPLC-MS/MS). The comparison was made with 199 human urine samples. The data analysis included Passing–Bablok and Deming regression, Bland–Altman test, Wilcoxon test, mountain plot and Lin’s concordance correlation coefficient. Results: The validation data indicated that both methods met the requirements of the European Medicines Agency. However, the statistical analysis revealed the systematic bias between the two assays. The Passing–Bablok and the Deming tests showed that the HPLC-FLD method overestimated results for cortisol and underestimated measurements for cortisone. The Bland–Altman analysis estimated the mean differences between the methods: 18.8 nmol/L for cortisol and −16.9 nmol/L for cortisone measurement. Conclusions: Both methods’ results led to the same conclusion in observational studies, but the techniques are not interchangeable. The literature data, the observations from the clinical setting and our experience clearly indicate that the future of steroid measurements will belong to chromatography coupled with mass spectrometry.