Influence of Pre-Pregnancy Obesity on Carbohydrate and Lipid Metabolism with Selected Adipokines in the Maternal and Fetal Compartment.

A higher body mass index (BMI) before pregnancy is associated with an increased risk of maternal and perinatal complications. This study aimed to analyze selected parameters of carbohydrate and lipid metabolism, including adipokines, in obese pre-pregnant women, and their influence on the birth weight of newborns. MATERIALS AND METHODS: The study group (O) consisted of 34 pregnant women with higher BMI (obese) before pregnancy. The control group (C) was 27 pregnant women with target BMI and physiological pregnancy. The BMI index: body weight [kg]/(height [m]2 was assessed on the first obstetrical visit. The research material was the serum of pregnant women collected in the third trimester of pregnancy and umbilical cord blood collected immediately after delivery. Selected parameters of carbohydrate and lipid metabolism and adipokines were determined. RESULTS: There were no statistically significant differences between the study group and the control group concerning the concentrations of insulin, glucose, VLDL, adiponectin, TNF-α, HOMA-IR, as well as LDH and cholesterol in maternal blood serum and umbilical cord blood serum. Total cholesterol and HDL in both maternal blood serum and umbilical cord blood were statistically significantly lower than those in the control group. The concentration of triglycerides (TG) and resistin in the blood serum of obese mothers were higher than those in the control group (p < 0.05). However, no statistically significant differences were found between the two groups regarding the concentrations of TG and resistin in the umbilical cord blood. The concentration of LDL cholesterol in the umbilical blood serum in the obese group was statistically significantly lower than that in the control group. The concentration of leptin in maternal blood serum and umbilical cord blood serum in the study group was statistically significantly higher than that in the control group. CONCLUSIONS: Pregestational obesity does not substantially affect the basic parameters of carbohydrate metabolism in pregnant women, but it disturbs the lipid profile, which is manifested by a significant increase in triglycerides and a decrease in the level of HDL cholesterol in the serum. Preexisting obesity increases the concentration of leptin and resistin in the serum of pregnant women, which may be caused by the increased volume of adipose tissue. The concentrations of leptin and resistin in the blood of pregnant women correlate positively, and the concentrations of adiponectin and TNF-α negatively correlate with pre-pregnancy BMI values. There is a positive correlation between the concentration of leptin in the serum of umbilical cord blood and the birth weight of the newborn, which suggests that this parameter contributes to the pathomechanism of macrosomia.

Inter-component immunohistochemical assessment of proliferative markers in uterine carcinosarcoma.

In the scientific literature, a selected number of reports have investigated the impact of proliferative activity on the development and progression of uterine carcinosarcomas (UC). The aim of the present retrospective study was to compare the immunohistochemical proliferation markers [Ki67, proliferating cell nuclear antigen (PCNA), minichromosome maintenance complex component 3 (MCM3), and topoisomerase IIα (topoIIα)] assessment in both components of UC. A total of 30 paraffin-embedded slides of UCs, obtained from patients who underwent surgery between January 1, 2006, and December 31, 2020, were analyzed. Medical records and clinicopathological data of patients were reviewed. Formalin-fixed, paraffin-embedded tissue sections were immunostained with monoclonal antibodies against Ki67, PCNA, MCM3 and topoIIα. Ki67-positive nuclear immunoreactivity was reported in 20 (67%) and 16 (53%) UC carcinomatous and sarcomatous components, respectively. In the epithelial component, Ki67 positive staining was related to the International Federation of Gynecology and Obstetrics (FIGO) stage (P=0.025), and histological grade (G1 vs. G2/G3, P=0.031). Nuclear PCNA reactivity was observed in 18 (60%) and 16 (53%) carcinomatous and sarcomatous components, respectively. Notably, all four cases with omental metastases were PCNA-positive, and a relationship between staining pattern and the existence of metastases was of significant value (P=0.018). MCM3-positive nuclear staining was found nearly twice as high in the carcinomatous (n=19; 63%), compared with the sarcomatous (n=11; 37%) component, respectively, and MCM3 expression in the epithelial component was related to clinical stage (P=0.030), and the existence of omental metastasis (P=0.012). In addition, out of the 30 UCs, 17 (57%) and 13 (43%) showed topoIIα positivity in the carcinomatous and sarcomatous UC components, respectively. A significant relationship between protein immunoreactivity and FIGO stage (P=0.049), and omental metastasis (P=0.026) was revealed to exist. However, no significant differences between expression of proliferation markers and clinicopathological features in the sarcomatous UC component were identified. Finally, a significant correlation between each protein immunohistochemical staining was demonstrated, particularly in the sarcomatous UC component. Collectively, a combined analysis of Ki67, PCNA, MCM3, and topoIIα may provide more detailed information of cell-cycle alterations determining the heterogeneity of uterine carcinosarcomas.

Cytokeratin Expression Pattern in Human Endometrial Carcinomas and Lymph Nodes Micrometastasis: a Mini-review.

Cytokeratins (CKs) are the largest subgroup of intermediate filament proteins, preferentially expressed in epithelial tissues. CKs play a critical role in determining epithelial structural integrity under stressful conditions in addition to their various fundamental functions in cellular proliferation, apoptosis, migration, adherence and molecular signaling. Immunohistochemical CKs staining could be evaluated with a proper comprehension of their task limitations and their association with the normal morphology to avoid misdiagnosis. Herein, we critically review the CKs expression patterns in ECs in relation to clinicopathological features and patients' outcome. We also briefly discussed the recent advantage of CKs immunohistochemical staining in the detection of EC micrometastasis.

Ovarian endometrioma - a possible finding in adolescent girls and young women: a mini-review.

Young girls before menarche or menstruating adolescent women may experience long-term drug-resistant chronic pelvic pain, as well as other symptoms associated with pelvic mass. In such cases, it is of great importance to consider ovarian endometrioma in the differential diagnosis. In general, endometrioma is recognized as an ovarian cyst. However, in most cases, the pathology represents pseudocyst with a partial or complete endometrial-like lining with extraovarian adhesions and endometriotic implants which are likely to occur at the sites of ovarian adhesions and at the ceiling of the ovarian fossa. Ovarian endometriomas occur in 17-44% patients with endometriosis and account for 35% of all benign ovarian cysts. The time span from the onset of menarche to the time of endometrioma formation, which requires surgical intervention, has been evaluated to be a minimum of 4 years. The pathogenesis of early-life endometrioma may be different from other types of endometriosis. Diagnosis is often delayed, especially in adolescents, who tend to wait too long before seeking professional help. The three specific aims of treatment in adolescents with endometriosis and endometriomas are control of symptoms, prevention of further progression of the disease as well as preservation of fertility. Increasing evidence demonstrates association between ovarian endometriosis and ovarian cancer. In the present mini-review, we draw the particular attention of clinicians to such a possibility, even if relatively infrequently reported.

Expression of p53 and selected proliferative markers (Ki-67, MCM3, PCNA, and topoisomerase IIα) in borderline ovarian tumors: Correlation with clinicopathological features.

BACKGROUND: The expression of p53 has been studied not only in primary human ovarian carcinomas, but also in borderline ovarian tumors, however, the results were discordant. Expression patterns of proteins involved in cell proliferation and apoptosis have been investigated in various human neoplasms, including female genital tract neoplasms. OBJECTIVE: The aim of this investigation was to assess the staining pattern and immunolocalization of p53 and selected proliferative markers (Ki-67, MCM3, PCNA, and topoisomerase IIα) in borderline ovarian tumors (BOTs). DESIGN: The study group consisted of 42 women who underwent pelvic surgery between 2006-2015. The median patients' age was 46 years. The immunoperoxidase technique was employed using antibodies against p53, Ki-67, MCM3, PCNA, and topoisomerase IIα. RESULTS: For p53, nuclear expression was observed in BOTs, however, cytoplasmatic immunoreactivity was also detected. Altogether, 25 (60%) tumors demonstrated positive p53 immunostaining, including overexpression found in 6 (14%). There were no significant differences in p53 expression between subgroups of clinicopathological variables. Immunoexpression of Ki-67, MCM3, PCNA, and topoisomerase IIα was nuclear. Ki-67 expression was positive in 12 (29%) cases and there was a trend towards a relationship between patients' age and Ki-67 staining (P=0.08). Interestingly, a significantly higher Ki-67 expression was found in tumors of ≥10 cm in diameter compared to smaller tumors (P=0.008). MCM3 expression was detected in 38 (90%) tumors, and PCNA expression in 28 (67%), yet none of clinicopathological factors was related to them. Topoisomerase IIα expression was present in 14 (33%) cases and, interestingly, its significantly higher expression was observed in BOTs of ≥10 cm in diameter compared to smaller tumors (P=0.008). Moreover, Spearman's correlation revealed highly significant positive associations between Ki-67 and topoisomerase IIα (R=0.403, P=0.008) and Ki-67 and MCM3 (R=0.469, P=0.001). CONCLUSIONS: We report a high positive immunostaining rate for p53, suggesting a role of TP53 alterations in the development of BOTs in humans. The new finding of higher topoisomerase IIα immunostaining positivity in BOTs of ≥10 cm may be clinically relevant and requires further studies on larger patient groups.

The Putative Role of TP53 Alterations and p53 Expression in Borderline Ovarian Tumors - Correlation with Clinicopathological Features and Prognosis: A Mini-Review.

Borderline ovarian tumors (BOTs) represent an independent group among ovarian malignancies, being diagnosed at clinical stage earlier than invasive ovarian carcinomas (OCs) and characterized by a rather favorable outcome after careful surgical management. Data published worldwide showed a substantial discordance of p53 expression in BOTs. The purpose of this work was to present the current status of knowledge on the significance of TP53 gene and p53 protein product alterations in BOTs. In general, higher p53 expression patterns were reported for ovarian malignancies compared to BOTs. Serous, mucinous, and endometrioid BOTs differ substantially in relation to p53 immunostaining, but data concerning the relationship between the protein's immunoreactivity and other clinico-pathological variables are scarce. Finally, reports published to date support the view that TP53 alterations may not be commonly associated with the borderline phenotype of ovarian tumors but they probably occur during the development of invasive OCs. In light of these uncertainties, the impact of TP53 alterations and p53 expression on overall survival in women affected by BOTs requires further multi-institutional studies in large cohorts of patients.

Well-differentiated mucinous uterine adenocarcinoma predominantly diagnosed as adenoma malignum: a case report with an immunohistochemical analysis.

Adenoma malignum (AM), also referred to as "minimal deviation adenocarcinoma", is an extremely uncommon variant of highly-differentiated adenocarcinoma of the uterine cervix. The study presented herein describes a case of uterine AM found out after hysteroscopy. An early-stage, well-differentiated mucinous uterine adenocarcinoma was diagnosed post-operatively. A subsequent immunohistochemical assessment of a panel of antibodies was applied, in order to distinguish between female genital tract malignancies.

Multiple recurrences of early-stage, endometrioid-type G2 endometrial cancer with a long-time follow-up: A case study.

The recurrence after a long-time free period of time, in women primarily operated on for early-stage of endometrial cancer (EC), is a unique phenomenon. Currently, we present the case of a 59-year-old woman with multiple recurrences from the moderately-differentiated, stage Ib, endometrioid-type, uterine cancer. All recurrences were pathologically proven to originate from the primary tumor, and the patient expired 12 years after the primary surgery for disseminated neoplasm. We summarize the current data to give a short overview of the role of late recurrences in women operated on for early-stage EC.

Coexistence of homologous-type cervical carcinosarcoma with endometrioid-type G1 endometrial cancer: a case report with an immunohistochemical study.

Coexistence of two or even more independent primary tumors derived from the female genital tract organs is a unique event. The most common combination is the coexistence of synchronous tumors in the ovary and endometrium. In the present case study, we described a coincidence of homologous-type cervical carcinosarcoma (CS) with endometrioid-type G1 uterine adenocarcinoma (EC) arising on the basis of hyperplastic endometrium. A panel of immunohistochemical markers was applied, either in both CS components or in endometrioid-type EC, to assess possible differences between both uterine malignancies. We also presented a short overview of the coexistence of cervical carcinosarcomas with other female genital tract malignancies.

Conservative management after prenatal ultrasound diagnosis of meconium periorchitis.

Meconium periorchitis is caused by the leakage of meconium from a bowel perforation into the peritoneal cavity via a patent processus vaginalis into the scrotal sac during fetal life or in the early postnatal period. Intrauterine meconium peritonitis causes sterile inflammatory response and calcification. Here, we describe a prenatally diagnosed case of meconium periorchitis. During the ultrasound scan at 29 weeks' gestation, enlargement of the scrotum with many small hyperechogenic masses and normal anatomy of testis was observed. Our case is the 11th prenatally diagnosed case presented in the worldwide literature and the first one described in Poland. This case confirms the latest tendency for the conservative management of meconium periorchitis and an asymptomatic postnatal course.

TGFß-pathway is down-regulated in a uterine carcinosarcoma: a case study.

Data assessing the role of various genetic alterations in uterine carcinosarcoma (CS), particularly the transforming growth factors-ß (TGFß) that play a crucial role in many cellular processes, including proliferation, differentiation, adhesion and migration, are scarce. TGFß exert their effects through specific receptors and associated auxiliary receptors. In the current study, we investigated the expression of TGFß isoforms and their receptors, as well as selected genes in a case of CS. We applied the real-time fluorescence detection PCR method with FAM dye-labeled TaqMan specific probes. In a comparison to the normal counterpart, TGFB1, TGFB2, TGFBRII, TGFBR3, ENG and CD109 were all down-regulated in uterine CS samples at different extents. BIRC5 and hTERT, markers of tumor survival, were up-regulated in CS as compared with normal counterparts. A concomitant increase of the hypoxia marker HIF1A expression pattern was noted, whereas the expression of GPR120, responsible for free fatty acids sensing, was not different in both counterparts evaluated. In conclusion, deregulation of various cellular mechanisms in uterine CS is associated with alterations at many levels - cell growth and proliferation, apoptosis, and impaired response to stimuli from extracellular environment.

p53 is not related to Ki-67 immunostaining in the epithelial and mesenchymal components of female genital tract carcinosarcomas.

Carcinosarcomas (CSs) are composed of two separate histological components and are rare neoplasms of the female genital tract. Therefore, CS pathogenesis has not yet been fully elucidated. In the present study, immunohistochemical techniques were used to determine the role of p53 and Ki-67 overexpression in female genital tract CSs. The study group was comprised of 36 patients with CSs originating from the uterus (n=31), cervix (n=3) and ovary (n=2), as well as 3 metastatic tissues. p53 was overexpressed in the epithelial component of 23 out of 36 (64%) tumors, and in the mesenchymal component of 20 out of 36 (56%) tumors. In both CS components, there was a significant correlation between p53 overexpression and patient age and ovarian metastases. Ki-67 overexpression was detected in the epithelial component in 15 out of 36 (42%) cases, and in the mesenchymal component in 13 out of 36 (36%) neoplasms. There was a significant correlation of p53 overexpression between the carcinomatous and sarcomatous components (R=0.884, P<0.001). A significant correlation was also found in Ki-67 immunoreactivity between the two CS components (R=0.676, P<0.001). However, p53 overexpression was not correlated with Ki-67 immunostaining in both tumor components. In conclusion, based on immunohistochemical results, p53 was overexpressed in more than half of the female genital tract CSs included in the present study, either at the epithelial or mesenchymal component. The correlation between p53 or Ki-67 overexpression in both tumor components supports the combination theory of histogenesis in the majority of these tumors.

Expression of genes coding for proangiogenic factors and their receptors in human placenta complicated by preeclampsia and intrauterine growth restriction.

The aim of the study was to investigate the expression of genes coding for vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) as well as their receptors, fms-like tyrosine kinase receptor 1 (VEGFR-1/Flt-1) and VEGF receptor 2 (VEGFR-2/KDR) in the placentae of patients with pregnancies complicated by preeclampsia (PE) and intrauterine growth restriction (IUGR). Tissue samples were collected from placentae of women with PE (n=31) and IUGR syndrome (n=25) as well as of healthy control women (n=31). Total RNA was extracted and purified, mRNA reversely transcribed, and amplified using real-time PCR. Expression of the examined genes was normalized to ß-actin. Higher levels of PlGF (p<0.001) and Flt-1 (p<0.05) transcription were found in PE placentae compared to normal ones. A positive correlation between PlGF and Flt-1 expression was revealed in the PE patients. In conclusion, the presented data indicate the upregulation of both PlGF and Flt-1 in placentae of women with PE, which could be induced by a pathological process possibly due to endothelial dysfunction.

Valproic acid transfer across human placental cotyledon during dual perfusion in vitro.

Valproic acid (VPA ) is a well-known antiepileptic drug with a significant teratogenic effect when administered during pregnancy. To investigate the transplacental transport of VPA, we used an in vitro experiment of dual perfusion of a human placental cotyledon. Eighteen normal placentas at term were investigated; ten were treated with a therapeutic dose of VPA (initial level at maternal circulation 75 microgram/ml), while the remaining eight were supplied with toxic VPA doses (initial level at maternal circulation 225 microgram/ml). VPA concentrations in fetal compartment were lower than those in the maternal compartment at all timepoints with both doses applied. The maternal and foetal VPA concentrations were stable at 60 min and 120 min for the therapeutic dose of VPA (transfer percentages from the maternal to the fetal circulation were 22.7 +- 9.1 percent and 22.7 +- 7.1 percent, respectively). Interestingly, a significant decrease of VPA level in the maternal perfusate was observed after 120 min due to the slightly higher transfer of the drug to the foetal compartment. In conclusion, our data confirmed an easy and rapid transfer of VPA accross the placental barrier. Since the incidence of congenital malformations in infants correlates positively with VPA concentrations in maternal serum, monitoring of VPA should be mandatory due to possible harmful effects on the foetus.

[Maternal serum concentration of angiogenic factors: PIGF, VEGF and VEGFR-1 and placental volume in pregnancies complicated by intrauterine growth restriction]. / Ocena lozyskowych czynników angiogennych (PIGF, VEGF, VEGF R1) oraz objetosci lozyska w ciazach powiklanych opóznieniem wzrastania wewnatrzmacicznego plodu (IUGR).

INTRODUCTION: Pathomechanism of intrauterine growth restriction is a complex issue, involving many different factors, and is still undergoing an investigation. Improper placental angiogenesis, resulting in placental pathology, is considered to be one of the most important causes of IUGR. Placental vascular growth factors--placental growth factor (PIGF), vascular endothelial growth factor (VEGF) and its receptor (VEGFR-1), are involved in the mechanism of placental vascular development and maternal endothelial function during the pregnancy. AIM: The aim of our study was to evaluate the maternal serum concentration of vascular growth factors (PIGF, VEGF) and their receptor (VEGFR-1), as well as the placental volume in pregnancies complicated by IUGR, and to compare the results with healthy control groups. MATERIAL AND METHODS: 20 patients with intrauterine growth restriction and 18 healthy pregnant women were recruited. Their blood serum samples were assayed for the placental growth factor (PIGF), vascular endothelial growth factor (VEGF) and their receptor (VEGFR-1). These placental factors were measured with the ELISA- method (R@D Systems Kits. In all cases the placental volume was assessed with an ultrasound (Voluson V730 GE) with VOCAL (Virtual Organ Komputer-aided AnaLysis). RESULTS: Our investigation revealed significantly lower maternal serum concentrations of PIGF in pregnancies with IUGR, comparing to the controls in the third trimester. In most cases, VEGF concentrations were undetectable in the maternal serum both, in the second as well as in the third trimester. In the 2nd trimester VEGFR-1 concentrations were statistically higher in the investigated group. In the 3rd trimester the concentrations of VEGFR-1 were higher in the investigated group, but the difference has not achieved the level of statistical importance. The mean placental volume was lower in the investigated group but with not statistical gnificance. CONCLUSIONS: Presented and documented dependencies may indicate the involvement of angiogenic factors in a pathomechanism of intrauterine growth restriction process. It seems that the measurement of placental volume may be useful in IUGR diagnosis. However, it should be a complementary examination only, due to technical limitations.

[Maternal serum concentration of placental growth factor (PIGF) and endothelial growth factor (VEGF) in pregnancies complicated by preeclampsia]. / Ocena stezenia lozyskowego czynnika wzrostu (PlGF) oraz naczyniowego czynnika wzrostu (VEGF) w surowicy krwi ciezarnych z preeklampsja.

UNLABELLED: Preeclampsia is one of the most frequent and dangerous complications of a pregnancy. In preeclamptic pregnancies the spiral arteries are not modified properly. Disturbed blood flow finally leads to hypoxia which is responsible for the dysfunction of the endothelium. Endothelial growth factor (VEGF) and placental growth factor (PIGF) play an important role in the angiogenesis and thus may participate in the pathomechanism of preeclampsia. AIM: The aim of our study was to estimate VEGF and PIGF level in serum of patients with preeclampsia. MATERIALS AND METHODS: The study comprised 25 gravidas with preeclampsia and a control group of 18 healthy gravidas. In 25 preeclamptic women the angiogenic factors levels were measured in the III trimester and in 7 of them in the II trimester. In the control group these parameters were assessed in both periods. Both factors were measured by commercial available ELISA KIT. RESULTS: PIGF concentrations were significantly (p < 0.0001) lower in sera of patients with preeclampsia in the II and III trimester in comparison to the controls: 17.4 vs. 290.3 pg/ml and 99.1 vs. 347.8 pg/ml, respectively. In most cases serum VEGF levels were undetectable. CONCLUSIONS: (1) PIGF is involved in the pathomechanism of preeclampsia and its maternal serum concentration decreases significantly in the course of the disease. (2) The sensitivity of the commercially available ELISA assay is too low to assess the serum VEGF concentration in women with preeclampsia.

[Prevalence of Leptotrichia amnionii sp. nov. in pregnant women]. / Czestosc wyst powania leptotrichia amnionii sp. nov. u kobiet ciezarnych.

INTRODUCTION: Leptotrichia bacteria belong to the group of Gram-negative anaerobes most frequently colonizing the oral cavity and reproductive organs. Leptotrichia sanquigenes constitute one of the bacterial factors in postpartum bacteremia of mothers and newborns, whilst Leptotrichia amnionii sp. nov., described for the first time in 2002, has turned out to be the etiopathogenetic factor in missed abortion in the second trimester of pregnancy. AIM: The purpose of this study was evaluation of the frequency of occurrence of Leptotrichia amnionii sp. nov. in patients in the 1st, 2nd and 3rd trimester of pregnancy. MATERIALS AND METHODS: The study involved 69 patients. Amplification reactions detecting the presence of Leptotrichia amnionii so. RNA in the smears were performed using specific starters complementary to 16SrRNA Leptotrichia amnionii--primer 1 Lam upper and primer 2 Lsp lower--complementary to Leptotrichia 16SrRNA. After amplification, the specimens were placed on 1% agarose gel in the presence of MassRuler marker (Fermentas). Next, PCR products were ligated to pGEM-T Easy Victor and then competent E. coli DH5 alpha cells were transformed with pGEM vector with an insert. Plasmid DNA isolation was performed using Plasmid Mini kit from A&A Biotechnology. Sequencing of inserts from the purified plasmids was performer in Molecular Biology Techniques Laboratory in the Department of Biology at Adam Mickiewicz University in Poznan. RESULTS: In the group of 69 pregnant patients Leptotrichia amnionii sp. nov. was identified in 8 women, which is 11.6%. CONCLUSION: Recently identified Leptorichia amnionii sp. nov. is a bacterie, which relatively frequently occurs in pregnant women.

[Effect of anti-epileptic drugs on human placenta and the fetus]. / Wplyw leków przeciwpadaczkowych na lozysko i plód.

The pregnancy in women with epilepsy is associated with an increased risk of complications and especially with an increased incidence of congenital malformations in offspring. Currently, anti-epileptic drugs (AEDs) are concerned to be a major etiologic factor of abnormal fetal development. The most of AEDs may cross the placenta and reach pharmacologically concentrations in the fetus. Although the pathomechanism of teratogenicity of AEDs is complex and not well understood, a AEDs--dependent folate deficiency is thought as crucial. The reasons may also theoretically include a primary effect of AEDs on placental function and morphology. In the own study on perfused human placental cotyledon, only toxic concentrations of valproic acid caused morphological changes in placental tissue, including microvascular degeneration of cytoplasm, atrophy of syncytiotrophoblast, colliquative necrosis of some mesenchymal cells. The toxic but not therapeutic dose of valproic acid influenced also hormonal function of placenta by lowering of chorionic gonadotrophin concentration in perfusate. Although a knowledge about an influence of AEDs on the placenta and fetus is not complete, the use of these drugs during pregnancy may be more safe. If a dosage of AEDs in pregnant women with epilepsy is reduced to a reasonable minimum and the monotherapy is preferred, the risk of congenital malformations in their offspring can be minimized.

[Urinary N-acetyl-beta-D-glucosaminidase (NAG) excretion in women with pregnancy complicated with hypertension]. / Aktywnosc N-acetylo-beta-D-glukozaminidazy (NAG) w moczu u kobiet w ciazy powiklanej nadcisnieniem tetniczym.

OBJECTIVES: Hypertensive disorders in pregnancy are one of the major mortality risk factors for mother and fetus. Although pathomechanisms of hypertension are extreme complex, the involvement of kidneys usually occurs. N-acetyl-beta-D-glucosaminidase (NAG) is a lysosomal enzyme which is located in renal tubular cells. Therefore an elevation of urinary NAG activity serves as a marker of tubular cell damage. AIM: Evaluation of renal tubular damage in pregnant women with different types of hypertension by determination of urinary NAG activity. MATERIAL AND METHODS: The study comprised 84 pregnant women in third trimester, divided according to type of hypertension into 3 subgroups: pregnancy induced hypertension (n = 58), preeclampsia (n = 13) and chronic hypertension (n = 13). The control group comprised 36 healthy pregnant women. Urinary NAG activity was measured in the second morning urine samples by colorimetric method and the results were expressed as NAG/creatinine ratios (NAG/Cr). RESULTS: The highest NAG/Cr ratios were found in women with preeclampsia (median-1.520 U/mmol) and in women with pregnancy induced hypertension (median-0.874 U/mmol) and both results differed significantly from those in controls (median-0.782 U/mmol). There was slight positive correlation between NAG/Cr ratios and systolic blood pressure (r = 0.225, p < 0.05). CONCLUSIONS: Hypertension in pregnancy may lead to renal tubular damage, however clinical significance of this phenomenon requires further studies.

[Influence of valproic acid (depakine I.V.) on human placenta metabolism--experimental model]. / Wplyw kwasu walproinowego (Depakine I.V.) na metabolizm lozyska ludzkiego w modelu doswiadczalnym.

OBJECTIVES: The pregnancy in women with epilepsy is associated with an increased incidence of congenital malformations in offspring. Currently, anti-epileptic drugs (AEDs) are concerned to be a major etiologic factor of abnormal fetal development but the pathomechanism of teratogenicity of AEDs is complex and not well understood. The purpose of this study was to evaluate an influence of one of the AED-valproic acid (VPA) on placental metabolism (glucose consumption and lactate production). MATERIAL AND METHODS: Term human placental cotyledons were perfused in vitro using a recycling perfusion of maternal and fetal circulations. A total 18 placentas were perfused either with 75 micrograms/ml of VPA (therapeutic dose) or with 225 micrograms/ml of VPA (toxic dose). Eight placentas were perfused with a medium without VPA and served as controls. During 2.5 h of experiment, both maternal and fetal glucose consumption and lactate production were measured every 30 minutes. RESULTS: The introduction of different concentrations of VPA into the perfusion system did not effect placental glucose consumption and lactate production rates in both maternal and fetal compartments. CONCLUSIONS: The teratogenic effect of valproic acid is not associated with metabolic disturbances of glucose or lactate in the placental tissue.