Iris Publishers_World Journal of Gynecology & Womens Health (WJGWH)

Prevalence of Dyslipidemia among Women with Polycystic Ovary Syndrome Based on Body Mass Index

Abstract

Objective: The purpose of this study was to detect the prevalence of dyslipidemia among polycystic ovary syndrome (PCOS) women with different BMIs.

Study design: We conducted a cross-sectional study whereby one hundred and fifteen women diagnosed with PCOS were recruited from a fertility clinic in a 6-month period. All participants had their weight and height measured and body mass index (BMI) calculated.

Thereafter, they were divided into two groups: normal BMI (BMI ≤25 kg/m2) and high BMI (BMI >25 kg/m2). Fasting blood samples were obtained and total cholesterol, triglycerides, LDL-C, HDL-C, glucose, and insulin levels were measured in both groups. Insulin resistance was calculated using the homeostasis model assessment of insulin resistance (HOMA-IR) equation. Differences in these variables were assessed using the Chi-square test and Fisher’s exact test.

Results: No statistically significant differences were found between both groups of women in terms of total cholesterol, triglycerides, LDL-C, and HDL-C levels. Insulin resistance was significantly more prevalent in the high BMI (78.3%) than in the normal BMI group (59.1%) (P < 0.05).

Conclusions: Dyslipidemia in women with PCOS is not related to their BMI. Early detection and treatment of dyslipidemia in this group of women will protect them from cardiovascular diseases.

Keywords: BMI; Dyslipidemia; Polycystic ovary syndrome; Cardiovascular risk; Atherosclerosis; Dubai

Introduction

Polycystic ovary syndrome (PCOS) is an endocrinological disturbance characterized by menstrual irregularities, androgenic manifestations, and a polycystic morphological appearance of one or both ovaries. It affects 5 to 20% of women of reproductive age [1].

Furthermore, PCOS encompasses a variety of cardiovascular risk factors such as hypertension, dyslipidemia, and hyperglycemia, all of which are characteristics of the so- called “metabolic syndrome.”

The cause of PCOS in not yet clear. However, insulin resistance seems to play a major role in its pathogenesis. Insulin is an essential orchestrator of fat, carbohydrate, and protein metabolism; reduced sensitivity to its effects results in major metabolic disturbances such as defective intracellular glucose transport, lipotoxicity, and ultimately, impaired energy production [2]. In this setting, adiposities retain their sensitivity to insulin action; therefore, lipid deposition continues and results in increased weight gain, which in turn worsens insulin resistance [3].

Impairments in the antioxidant system and accumulation of free radicals could be the spark that triggers inflammation, which in turn result in a plethora of pathogenic phenomena, such as PCOS and dyslipidemia [4].

Dyslipidemia in women with PCOS is a source of concern given its negative effects on cardiovascular health. In the general population, most epidemiological studies show a steady increase in cardiovascular disease when cholesterol levels exceed 5mmol/L [5]. The pathogenesis of dyslipidemia in PCOS has not been fully elucidated; over production of free radicals, defects in lipolysis, glucose receptor abnormalities, insulin resistance, and obesity have all been proposed as possible mechanisms [6].

In the current study, we aimed to evaluate cholesterol and lipoprotein levels among women with PCOS and assessed their relation to body mass index (BMI).

Materials and Methods

Subjects

Women included in this cross-sectional study were randomly selected during their visits to the fertility clinic in Saudi German Hospital in Dubai between August 2018 and February 2019. Participants were included if they had PCOS diagnosed according to Rotterdam criteria [7] and an age between 19 and 42 years. Women with concurrent hypothyroidism, hyperprolactinemia, or hyperandrogenism due to causes other than PCOS were excluded from the study.

The weight and height of each participant were measured (in kilograms and centimeters, respectively), and the participants were categorized into two groups according to their BMI: normal BMI (BMI ≤ 25 kg/m2) and high BMI (BMI > 25 kg/m2).

Blood samples were collected after a 12-hour fast. Total cholesterol, LDL-C, triglycerides, HDL-C, glucose, and insulin were measured.

Cardiovascular risk factors such as hypertension, diabetes mellitus, family history of dyslipidemia, and smoking status were assessed using a questionnaire filled out by the participants.

Laboratory assays

Venous blood samples were centrifuged, and sera were used to assess total cholesterol, LDL-C, and triglycerides using Adevia 1650 biochemical analyzer (Erba Lachema reagents). HDL-C was determined via direct immune-inhibition method. Insulin level was detected using electro-Chemiluminescence immunoassay (ECLIA) (Cobas E, Roche Diagnostics, and Mannheim, Germany). Hexokinase method (Cobas C, Roche Diagnostics GmbH, and Mannheim, Germany) was used to calculate the glucose level. Insulin resistance was calculated using the homeostasis model assessment of insulin resistance (HOMA-IR) equation.

Variable classification

Cholesterol and lipoprotein reference values were based on the American College of Cardiology and American Heart Association recommendations [8]. Abnormal blood levels were considered as follows: total cholesterol > 6.2mmol/L, HDL-C < 1.3mmol/L, LDL-C > 4.1mmol/L, and triglycerides > 2.2mmol/L. Insulin resistance was defined if HOMA-IR exceeded 1.9.

Data analysis

All data were analyzed using IBM-SPSS for Windows version 23.0 (SPSS Inc., Chicago, IL). Categorical variables were crosstabulated to examine independence between variables; for such variables, the Chi-squared test or Fisher’s exact test was used. Frequency tables bar and pie graphs, measures of percentage, tendency, and dispersion were used as descriptive tools. The Mann- Whitney test was used to compare the ages between both groups. A P-value of less than 0.05 was considered significant in all statistical analysis.

Ethical approval

Written informed consent was obtained from all the participants, and the study was approved by the Research Ethics Review Committee of Dubai Health Authority (approval number: DSREC-09/2018_12). The study was carried out in accordance with the code of ethics of the Declaration of Helsinki.

Results

A total of 115 women were included. Thirty-two of them were Emirati (27.8%), and eighty-three (72.2%) were of other nationalities. Forty-five women were grouped as normal BMI, and seventy as high BMI (Figure 1). The average BMI was 27.4kg/m2 (±5.7).

No age difference was observed between both groups.

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Iris Publishers_World Journal of Gynecology & Womens Health (WJGWH)

Updates in the Prevention of Preeclampsia, What’s Beyond Aspirin?

Abstract

Hypertensive disorders of pregnancy are among the most common medical problems during pregnancy and they are associated with significant mortality and morbidity rate. Low dose Aspirin is already approved by many societies like ACOG and WHO to be used as prophylaxis for preeclampsia in high-risk patients. Recent studies showed a possible reduction in the incidence of preeclampsia and intrauterine growth restriction for high-risk mothers who taking LMWH during pregnancy. Although, the published evidence supporting LMWH is characterized by profound heterogeneity and inconsistency in terms of selection criteria and treatment regimens. Antepartum treatment with a combination of LMWH with low-dose ASA is endorsed by the American College of Chest Physicians and The American College of Obstetricians and Gynecologists for treatment of Antiphospholipid syndrome during pregnancy. WHO recommends Calcium as the first nutritional supplementation to prevent preeclampsia among population with low calcium in the diet. Folic acid and statins showed possible reduction in incidence of preeclampsia in high-risk patients but there is a need for further studies to confirm that. Dietary and lifestyle interventions have the potential to reduce the risk of preeclampsia. Both Metformin and vascular endothelial growth factors has promising preventive role that has been found through recent studies.

Keywords: Preeclampsia; Prevention; Hypertensive disorders of pregnancy

Introduction

Hypertensive disorders of pregnancy are among the most common medical problems during pregnancy and they are associated with significant mortality and morbidity rate [1]. They affect 4 % of pregnant women and may cause serious complications like stroke, heart failure, and renal failure [2]. Those diseases are among the top 6 causes of maternal mortality in the USA being responsible for 10% of maternal deaths [3]. They should be considered as a syndrome rather than a single disease entity [4]. Highest mortality rates were found to be related to eclampsia, HELLP syndrome, hemorrhage, delayed diagnosis [5]. The incidence may be affected by parity, socioeconomic level, race, and environmental factors [6]. African Americans have a high incidence of preeclampsia, eclampsia, related maternal mortality [5]. Their incidence has been dramatically increased recently with significant health burden in terms of affection of both mother and fetus health [3]. Having standardized health care for those patients is associated with a significant reduction in both mortality and morbidity [7,8].

Many societies contribute to Classifying hypertensive disorders of pregnancy in order to determine proper management lines and timelines for each category.

Chronic hypertension is defined as systolic BP of 140 or greater Or diastolic BP of 90 or greater Or both on 2 separate occasions at least 4 hours apart, This condition is diagnosed at or before 20 gestational weeks or already documented before pregnancy [9]. However, ACOG suggests that gestational hypertension or earlyonset preeclampsia should be considered if 1st trimester BP measures are within normal range [10]. Gestational hypertension is defined as elevated BP above 140/90 mmHg after 20 weeks at two separate occasions 6 hours apart in the absence of features of severe preeclampsia [11]. Severe gestational hypertension is defined by sustained elevated BP at more than or equal 160/110mmHg [12]. SOMANZ defines preeclampsia with severe features as a unique condition of pregnancy with multisystem effects involving liver, kidney and hematological parameters [13]. ACOG criteria for diagnosis include new-onset hypertension after 20 weeks associated with new-onset proteinuria (>300 mg/24 hours urine collection) [14]. In absence of proteinuria, diagnosis can be made upon presence of gestational hypertension plus any of the following: low platelet count less than 100.000/cc, creatinine level more than 1.1 (double the baseline creatinine level in absence of other renal problem), raised liver enzymes (double baseline), pulmonary edema, visual or cerebral symptoms [15].

Low dose Aspirin is already approved by many societies like ACOG and WHO to be used as prophylaxis for preeclampsia in high-risk patients. In this article, we are going beyond Aspirin to know more updates about other possible prophylactic measures of preeclampsia including Low molecular weight heparin, Calcium, vitamin D, Arginine, statins, and Folic acid.

Pathogenesis

The pathogenesis of preeclampsia is not completely understood despite extensive researches focused on it [16,17]. Placental ischemia remains the most accepted theory that was postulated to explain the pathogenesis of preeclampsia because delivery of the fetoplacental unit remains the main curative line of treatment [17,18]. In addition to that, placental ischemia also explains other complications e.g. IUGR and oligohydramnios. Also, it explains a higher incidence of disease in patients with chronic hypertension, DM and autoimmune diseases. Placental ischemia may explain the effectiveness of both low dose Aspirin and Low molecular weight heparin [19,20]. In normal pregnancy, invasion of uterine arteries to cytotrophoblast causes their transformation from epithelial to endothelial cells with low resistance pressure allowing enough blood supply to fetus through a process called ‘’pseudovasculogenesis’’ [18]. Cytotrophoblast cells initiate migration of extra villous trophoblast to decidua of uterus and invade partially myometrium inducing remodeling of spiral arteries [16]. 2-stage theory has been hypothesized recently to understand this pathology [17,21]. The first stage is abnormal events during embryogenesis of trophoblast which contribute to fetoplacental oxidative distress and abnormal release of antiangiogenetic factors in maternal circulation and subsequent multisystem endothelial dysfunction [17,22]. Abnormal remodeling of spiral arteries and early immunologically mediated events are considered major causes of those events [18]. Moreover, trophoblast fails to adequately invade uterine wall and spiral arteries so subsequently vascular resistance in this area could not be decreased to allow adequate placental transfusion [23]. Also, the failure of obliteration of tunica media of myometrium vessels contributes to inability of placenta to accommodate enough blood supply due to lack of thinning of those vessels [17]. This leads to excessive secretion of sFlt-1 (soluble-fms like tyrosine kinase-1) and soluble endoglin [24]. sFlt-1 binds in the blood to both the vascular endothelial growth factor (VEGF) and the placental growth factor (PLGF). Both sFlt-1 and low VEGF/PLGF play a major role in the development of systematic hypertension [21,24]. Later on, maternal syndrome may occur in terms of vascular endothelial dysfunction, intravascular hypercoagulability, and vasospasm leading to multiple systems dysfunctions [21]. Abnormal vascular changes in placenta are confirmed by histopathological examination of postpartum specimens of placenta which showed vascular infarcts and sclerosis of arterioles [17]. Immunological maternal reaction towards fetal and paternal derived Antigens may also contribute, which is considered a certain type of immunological intolerance [25]. Immunological theory is supported by high serum level of cell-free fetal DNA. This theory has been also postulated to understand pathogenesis of hyperemesis gravidarum [26,27]. Recently genetic factors were found to contribute to preeclampsia; Angiotensinogen gene T235 and Leiden factor deficiency were found to be associated with disease [28]. Also, the higher incidence of preeclampsia was found in trisomy 13 pregnancy than pregnancy with normal karyotyping [29,30]. Interestingly, the gene for sFlt-1 which is known for contributing to preeclampsia is also encoded in chromosome 13q [31].

Low molecular weight Heparin (LMWH)

Recent studies have shown potential reduction in the incidence of preeclampsia and IUGR for high-risk mothers who take LMWH during pregnancy [32]. Since preeclampsia has been hypothesized to be linked to thrombotic and vasoconstrictive events in placenta, It is proposed that LMWH has beneficial effects on certain patients [33]. Examination of the placenta of patients with preeclampsia or restriction of fetal growth after delivery revealed ischemic thrombotic lesions (33). Another research investigated the impact of LMWH on both in vitro and in vivo endothelial functions and reported that pregnant women at high risk of preeclampsia had major cardiovascular abnormalities relative to low-risk women at 24 weeks of gestation, validated by in vivo and in vitro tests [34]. They also reported with proof that LMWH affects the endothelial function and serum level of angiogenic proteins in pregnant women at elevated risk of preeclampsia. In parallel, LMWH also influenced the in vitro endothelial cell function, with significant proangiogenic reactions [34]. Researchers also investigate the effects of low molecular weight heparins (LMWHs) on the invasiveness of extra villous trophoblast and its expression of heparin binding- EGF and cysteine-rich angiogenic inducer 61 (Cyr61) related to the trophoblast invasion process [35], They found that LMWHs are capable of promoting trophoblast development and invasion because they are capable of stimulating the invasive extra villous trophoblast properties that provide a possible biological rationale for the clinical use of LMWH for placental-mediated complications of pregnancy not related to thrombophilia [35]. In addition, low molecular heparin (LMWH) may control invasiveness and placental development of matrix metalloproteinase’s (MMPs) and other tissue inhibitors in vitro trophoblast (36). Heparin greatly improved pro-MMPs and active forms, as well as the invasiveness of extra villous trophoblast and choriocarcinoma cells [37]. Heparin also blocked apoptosis caused by other agents including Staurosporin, kinase inhibitor of broad range, and Thrombin. In addition, Heparin decreased caspase-3 function, a hallmark of apoptosis in first trimester villous and extra villous trophoblast cell lines in human studies [37].

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Iris Publishers_World Journal of Gynecology & Womens Health (WJGWH)

Black Box Warning: Cardiovascular Complications Make Motherhood Unsafe for African American Women

Abstract

Background: In the United States, cardiovascular disease and its complications in pregnancy is the leading killer in mothers. The black maternal mortality rate is quadruple the rate among white women.

Main Body: The reasons for this staggering discrepancy hinge on two central issues: First, black women are more likely to have pre-existing cardiovascular morbidity that increase the risk of maternal mortality. Second, black women are more likely to experience adverse pregnancy outcomes including small for gestational age, gestational diabetes and preeclampsia. These perinatal complications put them at risk for developing long-term cardiovascular disease.

Conclusions: This article is a call to action to recognize that adverse pregnancy outcomes represent an opportunity to intervene in order to change the long-term cardiovascular health of black women.

Keywords: Maternal mortality; Cardiovascular; African American; Blacks; Whites

Abbreviations: APO (adverse pregnancy outcomes); GDM (Gestational Diabetes Mellitus); PTB (Preterm birth); PEC (Preeclampsia); FGR (Fetal growth restriction); IUFD (Intrauterine Fetal Demise).

Background

In the United States, maternal mortality is on the rise. In the United States, the causes of maternal death have shifted over time. While the mortality for haemorrhage, infection and hypertensive disorders of pregnancy have decreased from 1987 to 2005, the incidence of mortality due to cardiomyopathy and cardiovascular conditions has increased. Whereby, cardiovascular causes are now the leading cause of maternal mortality in the United States [1]. Adverse pregnancy outcomes, such as preterm birth, gestational diabetes, preeclampsia, placental abruption and fetal growth restriction, are independent risk factors for the development of long-term cardiovascular disease and are overrepresented in black women [2].

Cardiovascular deaths are the leading cause of maternal mortality and black women are disproportionately affected

Cardiovascular deaths are now the leading cause of maternal mortality in the United States [1]. Contrary to trends in other wealthy nations, maternal mortality is on the rise in the United States. Black pregnant women are four times as likely to die as white women.

Black women are more likely to have existing cardiovascular morbidity that increases the risk of maternal mortality

Pre-existing medical complications such as chronic hypertension and Type 2 diabetes mellitus are more common in obese patients and increase the risk of death. Black women are disproportionately obese and are predisposed to these chronic conditions that often predate pregnancy.

Black women are at higher risk for perinatal complications which lead to the development of cardiovascular disease

Black women are at higher risk for adverse pregnancy outcomes (APO), which increase the risk of developing cardiovascular disease. APO such as preterm birth, gestational diabetes, preeclampsia, placental abruption, and fetal growth restriction are independent risk factors for the development of long-term cardiovascular disease and are essentially a “stress test”. Shown in Figure 1 is the common correlation of cardiac markers in cardiovascular disease sharing similar pathophysiology of perinatal complications.

Women who have delivered preterm have elevated total cholesterol, elevated systolic blood pressure and coronary intimal vessel thickness. Additionally, women who deliver prematurely are more likely to have inflammatory markers such as TNF-alpha and IL-6, both of which are markers for cardiovascular disease [3-5].

Both preeclampsia and coronary artery disease share common biologic markers, including excessive circulation maternal hypertriglyceridemia, free fatty acids, reduced high density lipoprotein, and increased concentration of small LDL and oxidized LDL. Common histopathological features such as foam cells or lipid laden macrophages exist in the spiral arteries of preeclampsia placentas and the vessels of individuals that had fatal coronary artery disease [6].

Gestational diabetes mellitus (GDM) has a higher incidence in minorities, including blacks and Hispanics, versus whites. Over half of women that are diagnosed with gestational diabetes will develop Type 2 diabetes (a cardiovascular risk equivalent) within 10 years of their GDM diagnosis.

Black women are also more likely to have a small for gestational age (SGA) infant, which correlates with an increased risk of both the child and the mother experiencing cardiovascular disease and an increased risk of premature death in the mother.

It’s time to act

Black mothers have an increased risk of dying in the peripartum period and are also at risk of dying in the long term should they develop cardiovascular disease. The United States’ disproportionately high black maternal mortality ratio reflects a lack of appreciation for the significance of the pregnancy co-morbidities of black women in this country. Implementing strategies to improve cardiovascular health before and after pregnancy will likely result in a significant reduction in mortality among black women.

Focusing on black maternal cardiac health may reduce perinatal complications

Cardio-obstetrics is a promising approach that is emerging in many tertiary institutions. This care model uses interdisciplinary teams (Cardiology, Maternal Fetal Medicine, Anaesthesia, Nursing) to care for pregnant patients with heart disease. It focuses on how the pregnancy-associated hemodynamic changes potentially exacerbate cardiac disease. At our institutions, the primary focus of our interdisciplinary team is to reduce cardiac death around the time of labour and delivery and the immediate post-partum period. At Vanderbilt, between October 2016 and August 2019, using a Redcap database, we have used a Cardio-obstetrics model to care for 37 women with significant cardiac disease of which 6/37 self-identified as black. The most common groups of cardiac lesions are valve disease (aortic stenosis, mitral stenosis and pulmonary stenosis) and corrected congenital heart disease (Fontan procedure, arterial switch procedures, and septal closure) accounting for 15/37 or 40% and 12/37 or 32% respectively. Other groups of cardiac lesions include coronary artery disease (5/37 or 13%), pulmonary hypertension/heart failure (3/37 or 8%) and arrhythmias (2/37 or 5%). Black women’s heart lesions (2/group) were distributed evenly amongst heart failure, repaired congenital heart defects, and valve disease. There was 1 maternal death and no black maternal deaths. Historically, high risk cardiac lesions such as aortic stenosis and mitral stenosis carried a maternal death rate of 10% and upwards of 25-50% for pulmonary hypertension. However, this model in our institution has been associated with a maternal mortality of <3%.

While cardio-obstetrics has shown promise for reducing maternal mortality in pregnant patients with known cardiac disease, it does not consider long-term follow-up care for patients who are at greatest risk of cardiovascular complications (i.e., APO) after their pregnancies is completed. We postulate that similar reductions will be observed with black females identified as being high risk for the development of cardiovascular disease if we use that critical period for prevention and intervention.

Collaboration between Maternal Fetal Medicine Specialists and Cardiologists are essential for long-term follow up for at-risk patients

The immediate post-partum period is a critical window to establish long-term care with a cardiologist with expertise on management of cardiovascular risk factors. Treatment of an atrisk black patient has the potential to alter the trajectory of her cardiovascular health. It is important for maternal fetal medicine providers to join forces with cardiology national leadership to enhance the education of primary health care providers in recognizing the implications of pregnancy complications for longterm cardiovascular health, particularly among black women. APO should be a routine part of history-taking and should be factored into the cardiovascular risk score.

Conclusion

Reducing black maternal mortality requires system-level changes, behavioural interventions, and adjustments to clinical care. The cardio-obstetric model has the potential to reduce shortterm mortality in patients with a known history of cardiovascular disease and should be expanded to address the care of women at risk of developing cardiovascular disease long-term. High-risk obstetric providers and cardiologists should join forces leading the way in educating the medical community that APO are associated with cardiovascular complications such as Type 2 Diabetes Mellitus, chronic hypertension, metabolic syndrome and stroke. Pregnant women with elevated cardiovascular risks should have life-long health care.

Similar pathophysiology exists for both clinical entities that lead to adverse perinatal events and cardiovascular events. Abbreviations: GDM (Gestational Diabetes Mellitus), PTB (Preterm birth), PEC (Preeclampsia), FGR (Fetal growth restriction), IUFD (Intrauterine Fetal Demise).

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Fetal Congenital Hepatic Cyst

Introduction

Congenital hepatic cyst is a rare and nonsymptomatic condition in infants. Its incidence is 2.5% in the postnatal life with a much lower incidence in the prenatal period. Incidental finding on antenatal imaging is the most common presentation.

We present a case of a female new-born in which fetal ultrasound detected a cyst within the fetal liver. Postnatal imaging revealed a liver cyst in the right lobe of the liver, fortunately the neonate presented with no other intrahepatic structure affected. Liver function tests were normal and patient was asymptomatic after birth and in further controls. An abdominal ultrasound scan showed a complete disappearance of the cyst by 9 months.

Case Presentation

A 24-year-old female presented to our institution for her prenatal care at her first pregnancy.

At 22 weeks of gestation, a structural fetal sonogram did not report any substantial mass or abdominal disorder (gall bladder was described as visualized).

At 33 + 1 weeks of gestation, a third trimester normal pregnancy evaluation was performed. The exam showed an echogenic structure in the upper right fetal abdomen, showing a dimension of 25 x 27 x 39 mm (Figure 1). No signs of ascitis or any other abdominal organ compromise were noted, including a normal fetal maternal Doppler velocimetry evaluation in a normal growth fetus. The gallbladder appeared unremarkable, with no intrahepatic biliary duct dilatation. A magnetic resonance imaging (MRI) was performed a week after, which confirmed the ultrasound scan diagnosis of congenital hepatic cyst.

The female neonate was uneventful at birth (39 wks. gestation), with an optimal Apgar score and with a birth weight of 3220g. Neonatologist abdominal examination revealed a no distended abdomen, with no masses palpated. On the first day after birth, an abdominal sonogram revealed a hepatic cyst in the right lobe of the liver, measuring 30 x 40 mm. The infant remained asymptomatic and was discharged presenting a hepatic function panel and total bilirubin within normal ranges. The baby was evaluated by the paediatric gastroenterologist who recommended repeating the sonogram to ensure stability. As such, a follow-up sonogram was performed at 6 months of life showing a cyst measuring 21 x 22.5cm in the right lobe of the liver with no increased vascularity. She was re-evaluated by paediatric gastroenterologist at 9 months of age when a new ultrasound was performed, showing the complete disappearance of the simple hepatic cyst.

Comment

The incidence of congenital hepatic cyst in the postnatal life is 2.5%. They are more common in girls, not associated with cysts in other organs, and rarely communicate with the biliary tree [1].

Incidental finding of an asymptomatic lesion on antenatal imaging is the most common presentation of a congenital hepatic cyst. Cholestasis may also be observed in some cases due to the compression of the hepatic parenchyma and the biliary system by a large cyst. Ultrasonography shows the congenital hepatic cyst as an anechoic unilocular fluid-filled space with a posterior acoustic enhancement. Magnetic resonance imaging (MRI) typically reveals a well-demarcated water-attenuated lesion without enhancement after gadolinium with low-intensity signal on T1 and high-intensity signal on T2 images. In our case, MRI was indicated, confirming the fetal US scan findings. Management of congenital hepatic cyst is conservative with periodic ultrasound monitoring to ensure their stability. Regarding surgical interventions, only few infants with simple hepatic cysts required surgical intervention due to gradual enlargement and symptoms, and the others needed no further intervention [2,3]. A simple US scan revealed the fetal hepatic cyst at 9 months extra uterine life in this case.

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Experience in Using Liquid Cytology in the Diagnosis of Endometrial Pathologies

Introduction

The method of liquid Cytology is the most promising in the screening diagnosis of precancerous diseases of the cervix [1]. At the same time, various types of endometrial pathology cannot always be verified based on the results of liquid Cytology, despite its high prognostic value in the diagnosis of endometrial cancer.

Purpose of the Study

The purpose of our study was to compare the histological results of endometrial pathology and conclusions of liquid Cytology diagnostics.

Material and Methods

Sampling of material from the uterine cavity for liquid Cytology was performed according to the standard method in the second phase of the menstrual cycle with the placement of the obtained material in a specific liquid. Diagnostic scraping of the walls of the uterine cavity was performed after taking the material for liquid Cytology [2].

A total of 88 women were examined with suspected endometrial hyperplasia, glandular fibrotic polyp, adenomyosis, chronic endometritis, endometrial adenocarcinoma, and uterine fibroids.

Women with vaginal manipulations, hormone therapy, and recent (within 2 days) sexual contact were excluded from the study, signs of endometritis that use COCA for contraception.

Results

The Average age of the women surveyed was 36.8±1.7 years. All the women had a history of childbirth. Medical abortions in 52 women. Complications after a medical abortion in 18. Uterine fibroids in 20 women.

The coincidence of the cytological conclusion and histological examination was noted in 47 (53.4%) observations. In 41(46.6%) cases, the findings of histological examination and liquid Cytology did not match. Out of 7 cases histologically diagnosed with endometrial adenocarcinoma, the result of liquid Cytology coincided with the histological conclusion only in 3 (42.9%) cases. In the presence of endometrial hyperplasia (37 cases), according to histological research, the identical pathology was confirmed by liquid Cytology only in 12 (32.4%) cases [3]. Atrophic endometrium was detected in 39 women based on histological examination. Cytological confirmation of the histological result of the study in these women was confirmed in 22 (56.4%) cases.

Thus, even when the visible benefits of liquid-based Cytology of abnormalities of the endometrium ( the speed of obtaining results , quality material, multiple studies without re-sampling, and HPV PCR study) frequency of coincidence of the histological result and outcome of liquid based Cytology at different pathological States of the endometrium according to our data, ranged from 32.4% to 56.4%.

Conclusion

The method of liquid Cytology, with all its advantages, does not have an absolute degree of accuracy in the diagnosis of pathological conditions of the endometrium.

Liquid Cytology for screening endometrial pathology should be accompanied by additional histological examination.

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