The objective of this study is to evaluate fetal and maternal outcomes of twin pregnancies with intrauterine single fetal death. In 13 cases, intrauterine death of one fetus was found during the first trimester; in 25 cases, it was found after the first trimester. Obstetric complications and fibrinogen levels were compared. There were no significant differences in the number of preterm delivery, preeclampsia, and intrauterine growth restriction and there were significant differences in gestational age at delivery and birth weight between groups. Coagulation disorders did not occur. The risk for adverse pregnancy outcomes with a single fetal death during and after the first trimester is similar.

A 27-year-old primigravid female was referred to our clinic with severe preeclampsia at 35 weeks of gestation. Her medical history was uneventful. She was administered 1000 mg/day alphamethyldopa since, 28 weeks of gestation. On admission, her blood pressure was 180/ 110 mmHg and urinary albumin 2+. Complete Blood Count (CBC) was in normal limits. Her serum biochemical analysis revealed: ALT: 401 U/L, AST: 292 U/L, creatinine: 1.39 mg/dL, urea: 40 mg/dL (16.6-48.5), uric acid: 8 mg/dL (2.4-5.7), total protein: 6.25 g/dL (6.4-8.3) and albumin: 3.3 g/dL (3.5-5.2). Her coagulation profile was within normal limits. A single live fetus of 31 weeks gestation along with 85 mm amniotic fluid index was detected by USG. Colour flow doppler USG revealed increased umbilical artery resistance. There were no subjective symptoms such as headache, epigastric pain and visual symptoms. Late decelerations were detected on cardiotocography trace and she was diagnosed to have fetal distress. An emergency cesarean section was performed and 1450 gm male fetus was delivered with APGAR score of 8/10. Postoperatively, she was given amlodipine 20 mg/day. Her blood pressure recordings were within normal limits. On first postoperative day 20-30 cc/hour urine output was detected. Serum transaminases were lowered. On the second postoperative day, she had abdominal distension and Massive Ascites and Pleural Effusion in PreeclampsiaKeywords: Hypertension, Peritoneal effusion, Pregnancy ABSTRACTPreeclampsia is defined as new onset hypertension and proteinuria after 20 weeks of gestation and complicates approximately 2-8% of all pregnancies. Release of vasoconstrictive agents, endothelial damage, hyperpermeability of the capillaries and microangiopathic haemolysis involves the basic pathophysiology. It has variable clinical presentation. Here, we report a case of severe preeclampsia who developed postpartum massive ascites and pleural effusion. Primigravid patient was admitted to our clinic at 35 weeks of gestation with very high blood pressure. In biochemical analysis, Alanine aminotransferase (ALT) was 401 U/L, Aspartate aminotransferase (AST) was 292 U/L. An emergency caesarean section was performed because of fetal distress. On the 2 nd post-operative day, abdominal distension and severe abdominal pain occurred. On the 3 rd post-operative day, her abdominal distension increased and Ultrasonography (USG) revealed massive ascites. Abdominal drainage was performed and albumin infusion was administered. On postoperative day 4, she still had abdominal distension and concomitant respiratory distress. Computed Tomography (CT) showed ascites and bilateral pleural effusion. Her complaint regressed on the following days.severe abdominal pain. The USG showed minimal ascites fluid. CBC was normal and serum albumin level was 2.5 gm/dl. Serum sodium level was normal. She had 320 µg albumin/mg creatinine (albumin:creatinine ratio) on spot urine sample. On the 3 rd postoperative day, her abdominal distension increased and USG revealed massive ascites. Abdomi...

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BackgroundThe aim of the study was to investigate the presence of possible markers in the prediction of polycystic ovary syndrome (PCOS)-related metabolic alterations and cardiovascular events in adolescent PCOS cases and also to investigate the applicability of anti-Mullerian hormone (AMH) levels for the diagnosis of PCOS.MethodsIn this cross-sectional study, a total of 75 non-obese women (adolescent PCOS group, n = 25; adult PCOS group, n = 25; control group, n = 25) were included. Measurements of copeptin, pentraxin 3 (PTX3), and AMH serum levels were performed.ResultsSerum copeptin, PTX3 and echocardiographic indices were not significantly different in PCOS subjects and they did not have higher common carotid artery intima-media thickness (CIMT) measurement. AMH levels were significantly higher in PCOS patients. There was a positive correlation between AMH and mean ovarian volume (r = 0.58, P < 0.001) and between AMH and total testosterone level (r = 0.63, P < 0.001). In order to predict a threshold value for the diagnosis of PCOS by using AMH, the receiver operating characteristic (ROC) method was used. Area under the curve was 0.820 and cut-off point was 6.66 ng/mL for AMH with a sensitivity of 62% and specificity of 76%.ConclusionsPossible markers for PCOS-related metabolic alterations may not present in the adolescent years. Serum AMH may be useful as a diagnostic test for adolescents.

The present study failed to demonstrate an association between the inherited thrombophilias and PE.

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The present study demonstrated that the levels of BNP, CRP and homocystein were not different in PCOS subjects. Serum insulin levels and HOMA-IR were significantly higher in PCOS subjects. Possible serum markers for PCOS-related metabolic abnormalities and cardiovascular events, may not present in the adolescent years.

Human chorionic gonadotropin (hCG) is commonly used for final oocyte maturation in "in vitro fertilization" (IVF)-treatment cycles, however, the main important risk is development of severe ovarian hyperstimulation syndrome (OHSS). OHSS can almost be avoided by using gonadotrophin-releasing-hormone agonist for final oocyte maturation in an antagonist protocol. However, primarily this approach lead to a very poor reproductive outcome, despite the use of a standard luteal phase support. The reason seems to be severe luteolysis. Obviously, luteolysis post-gonadotropin-releasing-hormone-agonist (post-GnRH-a) trigger is individual specific, and not all patients will develop a complete luteolysis, as expected previously. Luteolysis can been reverted by the administration of hCG. Unprotected intercourse around the time of ovulation induction and oocyte retrieval can lead to a spontaneous conception in IVF treatment and, endogenous hCG, produced by the trophoblast, will rescue the corpora lutea. Therefore, one should not rely on complete luteolysis after GnRH-a triggering and, especially patients for egg donation and pre-implantation-genetic diagnosis for single gene disorder, have to be counselled to avoid unprotected intercourse.