Objective: To determine the efficacy of the angiographic indexes of 3D power Doppler angiography (3D-PDA) for the diagnosis of malignancy in complex ovarian masses. Methods: A prospective, observational study of 72 patients with complex adnexal mass. Results: In the morphological study, 3D ultrasound showed sensitivity, specificity, PPV, NPV, PLHR and NLHR of 84.6%, 81.9%, 85.1%, 81.8%, 4.65 and 0.19. No differences in vascular indexes (VI, FI, VFI) between malignant and benign masses were found: VI 5.38 (CI 95% 3.06-7.7) vs. 6.29 (CI 95% 4.41-8.17) (p = 0.53); FI 29.6 (CI 95% 25.17-34.08) vs. 33.8 (CI 95% 30.03-37.3) (p = 0.15); VFI 1.68 (CI 95% 0.94-2.42) vs. 2.37 (CI 95% 1.49-3.25) (p = 0.24). When analysed according to different stages, VI was higher in patients with more advanced stages of disease; 4.34 (95% CI 2.21-6.47) vs. 7.38 (95% CI 4.7-10.06) (p = 0.11). FI was significantly lower in patients with early stages of disease; FI 29.07 (95% CI 21.49-36.68) vs. 36.46 (95% CI 32.31-40.62) (p = 0.04). For VFI, differences were not significant, although there was a strong trend; VFI 1.47 (95% CI 0.67-2.28) vs. 2.86 (95% CI 1.57-4.16) (p = 0.11). 3D-PDA indexes were significantly higher in patients with positive adenopathies. Conclusion: 3D-PDA values increase progressively, but not significantly, with the stage of the disease.

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Objective To determine the epidemiological and sonographic characteristics of patients with endometrial carcinoma of endometrioid and non-endometrioid subtype to analyse if any differences can be observed between the groups. Study design A case-control study was performed considering 122 patients with endometrial carcinoma where 96 (78.69%) had endometrioid carcinomas (controls) and 26 (21.31%) had non-endometrioid carcinomas (cases). Epidemiological, clinical, and sonographic variables (endometrial thickness and sonographic suspicion of myometrial invasion of the tumour) were analysed. Qualitative variables were studied with the Chi-square test and the Fisher's exact test and quantitative variables with the t test. A value of p < 0.05 was considered statistically significant. Results Tumours of the non-endometrioid type are observed in older patients (p = 0.003) and frequently show a higher sonographic tumoral invasion (p = 0.0036). Conclusions This study supports previous observations that non-endometrioid endometrial carcinomas present at older ages and provides new data that non-endometrioid carcinoma more frequently show sonographic images compatible with myometrial invasion.

Objectives: The clinical significance of sFlT1:PlGF ratio in late onset pre-eclampsia is unclear. The aim of the present study was to evaluate the relationships of this parameter with maternal and perinatal outcomes. Methods: This is a pilot prospective case-control study. In total 45 pregnant women, 16 with late onset pre-eclampsia (> 34 weeks) (8 mild and 8 severe) and 29 controls were studied. sFlT1, PlGF and ratio sFlT1:PlGF ratio was measured by immunoassay (Roche Corp). Patients were classified in mild and severe pre-eclampsia. Relationships with hematological, biochemical, Doppler parameters and perinatal outcomes were studied. Student t test, ANOVA test and Pearson's coefficient correlation were used. Statistical significance was set at 95% level (p <0.05). Results: sFlt1 and sFlT1:PlGF ratio were significantly increased and PlGF was decreased in women with late onset pre-eclampsia in comparison to controls. Overlapping was more pronounced for PlGF than for both sFLt1 and sFlT1:PlGF ratio. There were no significant differences between mild and severe cases in the level of angiogenic factors. However, sFlT1:PlGF ratio was significantly correlated with creatinine, ALT and AST (r = 0.53, p = 0.03, r = 0.54, p = 0.03, r = 0.58, p = 0.01 respectively). In the subgroup of women with pre-eclampsia sFlT1:PlGF ratio was significantly correlated with uterine artery PI (r = 0.82, p = 0.005) and both PlGF and sFlT1:PlGf were corrlelated with birthweight in centiles (r = 0.59, p = 0.02 and r = -0.65; p = 0.01). Conclusions: In women with late onset pre-eclampsia angiogenic factors may identify women with defective placentation but their relationships with maternal morbidity although present is poor.

Backgound: Ovarian abscesses are a rare complication encountered after vaginal hysterectomy. Few cases have been reported, and most of them have a late appearance between 15 months and 16 years after surgery. Moreover, most of the cases reported showed unilateral ovarian affection and no intervention of laparoscopic techniques. The physiopathology seems to be the hematologic or lymphatic progression of germs from the place of surgery to the ovaries. Case: In this article, we report the case of a 42-year-old patient who was operated on with a laparoscopicassisted vaginal hysterectomy (LAVH) for polymyomatous uterus. She was admitted 17 days after at the emergency room with abdominal pain and fever. Adnexal pathology was found by ultrasonography and confirmed by scanner, and a laparoscopic approach was carried out. Four (4) intraovarian abscesses were found during surgery, which forced us to remove that ovary. The postoperative course was satisfactory, and the infection was resolved. Conclusions: This case supports the importance of considering the ovarian abscess in the differential diagnosis of postoperative infections after LAVH. ( J GYNECOL SURG 26:49)

Pallister-Killian syndrome (PKS) is a rare genetic syndrome characterised by facial anomalies (prominent forehead with sparse temporal hair, broad nasal bridge, hypertelorism, wide mouth), variable developmental delay and intellectual impairment, hypotonia, seizures, pigmentary skin differences, diaphragmatic hernia, congenital heart defects, and other systemic abnormalities. It is caused by supernumerary isochromosome 12p (tetrasomy 12p). Prenatal diagnosis is difficult and mostly confined to second or third trimester. It can be suspected from ultrasound findings, however the proof by targeted FISH genetic analysis is essential for certain diagnoses. We report a case of Palliser-Killian syndrome, that was diagnosed prenatally at 18 gestational weeks in our clinic. The pregnant lady booked for second opinion scan in our centre due to the ultrasound finding of 7 minor markers in other centre. In this centre she already underwent CVS due to increased nuchal translucency. Karyotype and microarray investigation were normal, screening for deletion of exons 7 and 8 of the SMN1 gene and mutations of the FGFR3 gene were negative. Ultrasound examination in our centre revealed normohydramnion, asymmetrical fetal growth and spastic fetal movements. Several fetal abnormalities (many different from previous centre) were found: thick nuchal fold, mild bilateral hydronephrosis, omfalocele with partial herniation of the liver, facial anomalies (flat profile, high forehead, wide flat nose, outer eye corners pointing downwards and low insertion of ears). Fetal echocardiography showed tricuspid regurgitation in otherwise normal heart. Fetal thymus couldn't be identified. We asked for targeted genetic analysis for Killian-Pallister, DiGeorge and fragile chromosome X. Repeated genetic analysis (FISH) confirmed Pallister-Killian syndrome by finding of 80% mosaicism of tetrasomy 12p. The mother decided to terminate the pregnancy. EP13.05Upper limbs malformation and mutation in RECQL4 gene first trimester prenatal diagnosis At 12-5 weeks of gestation, the ultrasound findings showed a fetus corresponding to amenorrhea, with hypoplasia / agenesis of bilateral radii accompanied by malpositioned hands. Chorionic villus sampling was undertaken. The ultrasound was repeated one week later with the same findings, so the couple decided to terminate the pregnancy. The CVS analysis included karyotype and arrayCGH, but no alteration was detected. Seven months later, the couple came again to perform an ultrasound at 12-4 weeks of a new gestation. Similar findings were observed plus malpositioned feet and a discrete retrognathia. CVS was performed but shortly after the pregnancy was once again interrupted. Fetal necropsy of the second pregnancy confirmed the ecographic findings. The first fetus was subsequently analysed using a custom-designed Skeletal dysplasia Next generation sequencing panel (SkeletalSeqV6, n=368 gene). The fetus was found to be a compound heterozygote for two RECQL4 mutations, one novel and one previously described, p.(Met1?)(Ph...

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