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Despite the relatively small portion in the structure of the infertility causes, hypergonadotropic hypogonadism (HH) is one of the greatest challenges in reproductive medicine. Diagnosis of HH chromosomal causes often occurs with a significant delay. This is due to the widespread stereotype of the necessary presence of typical phenotypic characters (eunuchoid habitus, pterygoid folds on the neck). This review deals with clinical recommendations for diagnosis of the most common chromosomal causes of HH in women (Turner syndrome (TS)) and in men (Klinefelter syndrome (KS)).TS is a chromosomal pathology associated with the complete or partial absence of one X chromosome accompanied by one or more specific phenotypic features and comorbidities. Persons with suspected TS need to have karyotyping of at least 20 cells (venous blood material). This allows determining the karyotype 45,X, structural anomalies of X chromosome and mosaicism if it is present in more than 10% of the cells. If the mosaic form of TS is suspected but not diagnosed with standard karyotyping, options for investigating more cells or fluorescence hybridization in situ (FISH) are possible. It is important to verify the mosaic forms, especially in cases of a clone with Y chromosome in TS, since such a karyotype carries an increased risk of gonadoblastoma. FISH increases the diagnostic rate of mosaic forms of aneuploidy. Primary hypogonadism in men is the insufficiency of testosterone synthesis and spermatogenesis failure due to the pathology of gonads. Chromosomal causes of primary hypogonadism and nonobstructive azoospermia account for about 15% and are included in the mandatory list of diagnostic examinations. The variants of karyotypes in KS and their clinical manifestations are considered. KS is much more often diagnosed with delay compared to TS. The main diagnostic method for KS is karyotyping and using FISH to detect mosaic forms.Thus, cytogenetic testing (karyotyping) is the first line of examination for women and men with primary (non-iatrogenic) HH; the use of FISH increases the diagnostics efficiency of mosaic forms of sex chromosome aneuploidy.

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done initially to assess fetal head position by palpating fetal spine and cephalic prominence, followed by transvaginal digital examination after rupture of membranes fetal head position is determined after a uterine contraction, based on sagittal suture and posterior fontanelle. Then transabdominal ultrasound examination (also not during contraction) done using M Turbo Ultrasound System Fusifilm Sonosite to determine fetal head position. Ultrasonographic depiction of fetal head position was performed utilising midline intracranial structures (cavum septi pellucid, falx cerebri, thalami and cerebellar hemispheres), and anterior or posterior cranial structures (orbits, nasal bridge and cervical spine). fetal head position was classified as LOA, LOT, LOP, ROA, ROT, ROP. Person doing transvaginal digital examination was blinded from one doing transabdominal ultrasound. Results: The most frequently noted position was LOA (41%). In 78% (162/206) of fetal head positions determined by vaginal examination at <7 cms and 81% (63/77) at > 7 cms was consistent with those obtained by suprapubic transabdominal ultrasound (P = 0.02). Cohen's Kappa test of concordance indicated a good and excellent concordance of 0.70 (at <7 cms) and 0.86 (at > 7 cms). The rate of agreement between the two assessment methods for consultants versus residents was 80% versus 74% which was statistically significant (P = 0.01). Conclusions: The accuracy of transvaginal digital examination with transabdominal ultrasound was 78%, it was better by consultants than residents and also after 7 cms cervical dilatation. EP23.07Ultrasound in labour to predict a need for emergency Caesarean section (ECS): a prospective, blinded cohort study