This study reports 21 IVF cases with excessive ovarian response, who received gonadotrophin-releasing hormone agonist (GnRHa) triggering for final oocyte maturation, followed by a human chorionic gonadotrophin (HCG)-based, progesterone-free, luteal support, individually timed ('luteal coasting') according to endogenous luteal progesterone concentrations. One patient developed a brief early-onset moderate ovarian hyperstimulation syndrome (OHSS) condition. Six clinical pregnancies were achieved, two of which have resulted in live births thus far. To further individualize the luteal phase support post GnRHa trigger, the same principle that holds for follicular coasting, used in the context of OHSS prevention, may be valid. Monitoring luteal progesterone concentrations from the day of oocyte retrieval, and administering a bolus of HCG (1500 IU) when the concentration drops significantly, seems to facilitate fresh embryo transfer, even in patients with excessive ovarian responses.
New drug approval requires a new drug to undergo rigorous clinical trials to determine its efficacy and safety. A drug is approved only for the population on which it was tested, i.e. those who meet the inclusion criteria of the trial. The aim of this study was to determine what percentage of 'real life' patients in our clinic meet the inclusion and exclusion criteria used in large-scale clinical trials required for drug registration in the field of assisted reproduction. All 265 consecutive patients with pertinent data treated in a tertiary centre IVF Unit during 2015 were surveyed. Their demographic and clinical parameters were compared with inclusion and exclusion criteria used in nine major clinical trials. Only 97 out of 265 (37%) patients met the consensus inclusion criteria as defined by the nine clinical trials. The number of oocytes retrieved was 9.10 ± 5.34 in the patients that met the inclusion criteria (n = 97) versus 6.90 ± 5.23 (P = 0.00122) in those that did not (n = 168). Most 'real life' patients who come for treatment at a tertiary IVF centre do not meet the consensus of inclusion and exclusion criteria used for major clinical trials.
Introduction Preterm infants with necrotizing enterocolitis (NEC) are at increased risk of cerebral injury and neurodevelopmental dysfunction. N‐acetyl‐cysteine (NAC) is a known anti‐inflammatory and antioxidant agent. Currently, there is no prophylactic treatment in clinical use to prevent NEC and its neurodevelopmental sequelae. We sought to determine whether brain inflammation/apoptosis accompanies NEC systemic inflammation, and whether it can be attenuated by maternal NAC treatment during pregnancy and/or in the neonatal period in a rat model. Material and methods An established NEC newborn model (hypoxia 5% O2 for 10 min and formula feeding thrice daily, beginning on day 1 for 4 days) was used in Sprague‐Dawley rat pups (n = 32). An additional group of pups (n = 33) received NAC (300 mg/kg intraperitoneal thrice daily) in addition to NEC conditions (NEC‐NAC). Control pups (n = 33) were nursed and remained with the dam in room air. Two additional groups included pups of dams treated once daily with NAC (300 mg/kg intravenous) in the last 3 days of pregnancy. After birth, pups were randomized into NAC‐NEC (n = 33) with NEC conditions and NAC‐NEC‐NAC (n = 36) with additional postnatal NAC treatment. Pups were sacrificed on the fifth day of life. Pup serum interleukin (IL)‐6 protein levels, and brain nuclear factor kappa B (NF‐κB) p65, neuronal nitric oxide synthase (nNOS), Caspase 3, tumor necrosis factor alpha (TNF‐α), IL‐6 and IL‐1β protein levels were determined by ELISA, western blot and TUNEL staining, and the groups were compared using analysis of variance (ANOVA). Results NEC pups had significantly increased serum IL‐6 levels compared with the control group as well as increased neuronal apoptosis and brain protein levels of NF‐κB, nNOS, Caspase 3, TNF‐α, IL‐6 and IL‐1β compared with control. In all NAC treatment groups, levels of serum IL‐6, neuronal apoptosis and brain NF‐κB, nNOS, Caspase 3, TNF‐α, IL‐6 and IL‐1β protein levels were significantly reduced compared with the NEC group. The most pronounced decrease was demonstrated within the NAC‐NEC‐NAC group. Conclusions NAC treatment can attenuate newborn inflammatory response syndrome and decrease offspring brain neuroapoptosis and inflammation in a rat model of NEC by inhibition of NF‐κB, nNOS and Caspase 3 pathways.
While the need for progesterone-based luteal phase support is well documented, the required treatment duration is not well established, and a practitioners' survey showed a wide range of empiric stopping points. It is suggested that an early stop can be based on assessing endogenous luteal activity on the day of pregnancy test. To examine this approach, data were retrospectively collected on 99 patients with positive pregnancy test and high serum concentrations of oestradiol and progesterone (≥ 1000 pmol/l and ≥ 110 nmol/l, respectively), whose luteal support was stopped, and compared with those of 85 patients who did not meet the above criteria, and so luteal support was continued until gestational week 9. Both groups were comparable in terms of live birth and miscarriage rates. We conclude that in the face of strong endogenous luteal activity, exogenous support can be stopped on pregnancy test day, without affecting pregnancy outcome. Further research is needed to substantiate this finding.
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