Breaking bad news in assisted reproductive technology : a proposal for guidelines

Background: The issue of breaking bad news in assisted reproductive technology (ART) has been only partially explored by literature, and although some recommendations are available, specific guidelines are lacking. The present study aimed to explore the applicability of the oncologic SPIKES Protocol to the ART context. Methods: Thirteen ART clinicians (7 gynecologists; 4 psychologists; 1 biologist; 1 obstetrician) completed the Critical Incidents Report (CIR) to describe the experience of delivering bad news in ART. The CIRs were first discussed with clinicians, then a focus group was created composed of 13 clinicians, one health communication expert and a patient to discuss the applicability of the six-step (SPIKES) Buckman Protocol to ART. The discussion was audiotaped, transcribed and analyzed with content analysis. Results: The SPIKES Protocol seems to fit ART consultations and participants found it practical and easy to understand. Some specificities were found for the ART context: the reiteration of bad news, the "patient" as a couple and the fact that ability to conceive is closely related to self-esteem, as well as to social and family identity. During the discussion of the SPIKES Protocol, participants highlighted the importance of: 1) providing a caring setting, by adding a reflection on the value of communication by phone; 2) exploring patients perceptions but also misinformation; 3) exploring patients desires and expectations, while balancing the need to be honest and clear; 4) applying Buckmans suggestions for delivering information, and integrating clinical aspects with psychosocial ones; 5) managing and legitimizing patients emotions, in particular anger; 6) having a strategy for follow-up and supporting couples to make meaning of the ART experience. Conclusion: The proposal of a shared protocol for giving bad news in ART could be the starting point for training and experimental studies

Follicular fluid levels of vascular endothelial growth factor and early corpus luteum function during assisted reproductive technology cycles

BACKGROUND: The relation between vascular endothelial growth factor (VEGF) and early luteal function has rarely been proven in humans. The purpose of this study was to define the relation between follicular fluid concentrations of VEGF (FF VEGF) and early luteal function at the preimplantation stage during assisted reproductive technology (ART) cycles. METHODS: 71 women were divided into two groups, based on reproductive outcome: women who became pregnant after embryo transfer (ET) (n = 18, Group A) and non-pregnant women (n = 53, Group B). Serum progesterone (Se P) and inhibin A on ET day, and FF VEGF levels were measured in all women. Data were expressed as mean ± standard deviation. Statistical analysis was performed using Excel Office 98 for Student's t-test, linear regression test and chi-square test. A p value of < 0.05 was considered statistically significant. RESULTS: The groups were comparable for age, ovarian reserve, number and quality of the oocytes retrieved and of the embryos obtained and transferred. FF VEGF levels were increased (4235 ± 1433 vs 3432 ± 1231 pg/ml), while Se P and inhibin A levels were significantly reduced (83.1 ± 34.1 vs 112.0 ± 58.8 ng/ml and 397.4 ± 223 vs 533.5 ± 283 pg/ml, respectively) in the non-pregnant group and were negatively correlated with FF VEGF (r = -0.482, p < 0.05; r = -0.468, p < 0.05) only in pregnant women. CONCLUSION: Much has to be learned about the regulation and role of VEGF during the early luteal phase. We advance the hypothesis that the existence of a negative correlation between FF VEGF/Se P and FF VEGF/inhibin A in pregnant women might indicate the existence of a normal VEGF-mediated paracrine response when Se P and inhibin A levels are decreased. Excess production of FF VEGF and the absence of a correlation between FF VEGF/Se P and FF VEGF/inhibin A in non-pregnant women may be a paracrine reaction to immature luteal vasculature, resulting in luteal dysfunction

Follicular fluid vascular endothelial growth factor concentrations are increased during GnRH antagonist/FSH ovarian stimulation cycles.

Background: The aim of this study was to investigate the effect of GnRH antagonists (GnRH-ant) on follicular fluid vascular endothelial growth factor (FF VEGF). Methods: Sixty women undergoing assisted reproduction were randomised (computer-generated randomisation list) and assigned to two different GnRH analogue regimens: GnRH agonist (GnRH-a) (Group A; n = 30) and GnRH-ant (Group B; n = 30). Results: Mean (S.D.) FF VEGF concentrations were 1598 612 pg/mL and 2906 1558 pg/mL for Groups A and B, respectively ( p < 0.001). In the women treated with GnRH-ant, we found a statistically significant reduction in serum LH levels (1.72 0.74 IU/L in Group A versus 0.93 0.43 IU/L in Group B, p < 0.001), in serum oestradiol (E2) levels (1562.1 410.7 pg/mL in Group A versus 1214.67 779.9 pg/mL in Group B, p < 0.05), in FF E2 levels (1146 593 ng/mL in Group A versus 621 435 ng/mL in Group B, p < 0.05), and in FF androstenedione levels (136 55 ng/mL in Group A versus 78 31 ng/mL in Group B, p < 0.001), as well as a reduction in the number of pregnancies, though not statistically significant (23.3% in Group A versus 16.6% in Group B). Conclusion: The increase in FF VEGF levels in women treated with GnRH-ant might be explained by a suppression of LH and E2 levels

Ovarian response and pregnancy outcome related to midfollicular LH levels in down-regulated women undergoing assisted reproduction

OBJECTIVE: To assess ovarian response and pregnancy outcome related to midfollicular luteinizing hormone (LH) levels in nor-mogonadotropic women down-regulated with gonadotropin-releasing hormone-agonist (GnRH-a) (daily and depot) during an assisted reproduction cycle. STUDY DESIGN: In a prospective randomized trial, 50 women were down-regulated with leuprorelin, 0.5 mg/d subcutaneously (group A) and 50 with leuprorelin, 3.75 mg depot (group B), prior to ovarian stimulation with recombinant follicle-stimulating hormone (FSH). Midfollicular serum LH levels less than or equal to 0.5 mIU/mL (subgroups A1 and B1) versus > 0.5 mIU/mL (subgroups A2 and B2) were considered. A comparative analysis was carried out on the clinical effects (duration of stimulation, total FSH dose, number of oocytes retrieved and pregnancy rate). RESULTS: Maximum estradiol levels and pregnancy rates were higher in subgroups A2 and B2, with LH > 0.5 mIU/mL. No differences were observed in the cumulative amount of gonadotropin used, number of oocytes retrieved or fertilization rate. CONCLUSION: When FSH only is used for ovarian stimulation, very low LH serum concentrations in nor-mogonadotropic women profoundly suppressed with GnRH-a, especially if given as a depot, may adversely affect in vitro fertilization outcome

Gonadotropin-releasing hormone antagonists increase follicular fluid insulin-like growth factor-I and vascular endothelial growth factor during ovarian stimulation cycles.

The aim of the present study was to investigate the effect of gonadotropin-releasing hormone (GnRH) antagonists (GnRH-ant) on follicular fluid (FF) insulin-like growth factor-I (IGF-I) and FF vascular endothelial growth factor (VEGF) levels. Sixty women undergoing assisted reproduction were randomized and assigned to two different GnRH analog regimens: GnRH agonist (GnRH-a) and GnRH-ant. FF VEGF and FF IGF-I concentrations were significantly increased in the patients treated with GnRH-ant (ρ<0.001). In the same patients we observed a statistically significant reduction in serum luteinizing hormone (LH) and estradiol (E2 ) levels (ρ<0.001 and ρ<0.05, respectively), FF E2 and FF androstenedione levels (ρ<0.05 and ρ<0.001, respectively), as well as a reduction in the number of pregnancies although this was not statistically significant. In the GnRH-ant group, FF VEGF levels were positively correlated with FF IGF-I levels, and both were negatively correlated with serum LH levels. The increase in FF IGF-I and FF VEGF levels in women treated with GnRH-ant could be explained by a deleterious follicular environment in response to profound suppression of LH and E2 levels