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Impact of COVID–19 on Reproductive, Maternal and Child Health
Published in Srijan Goswami, Chiranjeeb Dey, COVID-19 and SARS-CoV-2, 2022
The world has lived with the COVID-19 pandemic since December 2019 and it is still ongoing. It was recognised to have begun in Wuhan, China. SARS-COV-2 is the new variant of human coronavirus that has caused the COVID pandemic. The spectrum of disease ranges from asymptomatic patients to severe complicated cases with full-blown clinical features of a cytokine storm (Coronavirus, 2020). SARS-CoV-2 infects the human body by binding with the angiotensin-converting enzyme-2 (ACE-2) receptor, which is in various human tissues like the lung, intestine, kidney, testis, ovary, uterus and vagina. Although the virus is found in semen and vaginal secretion, its potential for sexual transmission and resulting subfertility has not been established until now (Morelli et al., 2021). As the ACE-2 receptor is commonly found in Leydig cells and seminiferous tubules of the testis, SARS-CoV-2 can easily affect those areas. It may lead to orchitis but a full evaluation of reproductive function following SARS-CoV-2 infection is under research (Fan et al., 2021; Wang & Xu, 2020). Female reproductive processes necessitate the renin-angiotensin-aldosterone system. It helps in folliculogenesis, steroid genesis, oocyte maturation and ovulation (Li et al., 2020). Although no definite evidence of involvement in the female reproductive tract has been established, it has been postulated that the SARS-CoV-2 virus might affect ovarian tissue, including granulosa cells, leading to subfertility and miscarriage. ACE receptors are expressed in the endometrium, thus it might affect the endometrium and the implantation of the embryo.
Ultrasound-Guided Intervention in Assisted Reproductive Technology
Published in Arianna D'Angelo, Nazar N. Amso, Ultrasound in Assisted Reproduction and Early Pregnancy, 2020
It has been suggested that the presence of these ovarian cysts can disrupt folliculogenesis by reducing the area available for follicle development and by altering local blood supply [52], which could possibly lead to negative impact on IVF outcomes [53].
Principles of Pathophysiology of Infertility Assessment and Treatment*
Published in Asim Kurjak, Ultrasound and Infertility, 2020
Joseph G. Schenker, Aby Lewin, Menashe Ben-David
In normal folliculogenesis, FSH is detectable in the follicular fluid and the concentration of estrogens in the antral fluid exceeds that of androgens. When FSH is not detectable in the follicular fluid, then androgens predominate and further follicular development may cease.
Updates in diagnosing polycystic ovary syndrome-related infertility
Published in Expert Review of Molecular Diagnostics, 2023
Hélio Haddad-Filho, Jéssica A. G. Tosatti, Fernanda M. Vale, Karina B. Gomes, Fernando M. Reis
FSH acts through its receptor (FSHR) in the granulosa cells of ovarian follicles. The perfect link between FSH and its receptor is necessary to promote steroidogenesis, cellular proliferation and folliculogenesis. The FSHR gene is located at 2p16.3 consisting of 10 exons and 9 introns. The transmembrane receptor is expressed in GC and mediates FSH signal transduction through adenylate cyclase activation and elevation of intracellular cyclic adenosine monophosphate (cAMP) [92,100]. In a prospective cohort study of 240 normogonadotropic anovulatory patients (a category that includes mostly PCOS), those with FSHR genetic variation at position 2039 A > G (Asn680Ser, rs6166) had lower pregnancy rates after ovulation induction with clomiphene compared to the AA genotype [94].
Are all antral follicles the same? Size of antral follicles as a key predictor for response to controlled ovarian stimulation
Published in Journal of Obstetrics and Gynaecology, 2022
Isil Kasapoglu, Adnan Orhan, Kiper Aslan, Esra Sen, Aysenur Kaya, Berrin Avcı, Gurkan Uncu
Suboptimal response is a distinct entity and strategies that will improve oocyte yield could be found. The key question here is why these patients have suboptimal response and what will change the suboptimal response to normal. As the pathophysiology explaining suboptimal response is not fully understood, a genotype –based mechanism suggested (Alviggi et al. 2015). A common LH beta subunit variant was associated with increase FSH consumption and suboptimal response (Alviggi et al. 2013). As the importance of LH during folliculogenesis and recruitment is known (Raju et al. 2013), this mechanism could explain decreased recruitment and response to COH, although these patients have normal serum AMH levels which reflects primordial follicle pool. So, patients with low number of recruited 2–5 mm follicles could benefit from strategies that could improve recruitment. Among these, using aromatase inhibitors or LH in the early follicular phase could improve recruitment benefiting from the androgenic effect as the androgens play critical roles on folliculogenesis (Sen et al. 2014). As the follicles with a diameter of 2 mm could respond to FSH stimulation, the increase in the FSH starting dose might be also an option in women who show hypo-sensitivity to gonadotropin stimulation in a previous cycle. Also reported studies show that when a higher starting dose of FSH given during COS, the response was not significantly influenced by the presence of FSH receptor polymorphism (Genro et al. 2012).
Successful treatment of peritoneal inclusion cysts with dienogest: two case reports
Published in Journal of Obstetrics and Gynaecology, 2022
Hiroki Shinmura, Takashi Matsushima, Takehiko Fukami, Toshiyuki Takeshita
Dienogest, which is a synthetic progestin that is typically used for the treatment of endometriosis, reduces serum progesterone levels to anovulatory levels and inhibits folliculogenesis. One reason for peritoneal inclusion cysts is adhesion, which causes a decline in the ability of the peritoneum to absorb ovarian stroma-derived serous fluid (Fu and Su 2018). It is believed that dienogest can reduce the production of serous fluid derived from the ovarian stroma, which causes peritoneal inclusion cysts (Ruan et al. 2012; Maeda et al. 2014). It is thought that the presence of focal oestrogen and progesterone receptors on peritoneal inclusion cyst walls play a supportive role in hormonal management until menopause (Vallerie et al. 2009). Thrombus is a critical potential side effect of hormonal therapy, but dienogest does not exert the same effects as oestrogen, and therefore, its use is not associated with an increased risk of thrombus (Ruan et al. 2012). Irregular bleeding is a frequently encountered side effect of dienogest, but the two cases presented here experienced no adverse events because they had already undergone hysterectomy.