Journal of Obstetrics and Gynaecology Research
1447-0756
1341-8076
ÚC
Cơ quản chủ quản: Blackwell Publishing Asia , WILEY
Các bài báo tiêu biểu
Endometriosis, a common, benign, estrogen‐dependent disease affecting 3–10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue that is found primarily in the peritoneum, ovaries and rectovaginal septum. Recently, endometriosis has been alternatively described as an immune disease, a genetic disease and a disease caused by exposure to environmental factors, in addition to its usual description as a hormonal disease. In addition, accumulating evidence suggests that various epigenetic aberrations play definite roles in the pathogenesis of endometriosis. Epigenetic alterations reported to date in endometriosis include the genomic DNA methylation of progesterone receptor‐B, E‐cadherin, homeobox A10, estrogen receptor‐β, steroidogenic factor‐1 and aromatase. Aberrant expression of DNA methyltransferases, which attach a methyl group to the 5‐carbon position of cytosine bases in the CpG island of the promoter region and silence the corresponding gene expression, has also been demonstrated in endometriosis. This review summarizes the recent studies on the aberrant DNA methylation status and aberrant expression of DNA methyltransferases, which regulate DNA methylation, in endometriosis. We also discuss the recent information on the diagnostic and therapeutic implications of epigenetic alterations occurring in endometriosis.
Infertility is a serious social problem in advanced nations, with male factor infertility accounting for approximately half of all cases of infertility. Here, we aim to discuss our laboratory results in the context of recent literature on critical genes residing on the Y chromosome or autosomes that play important roles in human spermatogenesis.
The PubMed database was systematically searched using the following keywords: ‘genetics of male factor infertility’; ‘male infertility genes’, ‘genetics of spermatogenesis’ to retrieve information for this review.
Striking progress has recently been made in the elucidation of mechanisms of spermatogenesis using knockout mouse models. This information has, in many cases, not been directly translatable to humans. Nevertheless, mutations in several critical genes have been shown to cause male infertility. We discuss here the contribution to male factor infertility of a number of genes identified in the azoospermia factor (AZF) region on the Y chromosome, as well as the autosomally located genes: SYKP3, KLHL10, AURKC and SPATA16.
Non‐obstructive azoospermia is the most severe form of azoospermia. However, the presence of spermatozoa can only be confirmed through procedures, which may prove to be unnecessary. Elucidation of the genes underlying male factor infertility, and thereby a better understanding of the mechanisms that cause it, will result in more tailored, evidence‐based decisions in treatment of patients.
Adnexal torsion is a rare cause of acute abdominal pain during pregnancy. It is frequently associated with ovarian stimulation for
Hysteroscopic myomectomy is regarded as the best treatment for patients with submucous myomata. However, this procedure has a number of associated complications, including uterine perforation, cervical laceration, hyponatremia and hemorrhage, especially in cases of sessile submucous myomata. To avoid these problems, it is important to make well‐advised preparations and manipulations both pre‐ and intraoperatively. The main surgical considerations for safe hysteroscopic myomectomy are shortening the operating time and avoiding cutting too deeply into the myometrium. With these requirements in mind, a combination of techniques using vaporization and a powerful oxytocic agent, such as prostaglandin F‐2α, appears to be the safest method of carrying out hysteroresectoscopy for unpedunculated sessile submucous myomata.
Adenomyosis is a common gynecological disorder that causes dysmenorrhea, hypermenorrhea and metrorrhagia. Previously, we reported that 24 weeks of dienogest treatment is highly effective for pain in symptomatic adenomyosis. Up to present, there is no report that describes treatment of adenomyosis with long‐term dienogest administration for more than 2 years. In this retrospective cohort study, we investigated the course of long‐term dienogest treatment in patients with symptomatic adenomyosis.
This is a retrospective cohort study. Dienogest was continuously administered at a dose of 2 mg daily for patients with symptomatic adenomyosis. The outcome of long‐term administration of dienogest was investigated, and the characteristics of patients were compared between discontinued cases and long‐term administration cases.
Two patients were excluded from this study because of transfer to another hospital or discontinuation due to infertility treatment. Twelve of 18 patients (66.7%) received dienogest until menopause or for a period of >80 months. Four cases (22.2%) discontinued dienogest treatment because of severe metrorrhagia. In the discontinued cases because of severe metrorrhagia, the pain score for dysmenorrhea and serum CA125 level at baseline significantly elevated, and the hemoglobin level at baseline and the frequency of type 2 adenomyosis significantly decreased, compared to those with long‐term use. Moreover, long‐term dienogest use did not decrease the serum estradiol level.
Our report suggests that dienogest is tolerable for long‐term use until menopause and can be an alternative treatment option in some patients, especially those with type 2 adenomyosis, to avoid hysterectomy.
Emerging evidence suggests that adenomyosis, like endometriosis, may also be an epigenetic disease. In this study, we evaluated the effect of valproic acid (VPA) in ICR mice with adenomyosis, induced by neonatal dosing with tamoxifen. For all mice, we evaluated the bodyweight and the response to thermal stimuli by hotplate and tail‐flick tests 4, 8, and 12 weeks after dosing, respectively, and then treated mice with low‐ and high‐dose of VPA, progesterone (P4), P4 + VPA, or vehicle only. Three weeks after treatment, both bodyweight and thermal response tests were evaluated again before sacrifice, and the depth of myometrial infiltration was evaluated. We found that: (i) the induction of adenomyosis resulted in progressive generalized hyperalgesia as measured by hotplate and tail‐flick tests, along with decreased bodyweight; (ii) treatment with VPA, P4, or a combination was efficacious in improving generalized hyperalgesia; and (iii) drug treatment appeared to reduce the myometrial infiltration, but the difference did not reach statistical significance. Thus, VPA seems to be a promising therapeutics for treating adenomyosis, as reported recently in some case series in humans.
We aimed to investigate the safety and efficacy of dienogest (DNG), a progestational 19‐norsteroid, administered for 52 weeks in patients with symptomatic adenomyosis.
A total of 130 patients with adenomyosis received 2 mg of DNG orally each day for 52 weeks. In cases of complicated anemia, patients were treated for anemia prior to receiving the medication. Adverse events and adverse drug reactions were evaluated. The patients' pain symptoms (dysmenorrhea and pelvic pain from adenomyosis) were assessed using a pain‐scoring tool. This was a verbal rating scale comprising a 0–3‐point pain‐severity score measuring disability to work, and an analgesics‐usage score measuring need for analgesics.
The most common adverse drug reactions included metrorrhagia (96.9%) and hot flush (7.7%). However, in most cases, metrorrhagia was tolerable and no clinically significant changes were observed concerning the incidence or severity of reactions during the 52‐week treatment period. There were no serious adverse events. Both the pain‐severity score and analgesics‐usage score decreased after the start of treatment with DNG. The mean ± standard deviation changes from baseline for the pain score were −3.4 ± 1.8 at 24 weeks and −3.8 ± 1.5 at 52 weeks, respectively.
The long‐term use of DNG was well‐tolerated and effective in patients with symptomatic adenomyosis.