Two-Step Office-Based Hysteroscopic Operation for Submucosal Myoma.

BACKGROUND AND OBJECTIVES: In the past, diagnostic hys- teroscopy was used to diagnose an intrauterine mass or abnormality and surgical hysteroscopy was used to treat a uterine polyp, uterine synechia, uterine septum, and submucosal myoma. The old hysteroscope had large diameters. Thus, general anesthesia was needed for inpatient management. However, due to the development of smalldiameter hysteroscopes, hysteroscopic diagnosis and surgery are now possible on an outpatient basis. Despite the development of small-diameter hysteroscopes, resection of submucosal myoma is possible only through resecto- scopic operation under general anesthesia, including type 0 uterine myoma. The objective of the present study was to determine the usefulness of secondary office operating hysteroscopy after cutting the pedicle of submucosal myoma via primary office operating hysteroscopy. METHODS: We primarily cut the pedicle of type 0 submucosal myoma with the first rigid 5-mm operating mini- hysteroscopy in the outpatient clinic. We then expected the myoma to shrink. Two months later, we confirmed the size with use of 3-mm flexible diagnostic hysteroscopy. If the myoma was shrunk to less than one-third the original size, it was removed with the second rigid 5-mm operating mini-hysteroscopy. RESULTS: In 14 of 24 patients, the myoma had shrunk to less than one-third the size. The rest was successfully removed with the second operating mini-hysteroscopy. In 5 of 24 patients, the myoma mass was not present in the uterine cavity. However, in another 5 of 24 patients, the myoma size had not changed significantly. The myomas were removed via resectoscopic operation under general anesthesia. CONCLUSIONS: The trial with this 2-step operation was very useful for the removal of type 0 submucosal myoma in an outpatient clinic.

Clinical evaluation and management of endometriosis: guideline for Korean patients from Korean Society of Endometriosis.

Endometriosis is one of the most common diseases in reproductive ages, and it affects patients' quality of life and fertility. However, few Korean guidelines are available for the evaluation and management of endometriosis. Korean Society of Endometriosis reviewed various literatures and trials, and to provide seventy-one evidence-based recommendations. This review presents guidelines for the diagnosis and management of endometriosis with emphasis on: it's role in infertility, treatment of recurrence, asymptomatic women, endometriosis in adolescents and menopausal women, and possible association of endometriosis with cancer.

Erratum to "Long-Term Treatment of Native LDL Induces Senescence of Cultured Human Endothelial Cells".

[This corrects the article DOI: 10.1155/2017/6487825.].

Long-Term Treatment of Native LDL Induces Senescence of Cultured Human Endothelial Cells.

The study aimed to evaluate whether the treatment of primary cultured human endothelial cells with native low-density lipoprotein (nLDL) could induce their senescence and to uncover some of the putative mechanisms involved. For this purpose, human umbilical vein endothelial cells (HUVECs) were subcultured and/or continuously cultured with nLDL (0, 2, 5, and 10 µg protein/mL), for up to 9 days. The results indicated that nLDL inhibited the proliferation of HUVECs by arresting the cell cycle at G1 phase. The G1-arrested cells showed increase in cytosolic senescence-associated-ß-galactosidase (SA-ß-Gal) activity, a biomarker of cellular senescence. The causative factor of the cellular senescence was nLDL itself and not oxidized LDL (oxLDL), since blocking LDL receptor (LDLR) with the anti-LDLR antibody opposed the nLDL-induced increase of SA-ß-Gal activity and decrease of cellular proliferation. In addition, nLDL-induced cellular senescence by inhibiting the phosphorylation of pRb (G1 arrest) via p53 as well as p16 signal transduction pathways. G1 phase arrest of the senescent cells was not overcome by nLDL removal from the culture medium. Moreover, the nLDL-treated cells produced reactive oxygen species (ROS) dose- and time-dependently. These results suggested, for the first time, that long-term treatment of nLDL could induce the premature senescence of endothelial cells.

A randomized, multi-center, clinical trial to assess the efficacy and safety of alginate carboxymethylcellulose hyaluronic acid compared to carboxymethylcellulose hyaluronic acid to prevent postoperative intrauterine adhesion.

STUDY OBJECTIVE: To estimate the efficacy of alginate carboxymethylcellulose hyaluronic acid (ACH) gel to prevent intrauterine adhesions after hysteroscopic surgery in comparison with carboxymethylcellulose hyaluronic acid (CH) gel, which is known as an effective adhesion inhibitor. DESIGN: Randomized, multicenter, single-blind, clinical trial (Canadian Task Force classification I). SETTING: Tertiary university hospital. PATIENTS: One hundred eighty-seven patients with a surgically treatable intrauterine lesion (myomas, polyps, septa, intrauterine adhesion, dysfunctional uterine bleeding). INTERVENTIONS: Patients were randomized to 2 groups: hysteroscopic surgery plus intrauterine application of ACH or CH. MEASUREMENTS AND RESULTS: The rate of adhesion formation and the adhesion severity score with type and extent were calculated 4 weeks after surgery. The ACH group had results that were comparable to the CH group in terms of the development of intrauterine adhesions at 4 weeks follow-up. The adhesion severities were not different between the 2 groups. In a subgroup without baseline intrauterine adhesion, the ACH group showed a lower intrauterine adhesion rate than the CH group (p = .016). CONCLUSIONS: ACH had a comparable efficacy to CH in terms of the adhesion rate and severity. In the case of no baseline intrauterine adhesion, intrauterine application of ACH after hysteroscopic surgery had a lower rate of intrauterine adhesion than application of CH.

Endometriosis in a patient with Rokitansky-Kuster-Hauser syndrome.

Endometriosis in Rokitansky-Kuster-Hauser syndrome has been reported only once previously. We present here a case of endometrioma in a patient with Rokitansky-Kuster-Hauser syndrome. A 26-year-old patient with Rokitansky-Kuster-Hauser syndrome presented with abrupt pain in the left iliac quadrant. A mass was confirmed by sonography. Laparoscopic inspection revealed no uterus. The mass was removed laparoscopically. Endometriosis was confirmed histologically. If endometrioma in a patient with Rokitansky-Kuster-Hauser syndrome is associated with a small rudimentary unicornis uterus with a small endometrial cavity, endometriosis can be assumed to have developed by retrograde menstruation theory. Because the patient did not have a functioning endometrium, her endometrioma is assumed to have arisen from coelomic metaplasia.

Association of tumor necrosis factor-{alpha} gene polymorphisms with advanced stage endometriosis.

BACKGROUND: This study was performed to investigate whether specific haplotypes and several single nucleotide polymorphisms in the promoter region of the tumor necrosis factor (TNF)-alpha gene are associated with the risk of advanced stage endometriosis in a Korean population. METHODS: This study comprised women with (n = 246) or without (n = 248) endometriosis. The TNF:g.[-1031T > C], TNF:g.[-863C > A] and TNF:g.[-857C > T] polymorphism in the TNF-alpha gene were assessed by PCR-restriction fragment length polymorphism analysis, which utilized digestion by BbsI, HypCH4IV and HypCH4IV restriction enzymes, respectively. In silico haplotypes were deduced by using the Haploview version 3.32. RESULTS: The genotype distribution of TNF:g.[-1031T > C] was significantly different between total endometriosis patients and the controls (T/T of 56.9 versus 60.1%, T/C of 35.4 versus 37.5% and C/C of 7.7 versus 2.4%, respectively, P = 0.027). This difference at the TNF:g.[-1031T > C] tends to increase in Stage IV endometriosis (P = 0.01). However, there was no difference in the TNF:g.[-863C > A] and TNF:g.[-857C > T] site between the two groups. Even when the endometriosis cases were subdivided into American Society for Reproductive Medicine Stages III and IV, genotype differences were not found. The CC homozygote at TNF:g.-863 was more frequently found in the controls than Non-CC group (P = 0.04; odds ratio = 0.67; 95% confidence interval = 0.45-0.98). All haplotypes and diplotypes, deduced by in silico analysis, showed no association with subgroups or controls. CONCLUSIONS: Our results suggest that the genotype frequencies at the TNF:g.[-1031T > C] and the TNF:g.[-863C > A] sites may be associated with advanced stage endometriosis in the Korean population.

Effects of peritoneal fluid from endometriosis patients on the release of vascular endothelial growth factor by neutrophils and monocytes.

BACKGROUND: An increase in the level of the vascular endothelial growth factor (VEGF) production has been reported in the peritoneal fluid (PF) of endometriosis patients. This suggests that changes in the vascular permeability and angiogenesis play an important role in the pathophysiology of this disease. This study examined the effects of the PF obtained from endometriosis patients on the release of VEGF by neutrophils and monocytes. METHODS: Neutrophils and monocytes were obtained from young healthy volunteers and cultured with the PF obtained from either endometriosis patients (EPF) (n=18) or a control group (CPF) (n=4). A human monocyte/macrophage cell line, THP-1, was cultured with either 10% EPF or 10% CPF. The PF and culture supernatants were assayed for VEGF using ELISA. Real-time PCR and Western blotting were used to measure the VEGF mRNA and protein expression level, respectively. RESULTS: The VEGF levels were higher in the EPF than in the CPF (591+/-75 versus 185+/-31 pg/ml, P<0.05). However, the level of VEGF released by THP-1 cells in CPF and EPF was similar. The EPF induced the release of VEGF by neutrophils, but no VEGF was released by monocytes. The VEGF mRNA expression levels in the neutrophils were higher in the EPF, which was abrogated by cycloheximide, suggesting that the EPF induces the production of VEGF in neutrophils. Neutralizing antibodies against IL-8 and TNF-alpha did not completely prevent the EPF-induced release of VEGF by the neutrophils, even though these growth factors stimulated the release of VEGF by neutrophils. There was a positive correlation between the VEGF and IL-10 concentrations in the EPF (correlation coefficient=0.549, P=0.012, n=18), but the neutralizing antibody of IL-10 did not affect the release of VEGF by the EPF-treated neutrophils. CONCLUSION: The EPF induced the production and release of VEGF by neutrophils, suggesting that neutrophils may be a source of peritoneal VEGF. In addition, neutrophil-derived VEGF might be a marker for diagnosing endometriosis.

Nitric oxide inhibition of the proliferation of ovarian endometriotic stromal cells in vitro.

OBJECTIVE: To investigate the effects of nitric oxide on endometrial cell proliferation and the effects of peritoneal fluid from women with and without endometriosis on the production of nitric oxide and upon the nature of nitric oxide-induced changes. STUDY DESIGN: Ovarian endometriotic and endometrial stromal cells and peritoneal fluid were obtained from endometriosis patients and controls. Cell proliferation was determined by [3H]thymidine incorporation, and nitrite was measured using Griess reagent. RESULTS: Sodium nitroprusside (SNP), a nitric oxide donor, reduced the proliferation of endometriotic and endometrial cells in primary culture in a dose-dependent manner. SNP-induced production of nitric oxide and the inhibitory effect of nitric oxide on stromal cell proliferation were reduced by peritoneal fluid from women with endometriosis, although stromal cell proliferation was still inhibited by SNP in the presence of peritoneal fluid. However, this SNP-induced inhibition of cell proliferation was unaffected by interleukin-8, 17-beta, estradiol or transforming growth factor beta1. CONCLUSION: Nitric oxide inhibits the proliferation of endometrial stromal cells in vitro, and this inhibitory effect is abrogated by peritoneal fluid from women with endometriosis.