Bartosik, D., Jacobs, S. L., & Kelly, L. J. (1986). Endometrial tissue in peritoneal fluid. Fertility and sterility, 46(5), 796-800. https://doi.org/10.1016/s0015-0282(16)49813-4
Bartosik D, Jacobs SL, Kelly LJ. Endometrial tissue in peritoneal fluid. Fertil Steril. 1986;46(5):796-800. doi:10.1016/s0015-0282(16)49813-4
Bartosik, Delphine, et al. "Endometrial tissue in peritoneal fluid." Fertility and sterility, vol. 46, no. 5, 1986, pp. 796-800.
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Peritoneal fluid (PF) was studied for the presence of endometrial tissue in a consecutive series of 67 women (with documented tubal patency) undergoing diagnostic laparoscopy, tubal lavage, and hysteroscopy. PF was completely aspirated from the cul-de-sac both before and after uterine irrigation. The PF was then analyzed for the presence of endometrial tissue. In native PF no significant difference in the incidence of endometrial tissue between patients with (19%) and without (11%) endometriosis (P = 0.6) was observed. Refluxed PF, obtained after uterine irrigation, showed a significantly higher incidence of endometrial tissue in women with endometriosis (76%) as compared to controls (42%) (P = 0.03). We propose two models to explain the development of endometriosis. These are not mutually exclusive, may be independent of each other, and may represent two distinct pathophysiologic disease processes.
Interstitial cystitis/painful bladder syndrome (IC/PBS) is a chronic disease primarily in women that is of low incidence and unknown etiology and manifests as bladder pain and urinary symptoms. Acute urinary tract infection (UTI) is of high incidence in women, presents as dysuria and urinary symptoms, and is caused by uropathogenic bacteria. We hypothesized that UTI is present at the onset of IC/PBS in some women. For a case-control study seeking risk factors for IC/PBS, women with IC/PBS symptoms of 12 months or less were recruited and evaluated by interview and medical record review. The date of symptom onset was identified by a six-step process. Three evidence-based methods using culture, urinalysis, and symptoms were used separately and in combination to diagnose UTI at IC/PBS onset. Of 1177 screened women, 314 with recent-onset IC/PBS, including numerous confirming characteristics, were enrolled in the study; 98% of the requested medical records were obtained and reviewed. Evidence of a UTI at the onset of IC/PBS was found in 18% to 36% of women. Common UTI features not used in its diagnosis (short interval to medical care, hematuria, antibiotic treatment, and improvement after antibiotics) were significantly more common in those with onset UTI than in those without. These retrospective data suggest that a proportion, probably a minority, of women at IC/PBS onset had evidence of UTI or inflammation. Our results indicate that UTI is present at the onset of IC/PBS in some women and might reveal clues to IC/PBS pathogenesis.
To review and evaluate published studies that have examined the role of peritoneal fluid (PF) in the development of endometriosis. Important studies related to this topic have been identified through a computerized bibliographical search (MEDLINE), as well as by manually scanning the published literature of major reproductive journals over the last several years. Studies that examined the effect of PF or its components on the pathophysiology of endometriosis are discussed. These include reported effects on the histogenesis, maintenance and proliferation of endometriosis, as well as related actions on infertility. The majority of investigations into the role PF plays in the pathogenesis of endometriosis have evaluated how it may adversely affect fertility. Suggestive but inconclusive data in the literature indicate that degenerating endometrial tissue may release a biochemical factor(s) into the peritoneal environment that is capable of inducing ectopic endometrium formation. Peritoneal fluid itself contains growth factor that may play a role in the implantation and maintenance of the ectopic endometrium. The PF of women with endometriosis has been shown to contain angiogenic as well as other growth factors. These compounds may contribute to the proliferation of the ectopic endometrium.
Gogacz M et al., 2015·Ginekologia polska·Free to read
Endometriosis is a sex hormone-dependent and successively progressing gynecological disease, characterized by the presence of endometrial tissue outside the uterus. The etiology of endometriosis is known to be multifactorial, and its growth depends on immunological, hormonal, genetic and environmental factors. Angiogenesis plays a key role in implantation and growth of endometriotic lesions, as well as in adhesion formation. Physiologically angiogenesis is responsible for neoangiogenesis and recruitment of new capillaries from the already existing capillaries. It is well-documented that altered angiogenesis provokes improper follicular maturation, infertility recurrent miscarriages, ovarian hyperstimulation syndrome, and carcinogenesis. Factors stimulating angionesis include angiogenin, vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF).
The aim of the study was to analyze angiogenic factor concentration (angiogenin, VEGF, FGF) in blood serum and peritoneal fluid in patients with diagnosed endometriosis and idiopathic infertility.
A total of 39 patients were recruited for the study including 19 patients (study group) diagnosed with endometriosis during the laparoscopic procedure and 20 patients (control group) with idiopathic infertility and no morphologic changes within the pelvis revealed during the laparoscopic procedure. All patients underwent laparoscopy during the follicular phase of the menstrual cycle. Vein blood sample was obtained before the procedure and during laparoscopy the entire peritoneal fluid was aspirated for further measurement of VEGF, FGF and angiogenin concentrations.
Angiogenin concentration in peritoneal fluid was statistically higher in patient with idiopathic infertility in comparison to endometriosis (p<0.05). Higher angiogenin concentration was detected also in blood serum of patients with idiopathic infertility as compared to patients with endometriosis, but no statistical significance was found. VEGF and FGF concentration in blood serum and peritoneal fluid was similar in both groups (p>0.05). There were no significant differences between serum and peritoneal fluid in case of VEGF FGF and angiogenin in any of the groups.
Angiogenic factors concentration (VEGF FGF agiogenin) in the peritoneal fluid and blood serum during the follicular phase of the menstrual cycle is not a diagnostic criterion for endometriosis.
Fertility and Outcomes · Conception After Excision
The purpose of this study was to evaluate the effect of peritoneal fluid (PF) on in vitro cleavage of 2-cell mouse embryos. PF was aspirated from the posterior cul-de-sac at laparoscopy and centrifuged, and the cell-free supernatant was heat-inactivated at 56 degrees C for 30 minutes and filtered (0.22 micron). Five percent PF in Ham's F-10 media was prepared and eight to ten 2-cell mouse embryos cultured for 72 hours. There were two study groups, one consisting of 10 PF samples from infertile patients with no endometriosis (PF-NE) and 18 from infertile patients with endometriosis (PF-E). Each sample was assayed along with a control consisting of media only. At 72 hours, greater than 50% of the embryos in the control groups reached the blastocyst and hatching stages. Individual PF samples in both study groups were classified as toxic if less than 50% of the embryos reached the blastocyst and hatching stages at 72 hours. Eight of the 10 samples in the PF-NE group were nontoxic and 14 of the 18 samples in the PF-E group were toxic (P less than 0.01). For evaluation of the overall effect of PF, all results in the PF-E group were pooled (162 embryos) and compared by the Mann-Whitney U test to pooled results in the PF-NE group (100 embryos). The embryonic stages in the PF-NE group were significantly more advanced than those in the PF-E group (P less than 0.001) at 24, 48, and 72 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
Bulun SE et al., 2019·Endocr Rev·Free full text on PubMed Central
Pelvic endometriosis is a complex syndrome characterized by an estrogen-dependent chronic inflammatory process that affects primarily pelvic tissues, including the ovaries. It is caused when shed endometrial tissue travels retrograde into the lower abdominal cavity. Endometriosis is the most common cause of chronic pelvic pain in women and is associated with infertility. The underlying pathologic mechanisms in the intracavitary endometrium and extrauterine endometriotic tissue involve defectively programmed endometrial mesenchymal progenitor/stem cells. Although endometriotic stromal cells, which compose the bulk of endometriotic lesions, do not carry somatic mutations, they demonstrate specific epigenetic abnormalities that alter expression of key transcription factors. For example, GATA-binding factor-6 overexpression transforms an endometrial stromal cell to an endometriotic phenotype, and steroidogenic factor-1 overexpression causes excessive production of estrogen, which drives inflammation via pathologically high levels of estrogen receptor-β. Progesterone receptor deficiency causes progesterone resistance. Populations of endometrial and endometriotic epithelial cells also harbor multiple cancer driver mutations, such as KRAS, which may be associated with the establishment of pelvic endometriosis or ovarian cancer. It is not known how interactions between epigenomically defective stromal cells and the mutated genes in epithelial cells contribute to the pathogenesis of endometriosis. Endometriosis-associated pelvic pain is managed by suppression of ovulatory menses and estrogen production, cyclooxygenase inhibitors, and surgical removal of pelvic lesions, and in vitro fertilization is frequently used to overcome infertility. Although novel targeted treatments are becoming available, as endometriosis pathophysiology is better understood, preventive approaches such as long-term ovulation suppression may play a critical role in the future.
Endometriosis › Pathophysiology › Origin Theories
PMID 3780999 3780999 DOI 10.1016/s0015-0282(16)49813-4 10.1016/s0015-0282(16)49813-4 Bartosik et al. 1986, Bartosik 1986
Cite this article
Bartosik, D., Jacobs, S. L., & Kelly, L. J. (1986). Endometrial tissue in peritoneal fluid. Fertility and sterility, 46(5), 796-800. https://doi.org/10.1016/s0015-0282(16)49813-4
Bartosik D, Jacobs SL, Kelly LJ. Endometrial tissue in peritoneal fluid. Fertil Steril. 1986;46(5):796-800. doi:10.1016/s0015-0282(16)49813-4
Bartosik, Delphine, et al. "Endometrial tissue in peritoneal fluid." Fertility and sterility, vol. 46, no. 5, 1986, pp. 796-800.
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