Pathogenesis of endometriosis: Look no further than John Sampson.

Rather than consider endometriosis as an enigmatic disease, reading John Sampson's two theories/mechanisms explains virtually all cases affecting the female. It is true that Sampson's most recent publication, in 1940, which talks about retrograde menstruation via the fallopian tubes, clearly fails to explain many types of endometriosis, particularly that located in extra-pelvic sites. However, his earlier publications of 1911 and 1912, on radiographic studies of hysterectomy specimens that had been injected with various gelatin/bismuth/pigment mixtures examining the unique uterine vasculature, were more important. These studies enabled him to describe 'the escape of foreign material from the uterine cavity into the uterine veins' in 1918 and subsequently to demonstrate metastatic or embolic endometriosis in the first of his two important publications in 1927. Later in that same year, in response to 'academic banter' from other historic gynaecologists, he published a second article that indicated his studies had been redirected to explore the retrograde tubal menstruation idea; this required undertaking his hysterectomies during menses. That work led to his 1940 presentation at the invitation of The American College of Obstetricians and Gynecologists to focus on the second theory/mechanism of endometriosis. This appears to have caused his more important first theory/mechanism to have been forgotten.

Advanced fibroid study: paying homage to John Sampson.

A recent article supports our longstanding view that all intramural fibroids can cause disturbance of uterine function. This may be reflected in the symptom of menorrhagia or fertility-related issues, as well as pregnancy losses at all gestational stages. However, it was disappointing that there was no reference to either the mechanism by which fibroids disturb uterine function nor to the gynaecologist who described this more than 100 years ago, namely John Sampson. In fact, Sampson's findings about the unique venous drainage mechanism from the endometrium explains how menstrual loss is contained in normal physiology, but which can be excessive when the protective 'anaemic' zone is disturbed. Two more recent and pertinent observations include the hysteroscopic findings of Osamu Sugimoto, who showed in the 1970s that the endometrium overlying submucous fibroids is actually atrophic, hence the oft-cited reason of hyperplastic or excessive endometrium cannot be the cause of the associated menorrhagia. Furthermore, recent imaging techniques describe an additional 'junctional zone' adjacent to the endometrium in cases of fibroids and adenomyosis. We believe this all adds up to disturbed venous drainage as described by Sampson and needs to immediately enter the educational training of medical students, doctors and gynaecologists worldwide.

DHEA Supplementation Confers No Additional Benefit to that of Growth Hormone on Pregnancy and Live Birth Rates in IVF Patients Categorized as Poor Prognosis.

BACKGROUND: In vitro fertilization (IVF) patients receive various adjuvant therapies to enhance success rates, but the true benefit is actively debated. Growth hormone (GH) and dehydroepiandrosterone (DHEA) supplementation were assessed in women undergoing fresh IVF transfer cycles and categorized as poor prognosis from five criteria. METHODS: Data were retrospectively analyzed from 626 women undergoing 626 IVF cycles, where they received no adjuvant, GH alone, or GH-DHEA in combination. A small group received DHEA alone. The utilization of adjuvants was decided between the attending clinician and the patient depending on various factors including cost. RESULTS: Despite patients being significantly older with lower ovarian reserve, live birth rates were significantly greater with GH alone (18.6%) and with GH-DHEA (13.0%) in comparison to those with no adjuvant (p < 0.003). No significant difference was observed between the GH groups (p = 0.181). Overall, patient age, quality of the transferred embryo, and GH treatment were the only significant independent predictors of live birth chance. Following adjustment for patient age, antral follicle count, and quality of transferred embryo, GH alone and GH-DHEA led to a 7.1-fold and 5.6-fold increase in live birth chance, respectively (p < 0.000). CONCLUSION: These data indicated that GH adjuvant may support more live births, particularly in younger women, and importantly, the positive effects of GH treatment were still observed even if DHEA was also used in combination. However, supplementation with DHEA did not indicate any potentiating benefit or modify the effects of GH treatment. Due to the retrospective design, and the risk of a selection bias, caution is advised in the interpretation of the data.