Stepwise approach to the laparoscopic excision of bladder endometriosis.

OBJECTIVE: To describe a stepwise approach to the laparoscopic excision of bladder endometriosis. DESIGN: Narrated surgical video. SETTING: Academic tertiary care hospital. PATIENT(S): Surgical footage was obtained from three patients who underwent surgery for bladder endometriosis. Institutional review board approval was not required in accordance with the Tri-Council Policy Statement of Canada, article 2.5. INTERVENTION(S): Laparoscopic excision of bladder endometriotic nodules by partial cystectomy. MAIN OUTCOME MEASURE(S): Overview of the relevant anatomy, disease overview, surgical planning and perioperative care, and the approach to the excision of bladder endometriotic nodules. RESULT(S): The approach to excision of bladder endometriotic nodules can be standardized in six reproducible steps: cystoscopy with or without ureteral stent placement; abdominal survey and treatment of posterior compartment disease; bladder mobilization; partial bladder cystectomy under cystoscopic guidance; cystotomy closure; and water-leak test. CONCLUSION(S): The safe and complete excision of bladder endometriosis relies on the understanding of surgical anatomy, the multidisciplinary aspect of patient care, and the standardization of the surgical approach.

Laparoscopic excision of pericardial and diaphragmatic endometriosis.

OBJECTIVE: To present a five-step approach to the laparoscopic excision of pericardial and diaphragmatic endometriosis. DESIGN: Surgical video. SETTING: Academic tertiary care hospital. PATIENT(S): 35-year-old nulliparous woman observed for chronic pelvic pain and infertility with a diagnosis of diaphragmatic endometriosis at a prior laparoscopy. Symptoms included severe chest pain and right shoulder tip pain, refractory to multiple medical therapies. INTERVENTION(S): Laparoscopic excision of pericardial and diaphragmatic endometriosis. MAIN OUTCOME MEASURE(S): Description of the relevant anatomy, the literature surrounding pericardial and diaphragmatic endometriosis, and the approach to the surgical intervention and postoperative care. RESULT(S): The laparoscopic excision of the full-thickness pericardial and diaphragmatic endometriotic lesions was successfully completed according to five reproducible steps: upper abdominal survey, liver mobilization, excision of diaphragmatic endometriosis, intrathoracic laparoscopic exploration, and closure of the diaphragmatic defect. CONCLUSION(S): Although rare and challenging to diagnose and treat, pericardial and diaphragmatic endometriosis and its potentially debilitating symptoms can be successfully managed through a multidisciplinary and stepwise surgical intervention.

Bowel surgery for endometriosis: A practical look at short- and long-term complications.

Endometriosis involving the bowel requires a thorough evaluation prior to deciding upon surgical treatment. Patient symptoms, treatment goals, extent and location of disease, surgeon experience, and anticipated risks all play a part in the preoperative decision-making process. Short- and long-term complications after bowel surgery for endometriosis are the focus of this article. Unfortunately, the literature to date has inherent limitations that prevent generalizability. Most studies are retrospective or prospective single-center case series. Publication bias is unavoidable with mainly large volume experts sharing their experience. As a result, there is a need for high-quality prospective studies that standardize inclusion criteria and outcome measures among various centers with an aim to present long-term outcomes. In the meantime, care for those with endometriosis involving the bowel requires a thorough preoperative plan to minimize risks and a need for early diagnosis and management of complications unique to bowel surgery.

Progesterone and HMOX-1 promote fetal growth by CD8+ T cell modulation.

Intrauterine growth restriction (IUGR) affects up to 10% of pregnancies in Western societies. IUGR is a strong predictor of reduced short-term neonatal survival and impairs long-term health in children. Placental insufficiency is often associated with IUGR; however, the molecular mechanisms involved in the pathogenesis of placental insufficiency and IUGR are largely unknown. Here, we developed a mouse model of fetal-growth restriction and placental insufficiency that is induced by a midgestational stress challenge. Compared with control animals, pregnant dams subjected to gestational stress exhibited reduced progesterone levels and placental heme oxygenase 1 (Hmox1) expression and increased methylation at distinct regions of the placental Hmox1 promoter. These stress-triggered changes were accompanied by an altered CD8+ T cell response, as evidenced by a reduction of tolerogenic CD8+CD122+ T cells and an increase of cytotoxic CD8+ T cells. Using progesterone receptor- or Hmox1-deficient mice, we identified progesterone as an upstream modulator of placental Hmox1 expression. Supplementation of progesterone or depletion of CD8+ T cells revealed that progesterone suppresses CD8+ T cell cytotoxicity, whereas the generation of CD8+CD122+ T cells is supported by Hmox1 and ameliorates fetal-growth restriction in Hmox1 deficiency. These observations in mice could promote the identification of pregnancies at risk for IUGR and the generation of clinical interventional strategies.

Highway to health; or How prenatal factors determine disease risks in the later life of the offspring.

Fetal development is largely dependent on the mother. However, pregnancy maintenance and consequently fetal development are highly vulnerable and sensitive to disruption, triggered by, for example, prenatal stress challenge. Such prenatal stress challenge modulates the maternal endocrine and immune responses during pregnancy e.g. by decreasing levels of progesterone. Prenatal stress also has negative repercussions for the child's health later in life. It has been reported that prenatal stress increases the risk of the child to develop chronic immune diseases such as allergies and asthma. We therefore propose that prenatal stress challenge - associated with a decrease in maternal progesterone - impairs fetal immune development (immune ontogeny). Such impaired immune ontogeny carries over into postnatal life, rendering the child more prone to developing chronic immune diseases. This purported association urgently requires a fresh evaluation in order to identify biomarkers and cascades of events. In the present review, we outline candidate biomarkers involved in fetal immune ontogeny, which may be targets of prenatal stress challenge and subsequently determine offspring disease risk. Identification of these stress-sensitive biomarkers may allow detection of pregnant women at risk to deliver chronic immune disease-prone offspring. The creation of therapeutic interventions designed to prevent negative consequences of prenatal stress would then be within reach.