Vasopressin Injection Purse-String Ectopic Resection technique for laparoscopic management of cornual ectopic pregnancy.

Although cornual pregnancy is a rare form of ectopic pregnancy, the associated mortality rate is considerably higher than that of ectopic pregnancy overall. Historically, cornual ectopic pregnancy has been treated via laparotomy. With advancements in technology, equipment, and technique, laparoscopy offers a safer approach for the management of cornual pregnancy. However, laparoscopy of this nature requires excellent technique. The Vasopressin Injection Purse-String Ectopic Resection technique serves as an effective strategy for the laparoscopic management of cornual ectopic pregnancy. First, dilute vasopressin is administered into the myometrium surrounding the pregnancy. Next, a purse-string stitch is placed in the myometrium circumferential to the pregnancy. Finally, the pregnancy is excised by cornual wedge resection, and the defect is repaired using the attached remaining suture from the purse-string stitch. The Figure shows the graphical depiction of the Vasopressin Injection Purse-String Ectopic Resection technique, and the Video shows a laparoscopic recording of the Vasopressin Injection Purse-String Ectopic Resection technique. Between 2012 and 2022, 17 patients underwent a laparoscopic cornual ectopic pregnancy resection at a high-volume academic hospital and its affiliated community hospital. This case series revealed a mean operative time of 107 minutes, with a mean estimated blood loss of 41 mL for nonruptured ectopic pregnancies and 412 mL for ruptured ectopic pregnancies. No case was converted to laparotomy. Our findings suggest that the integration of the vasopressin administration and the pursue-string stitch placement minimizes blood loss and mitigates the risk of conversion to laparotomy for both nonruptured and ruptured cornual ectopic pregnancies.

Gut microbiota-derived short-chain fatty acids protect against the progression of endometriosis.

Worldwide, ∼196 million are afflicted with endometriosis, a painful disease in which endometrial tissue implants and proliferates on abdominal peritoneal surfaces. Theories on the origin of endometriosis remained inconclusive. Whereas up to 90% of women experience retrograde menstruation, only 10% develop endometriosis, suggesting that factors that alter peritoneal environment might contribute to endometriosis. Herein, we report that whereas some gut bacteria promote endometriosis, others protect against endometriosis by fermenting fiber to produce short-chain fatty acids. Specifically, we found that altered gut microbiota drives endometriotic lesion growth and feces from mice with endometriosis contained less of short-chain fatty acid and n-butyrate than feces from mice without endometriosis. Treatment with n-butyrate reduced growth of both mouse endometriotic lesions and human endometriotic lesions in a pre-clinical mouse model. Mechanistic studies revealed that n-butyrate inhibited human endometriotic cell survival and lesion growth through G-protein-coupled receptors, histone deacetylases, and a GTPase activating protein, RAP1GAP. Our findings will enable future studies aimed at developing diagnostic tests, gut bacteria metabolites and treatment strategies, dietary supplements, n-butyrate analogs, or probiotics for endometriosis.