Objective. To determine the effects of Mullerian inhibiting substance (MIS) treatment on endometriosis cells through study of apoptosis and autophagy. Design. Experimental in vitro study. Setting. University research laboratory. Cell Line. CRL-7566 endometriosis cell line. This line was established from a benign ovarian cyst taken from a patient with endometriosis. Interventions. In vitro treatment with MIS. Main Outcome Measures. The main outcome measures were cellular viability, proliferation, cell-cycle arrest, and induction of apoptosis and autophagy in endometriotic cells. Results. MIS treatment inhibited proliferation of endometriosis cells and induced apoptosis, as indicated by Annexin V staining, and induced caspase-9 cleavage and cell-cycle arrest, as evidenced by increased expression of p27 CDK-inhibitor. MIS treatment also induced autophagy in endometriosis cells as demonstrated by a significant increase in LC3-II induction, a hallmark of autophagy. Conclusions. MIS inhibits cell growth and induces autophagy, as well as apoptosis, in ectopic endometrial cell lines. Our results suggest that MIS may have a potential as a novel approach for medical treatment of endometriosis. Further studies may be needed to test the efficacy of MIS treatment in animal models and to develop MIS treatment specifically targeted to the endometriosis.

Routine use of prophylactic antibiotics reduces the risk of postcesarean fever and infections by over 50% in both nonelective and elective (scheduled) procedures. Although anaphylaxis to prophylactic antibiotics is rare, potentially fatal complications might occur. Herein, we present a case where disseminated intravascular coagulation and reversible ischemic neurological deficit complicated anaphylactic reactions to prophylactic antibiotics administered during cesarean delivery. A 27-year-old gravida 9, para 7 at 392/7 weeks underwent elective repeat cesarean delivery and bilateral tubal ligation. Her surgery was complicated by intraoperative hypotension, generalized itching, and urticarial skin rash consistent with anaphylactic reaction upon administering prophylactic cefazolin. In the recovery room, she continued to be hemodynamically unstable despite energetic resuscitation. Hemoperitoneum was suspected, and laboratory evaluation indicated disseminated intravascular coagulation. Abdominal exploration revealed massive hemoperitoneum, but there was no source of active bleeding noted. The postoperative course was complicated by reversible ischemic neurological deficit, which resolved on expectant management. Disseminated intravascular coagulation and reversible ischemic neurological deficit may complicate anaphylactic reaction to prophylactic antibiotics administered during cesarean delivery. Immediate recognition and intervention is crucial for a successful outcome.

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