ABSTRACT
INTRODUCTION: Ectopic pregnancy accounts for 1-2% of all pregnancies in the United States. The most common site of implantation for an ectopic pregnancy is the fallopian tube. We present the first case describing a recurrent ectopic pregnancy with a fetal heartbeat after ipsilateral salpingectomy that led to tubal rupture. PRESENTATION OF CASE: The patient presented with abdominal pain approximately six weeks after her last menstrual period. Seven years prior to presentation, a laparoscopic partial right salpingectomy had been performed for a tubal ectopic pregnancy. Physical exam was significant for diffuse abdominal tenderness and guarding. Ultrasonography revealed a right tubal pregnancy with a fetal pole and a fetal heart rate that was calculated to be 108 beats per minute. Free fluid was also noted. 1.5l of hemoperitoneum was subsequently evacuated and the right fallopian tube remnant with the ectopic pregnancy was removed. Pathology of the tubal remnant showed immature chorionic villi and fetal parts. DISCUSSION: The mechanism by which a recurrent ectopic pregnancy after ipsilateral salpingectomy occurs is unclear, but is theorized to be secondary to contralateral fertilization and/or tubal recanalization that may occur due to inadequate diathermy. CONCLUSION: Physicians should be aware that ectopic pregnancies may not only occur repeatedly but may also present a typically. We recommend when performing a salpingectomy that efforts be undertaken to minimize the length of the tubal remnant and to assure adequate coagulation of tissue so as to reduce the risk of recurrence.
ABSTRACT
OBJECTIVES: It is essential to understand the molecular basis of ovarian cancer etiology and tumor development to provide more effective preventive and therapeutic approaches to reduce mortality. Particularly, the molecular targets and pathways involved in early malignant transformation are still not clear. Pro-inflammatory lipids and pathways have been reported to play significant roles in ovarian cancer progression and metastasis. The major objective of this study was to explore and determine whether platelet activating factor (PAF) and receptor associated networking pathways might significantly induce malignant potential in BRCA1-mutant at-risk epithelial cells. METHODS: BRCA1-mutant ovarian epithelial cell lines including (HOSE-636, HOSE-642), BRCA1-mutant ovarian cancer cell (UWB1.289), wild type normal ovarian epithelial cell (HOSE-E6E7) and cancerous cell line (OVCA429), and the non-malignant BRCA1-mutant distal fallopian tube (fimbria) tissue specimens were used in this study. Mutation analysis, kinase microarray, western blot, immune staining, co-immune precipitation, cell cycle, apoptosis, proliferation and bioinformatic pathway analysis were applied. RESULTS: We found that PAF, as a potent pro-inflammatory mediator, induced significant anti-apoptotic effect in BRCA1-mutant ovarian surface epithelial cells, but not in wild type HOSE cells. With kinase microarray technology and the specific immune approaches, we found that phosphor-STAT1 was activated by 100 nM PAF treatment only in BRCA1-mutant associated at-risk ovarian epithelial cells and ovarian cancer cells, but not in BRCA1-wild type normal (HOSE-E6E7) or malignant (OVCA429) ovarian epithelial cells. Co-immune precipitation revealed that elevated PAFR expression is associated with protein-protein interactions of PAFR-FAK and FAK-STAT1 in BRCA1-mutant ovarian epithelial cells, but not in the wild-type control cells. CONCLUSION: Previous studies showed that potent inflammatory lipid mediators such as PAF and its receptor (PAFR) significantly contribute to cancer progression and metastasis. Our findings suggest that these potent inflammatory lipids and receptor pathways are significantly involved in the early malignant transformation through PAFR-FAK-STAT1 networking and to block apoptosis pathway in BRCA1 dysfunctional at-risk ovarian epithelium.
