Postpartum hemorrhage (PPH) remains a leading cause of maternal death worldwide, and it is important to understand the relative contributions of different risk factors. We assessed the incidence of these among cases of transvaginal delivery. Between June 2013 and July 2016, a prospective cohort study was conducted at a tertiary perinatal medical facility in Japan. Women were administered a questionnaire to ascertain risk factors for PPH, defined as a blood loss of 1,000 ml or more assessed using a calibrated under-buttocks drape and collection vessel at childbirth. We analyzed 1,068 transvaginal deliveries of singleton pregnancies. The incidence of PPH was 8.7%, and of severe PPH (1,500 ml blood loss or more) was 2.1%. Risk factors for postpartum hemorrhage among the deliveries were: fetal macrosomia (over 4000 g); pregnancy-induced hypertension; pregnancy generated by assisted reproductive technology; severe vaginal or perineal lacerations; and weight gain over 15 kg during pregnancy. Such high weight gain significantly increased the incidence of PPH compared with women showing less than 10 kg weight gain during pregnancy. Monitoring these identified risk factors could enable extra vigilance during labor, and preparedness for managing PPH in all women giving birth.

No abstract

No abstract

No abstract

Increased expression of heparin-binding EGF-like growth factor (HB-EGF) and membrane-type matrix metalloproteinase-1 (MT1-MMP) is frequently associated with various types of malignant tumor. HB EGF-like growth factor has been reported to promote the malignant progression of ovarian carcinoma. Based on this finding, inhibition of HB-EGF activity with CRM197 is now under phase I clinical evaluation. On the other hand, MT1-MMP expressed in ovarian carcinoma cells is thought to promote invasion and growth of tumor cells by degrading the extracellular matrix. However, we recently demonstrated that co-expression of MT1-MMP and HB-EGF in gastric carcinoma cells leads to cleavage of HB-EGF within its N-terminal heparin-binding region, converting it into a potent heparin-independent growth factor. In this study, we evaluated the importance of regulation of HB-EGF by MT1-MMP in clinical samples of ovarian carcinoma. We detected co-expression of HB-EGF and MT1-MMP in clear cell ovarian carcinoma tissues, particularly at the invasion front and in tumor cells that had disseminated into the ascites, whereas HB-EGF alone was expressed in non-invasive borderline ovarian tumor tissue. Furthermore, a soluble HB-EGF fragment that corresponds to that processed by MT1-MMP was detected in malignant ascites obtained from patients with metastatic ovarian carcinoma. Ovarian carcinoma cells that express MT1-MMP and HB-EGF exhibited enhanced cell growth in a 3D-collagen matrix and anchorage-independent growth in suspension. These results indicate that MT1-MMP coexpressed with HB-EGF in ovarian carcinoma cells potentiates the activity of HB-EGF to promote invasive tumor growth and spreading in vivo. (Cancer Sci 2011; 102: 111-116) O varian carcinoma has the greatest mortality among gynecological cancers, with a rate of cure that has not improved over the last 30 years.(1) The growth of many types of tumor cells is dependent on signals mediated by ErbB family receptors.(2) Indeed, inhibition of signaling by these receptors is a promising therapeutic approach to cancer, as has been shown with drugs such as gefitinib, lapatinib and erlotinib.(3) Members of the EGF family of growth factors bind to ErbB receptors and one or more such ligands have been exploited by tumor cells to support their growth. Heparin-binding EGF-like growth factor (HB-EGF) is the predominant growth factor responsible for supporting the growth of human ovarian carcinomas and it plays a key role in the acquisition of malignant tumor phenotypes such as rapid growth, spreading into the abdominal cavity and resistance to chemotherapy.(5) CRM197 is a mutant diphtheria toxin fragment that binds HB-EGF and prevents the latter from binding ErbB receptors. It is currently being evaluated in a phase I clinical trial to treat ovarian carcinoma patients. (5) Similarly to other members of the EGF family, HB-EGF is synthesized as a transmembrane protein (proHB-EGF).(6) Ectodomain shedding of proHB-EGF is mediated by members of the ADAM (A Disintegrin And Metalloprotease) family of ...

Small-cell carcinoma of the endometrium is a rare neoplasm, and its aggressive behavior has been reported. We report a case of small-cell carcinoma occurring primarily in the endometrium of a 62-year-old woman with postmenopausal vaginal bleeding and lower abdominal pain. The excised uterus showed a necrotic polypoid mass and histologically displayed an endometrial small-cell carcinoma. Immuno-histochemically, the tumor cells were positive for cytokeratin, the epithelial membrane antigen, neuron-specific enolase, and chromogranin, but were negative for the leukocyte common antigen and Grimelius stain. Ultrastructural analysis revealed the presence of dense core granules in the cytoplasm of tumor cells. The patient died 2 months after surgery because of aggressive behavior of the tumor. We wish to distinguish small-cell carcinoma of the endometrium from conventional epithelial tumors of the endometrium, because of the former's distinctive histopathologic, immunohistochemical, and ultrastructural characteristics.

The purpose of this study was to determine whether docetaxel has antitumour activity in patients with advanced or recurrent endometrial carcinoma. Chemotherapy-naïve or previously treated patients (one regimen) with histopathologically documented endometrial carcinoma and Eastern Cooperative Oncology Group performance status p2 entered the study. Docetaxel 70 mg m À2 was administered intravenously on day 1 of a 3-week cycle up to a maximum of six cycles. If patients responded well to docetaxel, additional cycles were administered until progressive disease or unacceptable toxicity occurred. Of 33 patients with a median age of 59 years (range, 39 -74 years) who entered the study, 14 patients (42%) had received one prior chemotherapy regimen. In all, 32 patients were evaluable for efficacy, yielding an overall response rate of 31% (95% confidence interval, 16.1 -50.0%); complete response and partial response (PR) were 3 and 28%, respectively. Of 13 pretreated patients, three (23%) had a PR. The median duration of response was 1.8 months. The median time to progression was 3.9 months. The predominant toxicity was grade 3 -4 neutropenia, occurring in 94% of the patients, although febrile neutropenia arose in 9% of the patients. Oedema was mild and infrequent. Docetaxel has antitumour activity in patients with advanced or recurrent endometrial carcinoma, including those previously treated with chemotherapy; however, the effect was transient and accompanied by pronounced neutropenia in most patients.

Histopathologic changes in lymph nodes were examined from ten patients with mild lymphadenopathy, a few atypical lymphocytes in their peripheral blood, skin lesions, and proviral DNA of human T‐cell leukemia virus type I (HTLV‐I) in their nodes. The proviral DNA of HTLV‐I was detected by southern blot analysis, in situ hybridization, and/or polymerase chain reaction techniques. The lymph nodes showed preserved nodal architecture with diffuse infiltration of small to intermediate‐sized lymphocytes in association with scattered transformed lymphocytes and a few immunoblast‐like cells in the enlarged paracortex. The infiltrating lymphocytes were positive for CD4, but neither rearrangement nor deletion of T‐cell receptors and immunoglobulin heavy chain genes was detected. Eight of ten patients received no therapy, and all patients were alive and healthy more than 5 months after the biopsies. The histologic findings resembled those of a viral infection and could be distinguished from HTLV‐I associated lymphomas.