Foley catheter induction of labor as an outpatient procedure.

OBJECTIVE: The aim of our study was to introduce outpatient induction of labor by Foley catheter, and to compare outcomes and preferences between in-patients and outpatients. STUDY DESIGN: This clinical cohort study was conducted in Helsinki University Hospital between January 2011 and January 2012. A total of 485 women scheduled for induction of labor by Foley catheter were included. The main outcome measures were cesarean delivery rate, and maternal and neonatal infectious morbidity. Maternal satisfaction of outpatients was measured after delivery. RESULTS: Two hundred and four (42.1%) women were managed as outpatients and 281 (57.9%) women as in-patients. The rates of cesarean delivery, and maternal or neonatal infections did not differ between outpatients and in-patients. Of the outpatients, 85.3% were satisfied. CONCLUSION: Induction of labor by Foley catheter appears suitable for outpatients, and resulted in no differences in cesarean delivery or infection rates compared with in-patients. Most women were satisfied with the outpatient induction.

Monitoring and treatment of anti-D in pregnancy.

Prophylactic anti-D is a very safe and effective therapy for the suppression of anti-D immunization and thus prevention of haemolytic disease of the foetus and newborn. However, migration from countries with low health standards and substantial cuts in public health expenses have increased the incidence of anti-D immunization in many "developed" countries. Therefore, this forum focuses on prenatal monitoring standards and treatment strategies in pregnancies with anti-D alloimmunization. The following questions were addressed, and a response was obtained from 12 centres, mainly from Europe.

Overlap technique improves results of primary surgery after obstetric anal sphincter tear.

PURPOSE: This study was designed to evaluate prospectively the results of the overlap technique in primary sphincter reconstruction after obstetric tear. METHODS: Obstetric tears in 44 women were operated on with primary overlap reconstruction. These women were investigated six to nine months after the operation. Results were compared with those of a historical control group of 52 women whose obstetric sphincter rupture had been treated with the end-to-end technique. RESULTS: The overlap group had significantly more incontinence symptoms after delivery and repair of the sphincter tear than before delivery (P < 0.0001); however, their incontinence symptoms were significantly fewer than those of the end-to-end group (P = 0.004). The prevalence of persistent rupture of the external anal sphincter was significantly lower in the overlap group (6/44, 13.6 percent) than in the end-to-end group (39/52, 75 percent; P < 0.0001). Internal anal sphincter rupture occurred in 5 patients (11.4 percent) in the overlap group and in 40 patients (76.9 percent) in the end-to-end group (P < 0.0001). CONCLUSIONS: The overlap technique should be adopted as the method of choice for primary sphincter repair after obstetric tear.

Impact of infertility characteristics and treatment modalities on singleton pregnancies after assisted reproduction.

Obstetric and neonatal outcomes of assisted reproduction and control singletons were evaluated after taking into account treatment characteristics and infertility background. The elective single embryo transfer (eSET) group (n = 45) was compared with the compulsory single embryo transfer (cSET; n = 52), double embryo transfer (DET; n = 227) and control (n = 304) groups. Infertility-related prognostic factors for neonatal outcomes were also analysed. Data were collected with structured questionnaires at gestational week 20 and 8 weeks after delivery. Spontaneous onset of delivery was more typical of the eSET group than of cSET and DET groups (68.9 versus 52.0%, P = 0.02). Mean (+/-SD) gestation at birth (39.3 +/- 1.6 weeks) and mean birth weight (3,470 +/- 505 g) of eSET singletons were comparable with other assisted reproduction groups, but gestational duration was lower than in the eSET group than in the control group (39.9 +/- 1.4; P < 0.05). However, numbers of preterm births and low birth weight infants were similar between groups. History of induced abortion increased risk of preterm birth (OR 4.5 and 95% CI 1.2-17.1) in assisted reproduction singletons. A small though clinically unimportant difference in gestational age at birth and birth weight between assisted reproduction and control singletons was found regardless of the number of embryos transferred.

Motor vehicle accident during the second or third trimester of pregnancy.

OBJECTIVE: To evaluate the need of immediate treatment, follow-up and consequences of different types of traffic accidents during pregnancy. METHOD AND MATERIAL: A retrospective analysis covering five years involving thirty-five pregnant women involved in motor vehicle accidents at 22-39 weeks of gestation. RESULTS: Fifteen of the 35 women were involved in frontal impact collisions, and suffered mild subjective and objective symptoms; all their fetuses survived and were delivered at term. Fifteen other women were involved in broadside collisions; two of these were riding a bicycle. These 15 women had clear objective findings like uterine contractions or tenderness, and some of them needed tocolytic therapy and hospitalization up to eight days. This was significantly longer than in those involved in frontal impact collisions. However, the broadside accidents did not have any adverse effect on pregnancy outcomes either. Five women were involved in serious accidents at speeds of 80-110 km/h, and one mother and her fetus died immediately because of rupture of the uterus and the cervical joint and spinal canal. Four other fetuses were found dead on arrival at hospital or soon after. In all cases the cause of fetal loss was placental abruption. The presence of fetal blood cells in maternal blood was evaluated in 15 of 35 patients, but was positive in only one. CONCLUSION: Frontal collisions are associated with lower vehicular speed, less trauma and no acute or later effects on pregnancy, whereas broadside collisions and high speed (> 80 km/h) cause more symptoms. The latter type of accidents are associated with high risk of placental abruption and of fetal and maternal death. Fortunately the symptoms are evident immediately after the accident, and early hospital discharge is possible if no abnormalities are present during the first hours.

Effect of interleukin 2 on urinary excretion of degradation products of prostacyclin and thromboxane A2 in patients with ovarian cancer.

We studied the effect of intraperitoneal recombinant interleukin 2 (rIL-2) on the production of prostacyclin (PGI2) and thromboxane A2 (TxA2) in six patients with metastatic ovarian malignancy. Time-span urine samples collected before and after 17 intraperitoneal instillations of IL-2 (6 x 10(5) IU m-2) were assessed for 2,3-dinor-6-keto-prostaglandin F1 alpha (dinor-6-keto; a metabolite reflecting the in vivo product of PGI2) and 2,3-dinor-thromboxane B2 (dinor-TxB2; a metabolite reflecting the production of TxA2). Analysis was by high-pressure liquid chromatography, followed by radioimmunoassay. Recombinant IL-2 administration was accompanied by a significant rise (85%; P < 0.02) in the output of dinor-6-keto within the first 2 h, and this elevation persisted for up to 6 h. Moreover, output of dinor-TxB2 also rose; this rise (30%) was significant (P < 0.02) 6 h after the instillation. These effects may, in some yet unknown manner, prove significant in the anti-cancer action of rIL-2.

Urinary excretion of degradation products of prostacyclin and thromboxane is increased in patients with gestational choriocarcinoma.

Gestational choriocarcinoma metastasizes rapidly, in which process the vasoactive prostanoids may be significant. We therefore compared the urinary excretion of prostacyclin and thromboxane A2 (TxA2) metabolites in 19 women with gestational choriocarcinoma and 20 healthy age-matched women by assessing spot urine samples for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and 2,3-dinor-6-keto-prostaglandin F1 alpha (2,3-dinor-6-keto-PGF1 alpha) (degradation products of prostacyclin) as well as for thromboxane B2 (TxB2) and 2,3-dinor-TxB2 (degradation products of TxA2) by high-pressure liquid chromatography, followed by radioimmunoassay; the data were related to urinary creatinine concentration. The urinary output of 6-keto-PGF1 alpha [29.56 +/- 7.0 versus 25.08 +/- 3.91 ng/mmol creatinine (SE)] in patients with choriocarcinoma was normal, but that of 2,3-dinor-6-keto-PGF1 alpha in cancer patients was higher than in controls (24.44 +/- 5.20 versus 14.84 +/- 1.94, P less than 0.02), as was that of TxB2 (22.72 +/- 4.69 versus 9.69 +/- 1.52, P less than 0.001) and 2,3-dinor-TxB2 (114.21 +/- 30.81 versus 51.81 +/- 10.40, P less than 0.01). The ratio of net prostacyclin output (6-keto-PGF1 alpha plus 2,3-dinor-6-keto-PGF1 alpha) to the net TxA2 output (TxB2 plus 2,3-dinor-TxB2) in cancer patients [0.52 +/- 0.1 (SE)] was lower (P less than 0.03) than in the controls (0.83 +/- 0.1), and in an inverse relation (r = -0.54, P less than 0.05) to the scoring index of poor prognosis for the disease. We conclude that the prostanoid excess in gestational trophoblastic disease, as evidenced for the first time in this study, may originate from choriocarcinoma cells, or may be a paraneoplastic phenomenon, and we conclude also that TxA2 excess may contribute to the tumor growth and/or formation of metastases.

Prostacyclin and thromboxane synthesis by endometrial cancer and leiomyomas.

To study the role of prostacyclin (PGI2) and thromboxane A2 (TxA2) in uterine tumors, pieces of endometrial cancer (n = 12) and leiomyomas (n = 12) were incubated in vitro, and the productions of 6-keto-prostaglandin F1a (6-keto-PGF1a, a hydration product of PGI2) and thromboxane B2 (TxB2, a hydration product of TxA2), measured by radioimmunoassay, were compared to those of corresponding healthy tissues. The production of 6-keto-PGF1a by endometrial cancer (20.8; 15.1-85.0 ng/mg protein/min, median and interquartile range), by healthy endometrium (25.5; 10.0-55.0), by healthy myometrium (34.9; 25.0-59.9) and by leiomyoma (20.3; 10.2-45.1) was similar. The production of TxB2 was increased by endometrial cancer (55.5; 10.5-155.2, p less than 0.02) in comparison with endometrium (9.8; 4.3-35.1), myometrium (3.8; 2.1-8.0) and leiomyoma (1.9; 1.0-3.8). The 6-keto-PGF1a/TxB2 ratio in endometrial cancer (0.9; 0.3-1.5) was smaller (p less than 0.02) than that in healthy endometrium (3.3; 1.9-4.8). Thus, TxA2 may be a factor in endometrial cancer.

Urinary excretion of prostacyclin and thromboxane degradation products in patients with ovarian malignancy: effect of cytostatic treatment.

We studied the effect of ovarian cancer and its chemotherapy on the urinary excretion of prostacyclin (PGI2) and thromboxane A2 (TxA2) hydration and metabolic products. In six patients we measured 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha (PGI2 products) and thromboxane B2 (TxB2) and 2,3-dinor-TxB2 (TxA2 products) by HPLC followed by radioimmunoassay before, during and after the combined infusion of cisplatin, 4'epi-adriamycin and cyclophosphamide. Before the first cytostatic infusion, the urinary excretion of prostanoids was on average 4.4-5.8 times higher than in patients with ovarian endometriosis (n = 19). The infusion of cytostatics led to a 50-120% rise in the excretion of prostanoids during the first post-infusion 9 hours, but in the subsequent 10 hours their output was 25-45% below the initial value and remained low for at least 2 weeks. Following repetitive courses of cytostatics (2-4 per patient), prostanoid excretion tended to normalise. These data suggest that ovarian cancer is associated with increased production of PGI2 and TxA2, and that cytostatics suppress this production. This may be of biological significance in tumour behaviour and in the effect of cytostatics.

Increased synthesis of prostacyclin and thromboxane in human ovarian malignancy.

To study the production of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane (TxA2) by ovarian tumors, we incubated pieces of benign and malignant ovarian tissue in vitro, and measured by radioimmunoassay the release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (a hydration product of PGI2) and thromboxane B2 (TxB2) (a hydration product of TxA2). Healthy ovary (n = 10) produced both 6-keto-PGF1 alpha [mean, 8.9; 95% confidence interval (CI) from 5.4 to 15.2 ng/mg protein/min] and TxB2 (mean, 1.9 ng/mg protein/min; 95% CI from 1.0 to 3.7 ng/mg protein/min). The production of 6-keto-PGF1 alpha (mean, 12.2; 95% CI from 7.7 to 19.3 ng/mg protein/min) and that of TxB2 (mean, 4.8; 95% CI from 2.1 to 11.9 ng/mg protein/min) by benign cystic tumors (n = 12) was normal. Ovarian anaplastic cancer and adenocarcinoma (n = 12) produced 6-keto-PGF1 alpha on average 11.6-fold (95% CI from 5.2 to 26.0) 6-keto-PGF1 alpha and TxB2 on average 30.0-fold (95% CI from 13.5 to 66.7) over production by healthy ovaries, and the ratio of 6-keto-PGF1 alpha to TxB2 shifted to the dominance of TxB2. Similarly ovarian metastases of breast cancer, tubal cancer, and colon cancer produced increasingly 6-keto-PGF1 alpha (mean, 20.7 ng/mg protein/min) and TxB2 (5.1 ng/mg protein/min). The dominance of TxA2 in human ovarian cancer may contribute to the aggressing growth and spreading of this tumor.

Urinary 6-keto-prostaglandin F1a in patients with gynaecological tumours.

The production of the antiaggregatory and vasodilatory prostacyclin (PGI2) in patients with gynaecological tumours was studied by assaying urinary 6-keto-prostaglandin F1a (= 6-keto-PGF1a), a hydration product of PGI2), by radioimmunoassay following high performance liquid chromatography (HPLC) in 59 patients with gynaecological tumours and 12 non-tumourous control women. Urinary 6-keto-PGF1a excretion in patients with cervical cancer (28.3 +/- 3.6 pmol/mmol creatinine, mean +/- S.E., n = 12), endometrial cancer (22.8 +/- 3.7 pmol/mmol creatinine, n = 12, uterine fibroids (26.0 +/- 3.5 pmol/mmol creatinine, n = 12) benign ovarian cysts (22.4 +/- 1.8 pmol/mmol creatinine, n = 12) did not differ from that in the control women (29.9 +/- 3.6 pmol/mmol creatinine, n = 12). However, patients with ovarian cancer excreted increased amounts of 6-keto-PGF1a (55.4 +/- 10.4 pmol/mmol creatinine, n = 11, P less than 0.05), although this bore no relation to tumour histology, clinical stage or the outcome of the patients. Thus, ovarian cancer is accompanied by increased PGI2 production, perhaps in the kidneys and/or in the cancer tissue.

Prostacyclin and thromboxane in breast cancer: relationship between steroid receptor status and medroxyprogesterone acetate.

To study the production and significance of prostacyclin (PGI2) and thromboxane A2 (TxA2) in breast cancer, tissue fragments of breast cancer (n=23) and mastopathy (n=10) were superfused in vitro and the release of 6-keto-PGF1 alpha (a metabolite of PG12) and TxB2 (a metabolite of TxA2) measured by radioimmunoassay. Breast cancer formed more 6-keto-PGF1 alpha (4.5 +/- 0.9 ng min-1 g-1 of tissue dry weight, mean +/- s.e.) and TxB2 (2.5 +/- 0.6 ng min-1 g-1) (P less than 0.01) than did mastopathic breast (1.4 +/- 0.5 and 0.4 +/- 0.1 ng min-1 g-1, respectively). These productions were similar in steroid receptor positive and negative tumours. Breast cancer metastasized in 15 patients during the follow-up time of 3.7 +/- 0.7 years, but the initial prostanoid productions in these patients were not different from those in nonmetastatic patients. Two patients died from metastases, but their initial mammary production of prostanoids was not profoundly different from those in the survivors. In 8 patients (4 with steroid receptor positive and 4 with negative tumour), the cancer tissue was superfused in the presence or absence of medroxyprogesterone acetate (100-5000 ng ml-1), which is commonly used for treatment of breast cancer. This hormone had no effect on mammary PGI2 and TxA2 production. We thus conclude that the PGI2 and TxA2 productions are increased in mammary cancer but that this may not be of primary significance for metastastic spread.