gestational trophoblastic disease/プロゲステロン

The purpose of this study is to evaluate the immunohistochemical detection of telomerase enzyme and estrogen receptor (ER) and progesterone receptor (PGR) in gestational trophoblastic neoplasia (GTN) and its clinical significance. Formalin-fixed paraffin blocks for 30 patients (24 with molar

OBJECTIVE To evaluate the utility of the serum progesterone level for discriminating pregnancy from gestational trophoblastic neoplasia. METHODS Serum progesterone levels were measured in 61 women with histories of trophoblastic disease who developed a re-elevation in hCG during surveillance and

Serial assays of serum progesterone and serum human chorionic gonadotropin (HCG) were performed in eight cases of choriocarcinoma before and during treatment of the disease. Serum progesterone was measured by the competitive protein-binding technique and serum HCG was measured by the

To evaluate the influence of hormonal contraception (HC) on the development and clinical aggressiveness of gestational trophoblastic neoplasia (GTN) and the time for normalization of human chorionic gonadotropin (hCG) levels. A retrospective cohort study was conducted with women diagnosed with molar

Plasma prolactin, progesterone, and 17 beta-estradiol were measured by radioimmunoassay in 58 patients with complete moles, 17 patients with partial moles, and the same number of maturity-matched pregnant control subjects. In both complete and partial moles in the first trimester, the pre-evacuation

The effect of oral Etoposide (VP-16-213) on the ovarian function in 22 patients with residual gestational trophoblastic disease was studied by serial weekly measurement of serum follicle stimulating hormone (FSH), 17 beta-estradiol (E2), progesterone (P) and prolactin (PRL), and monitoring of the

Serum and urine steroids were examined in two subjects with trophoblastic disease accompanied by large ovarian theca-lutein cysts and compared with those from 10 patients with trophoblastic disease but without palpable cysts. In the patients without cysts normal values were obtained for serum

Thirty-four patients with low risk gestational trophoblastic disease were treated with etoposide alone. Within 60 days after treatment, synthetic luteinizing hormone releasing hormone (LH-RH: 100 micrograms) was injected intravenously. The serum concentrations of LH, follicle-stimulating hormone

The purpose of this study was to provide a diagnostic and a prognostic variable that could easily be measured in the laboratory, and that would predict the need for future therapy of persistent gestational trophoblastic disease. There would no longer be a need to treat all cases of hydatidiform mole

Serial serum progesterone and beta human chorionic gonadotropin (beta hCG) levels were measured during surveillance of 24 women at risk for development of gestational trophoblastic neoplasia (GTN) following evacuation of complete molar gestations. Six of the 24 patients developed post-molar GTN. The

BACKGROUND Gestational trophoblastic disease (GTD) consists of a spectrum of disorders that are characterized by an abnormal proliferation of trophoblastic tissue. Gestational trophoblastic neoplasia (GTN) refers to a subset of GTD with a persistently elevated serum hCG in the absence of a normal

Serum 17alpha-hydroxprogesterone (17-OHP), progesterone (P), and human chorionic gonadotropin (hCG) levels were measured by specific radioimmunoassay in 19 patients undergoing laparoscopy or laparotomy with either unevacuated molar pregnancy or nonmetastatic gestational trophoblastic neoplasms

Concentrations of human chorionic gonadotropin (HCG), human placental lactogen (HPL), prolactin (PRL), follicle-stimulating hormone (FSH), estradiol (E2) and progesterone (P) were measured in serum and fluid from ovarian theca lutein cysts (TC) in patients with gestational trophoblastic disease

Progesterone administration prevents spontaneous preterm birth (sPTB) in women at increased risk. Progesterone concentration is lower in women with subsequent sPTB. Conversely, high concentrations of progesterone are implicated in the pathogenesis of hyperemesis gravidarum (HG). We hypothesized that