The rate of VBAC was 77.8% in all women with a prior scar. During our management of VBAC, maternal or perinatal morbidity and mortality rates did not increase significantly.

We report a case of rectal cancer with microsatellite instability (MSI) that probably resulted from Lynch syndrome and that was diagnosed after Cesarean section. The patient was a 28-year-old woman (gravid 1, para 1) without a significant medical history. At 35 gestational weeks, vaginal ultrasonography revealed a 5 cm tumor behind the uterine cervix, which was diagnosed as a uterine myoma. The tumor gradually increased in size and blocked the birth canal, resulting in the patient undergoing an emergency Cesarean section. Postoperatively, the tumor was diagnosed as rectal cancer with MSI. After concurrent chemoradiation therapy, a lower anterior resection was performed. The patient's family history revealed she met the criteria of the revised Bethesda guidelines for testing the colorectal tumor for MSI. Testing revealed that the tumor did indeed show high MSI and, combined with the family history, suggested this could be a case of Lynch syndrome. Our findings emphasize the importance of considering the possibility of Lynch syndrome in pregnant women with colorectal cancer, particularly those with a family history of this condition. We suggest that the presence of Lynch syndrome should also be considered for any young woman with endometrial, ovarian, or colorectal cancer.

Fulminant type 1 diabetes is a new subtype of rapid-onset type 1 diabetes, with pancreatic exocrine dysfunction, that usually develops during the third trimester of pregnancy. We describe a patient with fulminant type 1 diabetes onset during her second trimester, resulting in premature delivery. The 34-year-old woman, without any known risk factors for diabetes mellitus, experienced a sudden stillbirth at 24-weeks gestation. Her blood glucose level was 950 mg/dL and she was positive for urine ketone bodies. The condition met all the diagnostic criteria for fulminant type 1 diabetes, and was diagnosed as such. Although this disease is rare, its progression is rapid, and its clinical course is severe and occasionally leads to death; therefore, a full knowledge of the disease is important to facilitate an accurate diagnosis.

To examine antiestrogenic effects of danazol through the receptor system and to clarify its direct effects on the endometrium in vivo, we applied danazol jelly directly into the rabbit uterine cavity and measured uterine estrogen, progesterone and androgen receptors (ER, PR and AR, respectively). Danazol significantly reduced ER, PR and AR (p < 0.05). Treatment with receptor-blocking agents (RU 486 and oxendolone) showed that the decrease in the ER level showed a closer association with that in PR than with AR. These results indicate that danazol directly administered into the uterine cavity is absorbed by the endometrial tissue and exerts its antiestrogenic effects possibly through PR in the cells.

Gestrinone has a biophysical antiestrogenic effect. But the mechanism of its antiestrogenic effect is not clear. Gestrinone blocked the increase of estrogen binding of nuclear type II sites and uterine weight in the estrogen-treated immature rabbit. Competitive assays indicated that gestrinone, at low concentrations (0.4 ∼ 4 nM), inhibited [³H]-estradiol binding to nuclear type II sites. This inhibitory effect was the same as the addition of 20 µM diethylstilbestrol. This inhibition with gestrinone on [³H]-estradiol binding to nuclear type II sites appeared only when used at concentrations less than an equivalent molar of [³H]-estradiol. Time course analysis of the gestrinone binding inhibition showed that within the first 6 min gestrinone did not inhibit specific [³H]-estradiol binding to nuclear type II sites. This gestrinone-mediated inhibition was not observed in soluble fractions such as the cytosolic and KCl-extracted nuclear binding sites. These results suggest that gestrinone acts primarily on the nuclear fraction and then it operates the inhibitory mechanism on estradiol binding to nuclear type II sites.