Endometrial rollerball ablation.

OBJECTIVE: To study a standardized technique for endometrial rollerball ablation and various methods of preoperative preparation. STUDY DESIGN: All patients had refractory symptomatic menorrhagia and previously failed conservative surgery and other forms of medical therapy, such as progestogens. Patients received a preoperative regimen of either leuprolide acetate, danazol, Nolvadex or Depo-Provera. They then underwent hysteroscopically controlled rollerball ablation at 80-100 W with 1.5% glycine as the distending medium. The endometrium was evaluated hysteroscopically and considered to be completely atrophic, intermediate or no response. RESULTS: Refractory symptomatic menorrhagia was treated successfully in 38 of 40 patients. Nineteen reported amenorrhea; the other 21 reported subjective and objective improvement of bleeding. Three patients, despite improvements in flow, were unhappy with the overall result. Two did not wish repeat ablation and subsequently underwent vaginal hysterectomy. The third underwent repeat ablation and became amenorrheic. The ability to achieve complete endometrial atrophy prior to ablation was improved with leuprolide acetate (19/24) and danazol (5/6) when compared to tamoxifen (0/4) and Depo-Provera (0/6). Attainment of amenorrhea after ablation was significantly improved when complete atrophy (19/24) was achieved prior to ablation as compared to the ability to achieve amenorrhea when no endometrial response was achieved (0/7). The only significant complication was one uterine perforation in a patient undergoing repeat ablation. CONCLUSION: Endometrial rollerball ablation is a safe, effective means of controlling refractory menorrhagia. Amenorrhea is best attained when complete preoperative atrophy is achieved. Leuprolide and danazol were superior to tamoxifen and Depo-Provera.

Interaction of the anti-oestrogen, nafoxidine hydrochloride, with the soluble nuclear oestradiol-binding protein in chick liver.

Nafoxidine hydrochloride (Upjohn, 11100A)injected with oestradiol into immature chicks inhibits the hormone-induced increase in [3H]oestradiol-binding activity in salt extracts of liver nuclei as well as the subsequent production by liver of egg-yolk phosphoprotein. Substantial inhibition of both oestradiol-induced responses is seen when nafoxidine is given in a dose approximately equimolar with that of oestradiol. In vitro nafoxidine competitively inhibits binding of [3H]oestradiol in nuclear extracts. The Ki for the inhibition is 43 nM, which indicates an affinity of nafoxidine for the binding protein about 4% of that of oestradiol. The inhibitory action of nafoxidine in vivo thus is more potent than the relative binding affinity determined in vitro might indicate. One possible explanation is that the primary site of nafoxidine action is at a point proximal to nuclear receptor interaction. Nafoxidine injected alone into the chick does not induce phosphoprotein synthesis, but it does increase [3H]oestradiol-binding activity in extracts of liver nuclei to a limited extent. No differences in the properties of the oestradiol-binding activity in extracts from nafoxidine-treated chicks or from oestradiol-treated chicks were detected. Chick liver cytosol does not contain detectable high-affinity oestradiol-binding activity. A low-affinity oestradiol-binding component with a sedimentation coefficient of 3.5S was found, but it was unaffected by treatment of chicks with earlier nafoxidine or oestradiol. The results suggest a difference in the mechanism of oestradiol action in the chick liver and in the widely studied rat uterus, on which the usual model for oestradiol action is largely based.