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Objective: The aim of this study was to compare the time length until the human chorionic gonadotropin titer became negative after medical or surgical treatment of ectopic pregnancy., Experimental Design: Prospective, randomized study. PARTECIPANTS AND INTERVENTIONS: We compared time to resolution in 30 cases of tubal pregnancies successfully treated, 15 underwent laparoscopic linear salpingostomy (group 1) and 15 medical treatment with single-ose methotrexate (group 2). The patients of both groups had no meaningful differences of age, gestational age and human chorionic gonadotropin mean values., Measures: During the follow-up human chorionic gonadotropin serum values were obtained every two days until the titer was negative., Results: The time to resolution was 33.6 +/- 6.6 days in group 1, 31.5 +/- 7.8 in group 2 with no statistically meaningful differences., Conclusion: The data, comparable with results obtained by laparoscopic treatment, suggest that human chorionic gonadotropin value becomes negative independently of type of treatment and residual trophoblast.

Objective: To evaluate the impact of endometriosis on bone metabolism., Materials and Methods: We compared bone mineral density and biochemical markers (plasma osteocalcin, bone alkaline phosphatase, fasting urinary hydroxyproline, urinary excretion of cross-linked N-telopeptide of type I collagen) of bone turnover in forty-nine perimenopausal women undergoing laparotomy because of benign gynecologic pathology: in twenty-four of them (group A) endometriosis was diagnosed, the remaining twenty-five represented the control group (group B). Statistical analysis was performed by means of Student "t"-test; significance was set at p < 0.05., Results: Bone density of the lumbar spine (0.898 +/- 0.325 vs 0.940 +/- 0.350) and bone markers failed to show statistically significant differences between the two groups. No significant correlation was observed between any bone density measurement and severity of endometriosis., Conclusion: Endometriosis does not seem to induce even in advanced stages, a reduction of bone density.

Objective: To evaluate the relationship between hormone replacement therapy and glucose metabolism, and the possible role played by the administration route., Design: Prospective randomized study., Materials and Methods: Eighty-four patients in either surgical or spontaneous menopause were randomly allocated into four groups: 15 patients in surgical menopause were treated with estrogens alone administered transdermically (17 beta-estradiol, 50 micrograms/day); 15 patients in surgical menopause were treated with oral conjugated equine estrogens (0.625 mg/day); 18 patients in spontaneous menopause were treated with transdermic estrogens plus oral progestagen (17 beta-estradiol 50 micrograms/day, acetate medroxyprogestogen 10 mg/day for 12 days per month); 16 patients in spontaneous menopause were treated with oral conjugated equine estrogens (0.625 mg/day) plus oral progestagen (10 mg/day for 12 days per month). Twenty patients not given any medication represented the control group. Before starting the trial and after six months of therapy, glucose and insulin levels before and after an oral glucose loading test were evaluated. Data analysis was performed by means of Student's "t"-test, ANOVA was used to compare mean levels between the groups. Significance was set at p < 0.005., Results: Dosages made after 6 months of therapy showed comparable basal glucose levels in all the studied group, while basal insuline levels in patients taking estrogen alone were lower (76.88 +/- 23.66 vs 95.91 +/- 24.57 in group 1, 80 +/- 13.34 vs 96.91 +/- 18.97 in group 2) than pretreatment values. No significant difference in glucose levels was found after glucose load in the four groups. CONCLUSION. Women treated with estrogen alone have a tendency to a lower insulin response, which could indicate a greater insulin sensitivity. This effect seems to be more evident in transdermic administration than with oral administration. The addition of progestagen seems to wane the increase in insulin sensitivity induced by estrogens.