Summary:findings are used to define the protocol survey and the indications for substitution treatment, and to propose a protocol for re-evaluating ovarian function to detect ovarian Ovarian failure is often brought about by the conditioning protocol used for bone marrow transplantation recovery. (BMT). We monitored ovarian function in 31 girls conditioned for BMT at 10.3 ؎ 0.6 (s.e., 3.2-17.5) years by chemotherapy alone (group 1, n = 8) or chemotherapy Patients and methods plus body irradiation (12 Gy, fractionated in group 2, n = 9, or 10 Gy single total body in group 3, n = 7, and A group of 31 girls who underwent BMT at 3.2-17.5 years were seen at 11.7-18.6 years at the Pediatric Endocrinology 5 or 6 Gy single thoraco-abdominal in group 4, n = 7, irradiation) at 13.4 ؎ 0.4 (11.7-18.6) years. BreastUnit for evaluation of their ovarian function. None of them had any CNS involvement, had been given additional crandevelopment was normal (n = 11), did not occur (n = 14), or did not progress spontaneously (n = 2) after ial or abdomino-pelvic irradiation, or had iron overload due to multiple blood transfusions. All patients had been suc-BMT. The other four girls who menstruated before BMT had permanent amenorrhea. Basal plasma gonacessfully transplanted, and all were considered to be free of their initial disease. Chronic graft-versus-host disease dotropin concentrations were measured in 29; folliclestimulating hormone was increased in them all and occurred in cases 15, 19, 25, 27, 28 and 31. They were assigned to one of four groups, according to luteinizing hormone in 23. At the last clinical evaluation at 16.3 ؎ 0.4 (12.1-21.6) years, 23 girls had complete the conditioning protocol used for BMT (Table 1): chemotherapy alone in group 1; chemotherapy plus body ovarian failure, two had partial ovarian failure, and six had normal ovarian function. Three of these were the irradiation in groups 2-4. Group 2 patients were given 12 Gy total body irradiation (TBI) as 6 fractions of 2 Gy youngest group 1 patients and those who had not received busulfan. We conclude that conditioning for over 3 consecutive days, group 3 patients 10 Gy TBI and group 4 patients 5 (cases 25 and 29) or 6 Gy thoraco-BMT given during childhood frequently prevents normal estrogen secretion at puberty. Adequate substitutabdominal irradiation (TAI) as a single 4-h exposure. At the Institut Curie, TBI was delivered using a 5.5 mV linear ive treatment may be necessary to induce growth acceleration and sexual development.accelerator at 50 cGy/min. Conditioning chemotherapy was melphalan (140 mg/m 2 ), cytarabine (18 g/m 2 ), etoposide Keywords: bone marrow transplantation; body irradiation; chemotherapy; ovarian function; puberty (400 mg/m 2 ) and carmustine (300 mg/m 2 ). At the Saint Louis Hospital, TBI was delivered using a 18 mV linear accelerator at 4.2 cGy/min. Conditioning chemotherapy was cyclophosphamide (120 mg/kg in cases 15, 18, 20, 21 The conditioning regimens used for bone marrow transplanand 23; 150 mg/kg in cases 26, 27, 28, 30 and 31;...

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To determine whether ultra-low doses of estradiol (E(2)) affect the serum lipid profile in elderly women, we analyzed changes in serum lipids and lipoproteins in 70 healthy women, 60 yr and older, randomly assigned to parenteral E(2) (7.5 microg per 24 h) delivered by a vaginal ring (Estring; Pharmacia-Upjohn, Malmö, Sweden) or no treatment for 12 months. Baseline serum estrone sulfate (E1S), but not E(2) or serum FSH, was negatively associated with serum total cholesterol (P = 0.026), low-density lipoprotein (LDL) cholesterol (P = 0.053), and apolipoprotein B levels (P = 0.023). Compared with no treatment, Estring treatment yielded nonsignificant increases within the normal postmenopausal range in serum E1S (+16%) and E(2) (+13%), but significantly reduced serum LDL cholesterol by 7.6% (-0.32 mmol/L; 95% confidence interval, -0.58, -0.07; P = 0.014) and LDL to high-density lipoprotein (HDL) ratio by 7.3% (-0.19 mmol/L; 95% confidence interval, -0.44, -0.06; P = 0.030). In Estring users values were significantly reduced in total cholesterol (by 4%), LDL cholesterol (by 7%), LDL to HDL ratio (by 7%), and apolipoprotein B (by 4%), and significantly increased in serum HDL triglyceride (by 25%) but not triglycerides. No significant changes were found in the untreated group. There was a significant interaction between age and both baseline serum E(2)/sex hormone-binding globulin (P = 0.006) and sex hormone-binding globulin (P = 0.009) and a marginal interaction between age and E1S (P = 0.083) with regard to effects on changes in LDL cholesterol levels during Estring treatment. We conclude that ultra-low doses of E(2), which previously were considered to have only local effects, may improve serum lipid profile in elderly women with a pattern and magnitude similar to that reported after conventional estrogen doses or first-generation lipid-lowering agents. The reduction in LDL cholesterol tended to be greater with a combination of high age and low baseline levels of biologically active estrogens.

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