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Readily Measured and Which Could Have Highly Vari- Ular Again Reflecting Differences in Absorption in the Able Effects, Depending on the Target Tissue

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Readily Measured and Which Could Have Highly Vari- Ular Again Reflecting Differences in Absorption in the Able Effects, Depending on the Target Tissue ORIGINAL ARTICLE Endocrine Research Pharmacokinetics and Pharmacodynamics of Oral and Transdermal 17␤ Estradiol in Girls with Turner Syndrome Martha Taboada, Richard Santen, John Lima, Jobayer Hossain, Ravinder Singh, Karen Oerter Klein, and Nelly Mauras Nemours Children’s Clinics in Jacksonville, Florida 32207 (M.T., J.L., N.M.), Orlando, Florida 32806 (M.T.), and Wilmington, Delaware 19805 (J.H.); University of Virginia (R.Sa.), Charlottesville, Virginia 22908; Mayo Clinic (R.Si.), Rochester, Minnesota 55905; and University of California, San Diego (K.O.K.), San Diego, California 92161 ␤ Context: The type, dose, and route of 17 -estradiol (E2) used to feminize girls with Turner syndrome (TS) is not well established. Objective: The objective of the study was to characterize pharmacokinetics and pharmacodynamics of oral vs. transdermal E2. Setting: The study was conducted at a clinical research center. Subjects: Ten girls with TS, mean age 17.7 Ϯ 0.4 (SE) yr and 20 normally menstruating controls (aged 16.8 Ϯ 0.4 yr) participated in the study. Interventions: TS subjects were randomized 2 wk each to: low-dose daily oral (0.5 mg) and biweekly transdermal E2 (0.0375 mg) with 2 wk washout in between or high-dose oral (2.0 mg) and trans- dermal (0.075 mg), studied for 24 h each. Tandem mass spectrometry E2 and estrone (E1) assays and a recombinant cell bioassay were used. Ϯ Ϯ Results: Controls consisted of the following: E2,96 11 pg/ml (SE), E1,70 7 (mean follicular/luteal). Ϯ TS consisted of the following: E2, average concentration on low-dose oral, 18 2.1 pg/ml, low-dose Ϯ Ϯ Ϯ transdermal, 38 13, high-dose oral, 46 15, high-dose transdermal, 114 31 pg/ml. E1 concen- trations were much higher on oral E2 (low or high dose) than transdermal in TS and higher than controls. Bioestrogen was closest to normal in the high-dose transdermal group. LH and FSH decreased more in transdermal than oral low-dose routes and similarly in the high-dose oral and transdermal groups. IGF-I concentrations were variable (P ϭ NS) among groups, and low-density lipoprotein/high-density lipoprotein cholesterol responses were variable. Conclusions: Transdermal E2 results in E2,E1, and bioestrogen concentrations closer to normal and achieves greater suppression of LH/FSH in lower doses compared with normal. Whether the long- term metabolic effects of estrogen differ using the same form of E2, depending on route, awaits further study in TS. (J Clin Endocrinol Metab 96: 3502–3510, 2011) hysiologically, estrogen is necessary for feminization drenprimarilyresultinbonematuration,skeletalconsolidation, P during puberty and to allow achievement of peak bone and skeletal growth, although they eventually also cause epiph- mass and normal bone health in the female (1). Estrogen pri- yseal fusion and completion of linear growth. Hence, proper marily lowers bone resorption in adults, yet the effects in chil- replacement is important in hypogonadal girls. ISSN Print 0021-972X ISSN Online 1945-7197 Abbreviations: AUC, Area under the curve; BMI, body mass index; C-average, average con- Printed in U.S.A. centration; CEE, conjugated equine estrogen; Cmax, maximum concentration; E1, estrone; E2, Copyright © 2011 by The Endocrine Society 17␤-estradiol; HDL, high-density lipoprotein; hsCRP, highly sensitive C-reactive protein; doi: 10.1210/jc.2011-1449 Received May 7, 2011. Accepted August 4, 2011. LCMSMS, liquid chromatography mass spectrometry/mass spectrometry; LDL, low-density First Published Online August 31, 2011 lipoprotein; PD, pharmacodynamics; PK, pharmacokinetics; PO, orally; TD, transdermal; Tmax, time of maximal concentration. 3502 jcem.endojournals.org J Clin Endocrinol Metab, November 2011, 96(11):3502–3510 J Clin Endocrinol Metab, November 2011, 96(11):3502–3510 jcem.endojournals.org 3503 There is wide variation in the types of estrogens used for Study subjects replacement as well as in doses and routes of administra- Ten girls with Turner syndrome (45X and related karyo- tion. Although ethinyl estradiol has been commonly used types), between the ages of 13 and 20 yr, were recruited. Study subjects were referred to the Nemours Children’s Clinic (Jack- as replacement therapy in research studies in Turner syn- sonville, FL) from several pediatric endocrine clinics and through drome (2–4), since 2004 this is no longer commercially web-based advertising. By design, subjects had completed or available as a single agent in the United States. The pre- nearly completed their linear growth (defined as a bone age equal Ͻ dominant type of estrogen used clinically to replace hy- or more than 14 yr and a growth velocity of 2 cm/yr) and any previous GH therapy discontinued at least 6 months before study pogonadal girls until recently in the United States has been participation. All were hypogonadal as indicated by elevated conjugated equine estrogen (CEE) (5), which has more FSH concentrations. Any subject on estrogen replacement ther- than 100 individual estrogenic compounds of different apy had medications discontinued for at least 6 wk before base- biologic potency and cannot be measured in conventional line studies. Subjects with significant obesity (body mass index Ͼ36 kg/m2) or history of systemic illness were excluded from assays. In the postmenopausal literature, a number of participation. studies have suggested that estrogen given orally (PO) has Twenty healthy, normally menstruating (every 28–30 d) girls deleterious effects on body composition and lipid oxida- on no medications and not on oral contraceptives were recruited tion compared with transdermal (TD) (6, 7) and that it for comparison. could serve as a GH antagonist (8), although these findings Study design have not been consistently confirmed (9, 10). However, A physical examination including pubertal staging and lab- the studies used not only different routes but also different oratory studies were performed at baseline in all the girls. Blood forms of estrogen altogether [CEE oral vs. 17␤-estradiol samples for measurement of plasma lipids, estradiol and estrone concentrations, LH, FSH, IGF-I, and highly sensitive C-reactive (E2) TD], and bioequivalencies are not well established protein (hsCRP) were obtained. Subjects were randomized into and have been based mostly on degree of suppression of two study groups, assigned to take estrogenic compounds as gonadotropins and vaginal cytology (11–13). follows. The lower-dose group took either E2 0.5 mg orally (Es- Girls with Turner syndrome represent an important trace; Bristol-Myers Squibb, New York, NY) daily for 2 wk or E2 case study for these issues because they have early primary 0.0375 mg twice weekly TD for 2 wk (Vivelle TD system; No- gonadal insufficiency or failure many years before the vartis Pharmaceuticals, East Hanover, NJ). The higher-dose group took either E2 2.0 mg orally daily or twice-weekly E2 0.075 achievement of peak bone mass. Micronized E2, identical mg TD for 2 wk. After the baseline samples were obtained, sub- with the product of the ovary, is available both orally and jects were started on daily doses of the assigned oral estrogen TD and should be considered when replacing young hy- preparations or twice a week changed estradiol patches for 2 wk pogonadal women because it is perhaps the most physio- (transdermal patches delivered stated concentrations of estradiol daily). On the morning of d 15, each patient was admitted to the logical form of estrogen available. In a previous study, we clinical research center while on the estrogen formulation and used the same type of E2 orally and TD in girls with Turner blood samples collected at 0, 4, 8, 12, 16, and 24 h after dosing. syndrome in 16-wk experiments and found no differences Estradiol was then stopped for 2 wk to achieve washout of es- in rates of protein synthesis, degradation, or lipid oxida- trogen and blood was withdrawn again; then the second assigned dose/form of estrogen was started for 2 more weeks, at which tion or whole-body lypolysis between the estrogens, de- time another PK/PD study was again repeated at the same time pending on route (14). This new study seeks to character- intervals. Each study lasted 6 wk. Doses chosen are within the ize the pharmacokinetics (PK) and pharmacodynamics therapeutic spectrum of prescribed Food and Drug Administra- (PD) of the exact same form of E using a very sensitive tion-approved dosing and presumably raise E2 concentrations 2 within physiological range of younger females in postmeno- liquid chromatography mass spectrometry/mass spec- pausal women. trometry (LCMSMS) assay and a recombinant cell bioas- Healthy girls serving as controls were examined and sampled say using a transformed yeast expressing the estrogen re- twice, once in the early follicular (within 1 wk following menses) ϳ ceptor in girls with Turner syndrome. and again in the luteal phase ( 3 wk after menses) of their men- strual cycle for determination of estradiol and estrone concen- trations using the same assays. Subjects and Methods Assays E2 and estrone (E1) concentrations were measured in serum These studies were approved by the Wolfson Children’s Hospital at the mass spectrometry laboratory at Mayo Clinic Rochester Institutional Review Committee. Informed written consent/as- (Rochester, MN) using LCMSMS methodology as previously sent was obtained before study entry from the parents/guardians described (15) with a quantitation limit of 2.5 pg/ml and an and subjects (if older than 18 yr) and children’s assent. The intrassay coefficient variation of 20%. This assay has proven PK/PD study was the first arm of a larger ongoing trial registered superior in accuracy and specificity over commercial RIA and [in Clinicaltrial.gov (NCT00837616)]. other assays (16–18). In addition, total bioactive estrogens ␤ 3504 Taboada et al. PK/PD of Oral and Transdermal 17 E2 in Turner Syndrome J Clin Endocrinol Metab, November 2011, 96(11):3502–3510 were measured in plasma by a recombinant cell bioassay with TABLE 1.
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