コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 istics, risk factors, and therapy (including hormone replacement therapy).
2 adduct induced by equine estrogens used for hormone replacement therapy.
3 h can be effectively treated with the use of hormone replacement therapy.
4 ive, and evidence is emerging for the use of hormone replacement therapy.
5 one concentration or by the need for thyroid hormone replacement therapy.
6 ancy, while using oral contraceptives and/or hormone replacement therapy.
7 he administration of oral contraceptives and hormone replacement therapy.
8 Premarin is the most widely used formula for hormone replacement therapy.
9 eproductive-age women, and/or treatment with hormone replacement therapy.
10 e of HDL and other intermediate endpoints to hormone replacement therapy.
11 the keywords of menopause, sex steroids, and hormone replacement therapy.
12 To review the randomized trials of hormone replacement therapy.
13 y mass index, education, and (in women only) hormone replacement therapy.
14 otic events among postmenopausal women using hormone replacement therapy.
15 ysicians of the utility and safety of growth hormone replacement therapy.
16 at menopause, marital status, and the use of hormone replacement therapy.
17 presence of diabetes, and use of aspirin or hormone replacement therapy.
18 ausal women, regardless of whether they took hormone replacement therapy.
19 dex, physical activity level and duration of hormone replacement therapy.
20 ence in postmenopausal women who do not take hormone replacement therapy.
21 strogen-regulated malignancies, and even for hormone replacement therapy.
22 vely used by women as a contraceptive and in hormone replacement therapy.
23 g mechanism that represents a new option for hormone replacement therapy.
24 ted between SP risk and physical activity or hormone replacement therapy.
25 enzyme inhibitors, beta-blockers, and growth hormone replacement therapy.
26 oid, and sex steroid production that require hormone replacement therapy.
27 ls and bone health can be limited by focused hormone replacement therapy.
28 r history of aspirin, oral contraceptive, or hormone replacement therapy.
29 sis, and history of fracture, and (in women) hormone replacement therapy.
30 possibly because of interactions with age or hormone replacement therapy.
31 g medication, season, menopausal status, and hormone replacement therapy.
32 oductive cancers observed in women receiving hormone replacement therapy.
33 lism have not revealed any adverse effect of hormone-replacement therapy.
34 an augmented response of HDL cholesterol to hormone-replacement therapy.
35 malignancy, or with any contraindications to hormone-replacement therapy.
36 those who are postmenopausal or those taking hormone-replacement therapy.
37 te end point and among users and nonusers of hormone-replacement therapy.
38 ss, diet, physical activity, medication, and hormone-replacement therapy.
39 med from the search for safe alternatives to hormone replacement therapies.
40 ignaling component as a candidate target for hormone replacement therapies.
41 men; 2) post-menopausal women not receiving hormone replacement therapy; 3) pre-menopausal women not
42 /-44 mg/L; P<0.0001), women on versus not on hormone-replacement therapy (398+/-89 versus 291+/-60 mg
43 postmenopausal women who had never received hormone replacement therapy, a stronger positive associa
44 effect of the most widely used modalities of hormone replacement therapy against cardiovascular disea
45 sex, smoking, physical activity, menopause, hormone replacement therapy, alcohol, and aspirin use; a
46 ificantly greater than in those treated with hormone replacement therapy alone (4.2% [3.8] vs 3.0% [4
47 ex, diabetes, use of oral contraceptives and hormone replacement therapy among women, intake of vitam
48 nitiative and the ensuing drop in the use of hormone-replacement therapy among postmenopausal women i
50 of postmenopausal (PMP) women were receiving hormone replacement therapy and 14%, bisphosphonate trea
52 st cancer screening, the association between hormone replacement therapy and breast cancer incidence,
55 lp resolve the current controversy regarding hormone replacement therapy and improve cardiovascular h
56 peutically to oppose the effect of E2 during hormone replacement therapy and in the treatment of uter
57 a synthetic progestin used in postmenopausal hormone replacement therapy and oral contraception, also
58 inical decision-making concerning the use of hormone replacement therapy and other novel estrogen ago
61 de screening for prostate and breast cancer, hormone replacement therapy and risk for breast cancer,
62 ific mortality), overall and with respect to hormone replacement therapy and tamoxifen treatment.
63 een postulated to occur in women who receive hormone replacement therapy and/or by additional molecul
64 e transient excess incidence associated with hormone-replacement therapy and adjusting for trends in
65 en who were receiving and had never received hormone-replacement therapy and who were naturally match
66 ersonal history of breast cancer, and use of hormone replacement therapy) and mammographic findings r
67 These findings indicate that BMI, parity, hormone replacement therapy, and alcohol consumption may
68 pregnancies, use of oral contraceptives and hormone replacement therapy, and BRCA mutation status.
71 l intake, type 2 diabetes and parity, use of hormone replacement therapy, and oral contraceptives in
72 min D measurement, menopausal status, use of hormone replacement therapy, and physical activity; P fo
73 9 %, 15.3 %, and 27.3 %) for postmenopausal, hormone replacement therapy, and premenopausal subjects,
74 was adjusted for nodal status, prior use of hormone replacement therapy, and prior chemotherapy (HR,
75 ter ovarian cancer treatment can safely take hormone-replacement therapy, and this may, in fact, infe
76 ceptives; 4) post-menopausal women receiving hormone replacement therapy; and 5) pre-menopausal women
77 g (AOR 1.569, 95% CI 1.292-1.905), or use of hormone replacement therapies (AOR 1.548, 95% CI 1.273-1
79 on and scattering properties for women using hormone replacement therapy are intermediate between pre
80 o inform dosage and timing of antihormone or hormone replacement therapies as part of a personalized
81 candidates received calcium, vitamin D, and hormone replacement therapy as indicated for hypogonadis
82 graine with combined oral contraceptives and hormone replacement therapy, as well as the risk of isch
83 activity, alcohol intake, menopausal status, hormone replacement therapy, aspirin use, and dietary fa
85 on of menopause, pretreatment assessment for hormone replacement therapy, benefits and risks of this
86 her CRP levels: age, gender (with or without hormone replacement therapy), body mass index >25 kg/m2,
87 menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, an
88 tabilized in subjects who were not receiving hormone replacement therapy but continued to decline in
89 e suggests the possibility of a benefit from hormone replacement therapy, but the optimal trial has y
90 menopausal symptoms and as an alternative to hormone replacement therapy, but they can produce potent
92 Women using combined estrogen and progestin hormone replacement therapy (CHRT) have an increased ris
93 that use of combined estrogen and progestin hormone replacement therapy (CHRT) increases breast canc
95 If the observed associations are causal, hormone replacement therapy could have a role in prevent
97 icantly more prevalent among women receiving hormone replacement therapy during the previous year.
98 We have previously reported that estrogen/hormone replacement therapy (E/HRT) has beneficial effec
99 lean body mass, pulse rate, pulse pressure, hormone-replacement therapy, educational status, and phy
100 s no compelling evidence that postmenopausal hormone replacement therapy either decreases or increase
101 typic relative risks were affected by use of hormone replacement therapy, either overall or for oestr
102 from menstrual history, gynecologic surgery, hormone replacement therapy, follicle-stimulating hormon
104 l management of a patient who is considering hormone replacement therapy for menopausal symptoms.
105 egnancy in the past 15 years, and the use of hormone replacement therapy for more than 4 years was as
106 nt practitioners to at least consider growth hormone replacement therapy for patients with definite g
107 a definitive statement can be made regarding hormone replacement therapy for women who have had stage
108 zed controlled trials in which no benefit of hormone-replacement therapy for postmenopausal women has
111 diabetes mellitus, and hypertension, whereas hormone replacement therapy had no effect on progression
116 ies suggest that postmenopausal women taking hormone replacement therapy have a reduced risk of radio
117 and breast cancer among women randomized to hormone replacement therapy have increased interest in o
119 ors were not increased by use of any form of hormone replacement therapy; however, small numbers of t
120 drugs (HR, 1.25; 95% CI, 1.08 to 1.43), and hormone replacement therapy (HR, 1.27; 95% CI, 1.08 to 1
122 reas those postmenopausal women who had used hormone replacement therapy (HRT) (primarily estrogen) h
123 of concerns and controversy about the use of hormone replacement therapy (HRT) after oophorectomy.
124 Many premenopausal women choose to take hormone replacement therapy (HRT) after undergoing BPO t
128 ed the association between the initiation of hormone replacement therapy (HRT) and early cardiac even
129 search has examined the relationship between hormone replacement therapy (HRT) and pulmonary function
131 ether with the epidemiological evidence that hormone replacement therapy (HRT) and, less consistently
133 ovarian cycle, pregnancy and with exogenous hormone replacement therapy (HRT) are currently unknown.
134 ted and often conflicting data on the use of hormone replacement therapy (HRT) as a possible risk fac
136 pausal women and women who consistently took hormone replacement therapy (HRT) between menopause and
137 Basic neuroscience findings suggest that hormone replacement therapy (HRT) could reduce a woman's
138 e clinical trials provoked major debate when hormone replacement therapy (HRT) did not reduce coronar
139 Recent clinical trials demonstrating that hormone replacement therapy (HRT) does not prevent coron
141 ntinues to be conducted on the mechanisms of hormone replacement therapy (HRT) effects, and the first
142 pproximately 10 million women were receiving hormone replacement therapy (HRT) for alleviation of men
147 ding to follow-up time, severity, and use of hormone replacement therapy (HRT) in a retrospective ana
148 nships among breast density, age, and use of hormone replacement therapy (HRT) in breast cancer detec
160 or absence of oestrogen and selective use of hormone replacement therapy (HRT) may alter these relati
161 en with clinically recognized heart disease, hormone replacement therapy (HRT) may be associated with
162 It has been hypothesized that postmenopausal hormone replacement therapy (HRT) may increase levels of
165 of menopausal status, age, race, and use of hormone replacement therapy (HRT) on 3-year changes in g
166 Furthermore, the effects of statins plus hormone replacement therapy (HRT) on cardiovascular outc
167 oximately 20%) who have augmented effects of hormone replacement therapy (HRT) on levels of HDL chole
168 gate whether female reproductive history and hormone replacement therapy (HRT) or birth control pills
170 omy produce relative risks for the effect of hormone replacement therapy (HRT) that are biased downwa
171 ostmenopausal women in the United States use hormone replacement therapy (HRT) to treat symptoms of m
176 nd measures of obesity and fat distribution, hormone replacement therapy (HRT) use, and serum sex hor
177 After excluding women with a history of hormone replacement therapy (HRT) use, the authors condu
179 at differentiate long-term (> or = 10 years) hormone replacement therapy (HRT) users from short-term
180 were not and 31 women were taking long-term hormone replacement therapy (HRT) using estrogen either
181 xamination, responded to questions regarding hormone replacement therapy (HRT), and provided a blood
182 as a component in both contraceptives and in hormone replacement therapy (HRT), both on their own and
185 n to use of hormonal birth control (HBC) and hormone replacement therapy (HRT), taken singly or cumul
195 d 140 postmenopausal women-31 not taking any hormone replacement therapy (HRT); 75 taking estrogen al
196 1.32; 95% CI, 1.02 to 1.70), current use of hormone replacement therapy (HRT; OR, 1.84; 95% CI, 1.38
199 me vigorous activity, vegetable consumption, hormone-replacement therapy (HRT), and estrogen exposure
201 ized that the progesterone component of some hormone replacement therapies in women is detrimental to
202 his observation highlights the importance of hormone replacement therapy in postmenopausal conditions
203 ovascular risks associated with conventional hormone replacement therapy in postmenopausal women (5-7
204 cancer epidemiology also support a role for hormone replacement therapy in prevention of colorectal
205 eplacement Study (HERS), studied the role of hormone replacement therapy in protecting women from cor
206 e associated with a differential response to hormone replacement therapy in several domains of estrog
207 n, underscores the unexplored utility of GCC hormone replacement therapy in the chemoprevention of co
208 an odor memory/discrimination task and that hormone replacement therapy in the menopause may be an e
210 Treatment intensity for diabetes and use of hormone replacement therapy in women were similar across
212 nal level, smoking, alcohol consumption, and hormone replacement therapy (in women), the upper quarti
213 n-users (age 58 +/- 1 years) and 32 users of hormone replacement therapy, including oestrogen alone (
215 re prevented with estrogen (E(2))-containing hormone replacement therapy initiated shortly following
224 ion concerning the cardiovascular effects of hormone replacement therapy is whether genetic factors c
225 ystemic estrogen replacement (in the form of hormone replacement therapy) is able to accelerate heali
226 tional data that excluded prevalent users of hormone replacement therapy led to attenuated discrepanc
229 essed whether different oral progestogens in hormone replacement therapy may differentially affect th
230 on health and cognitive status, suggest that hormone-replacement therapy may have a selective benefic
231 001), were lower among women currently using hormone replacement therapy (mean 0.98 mg/l vs. 1.23 mg/
232 for age, Tyrer-Cuzick risk, smoking, use of hormone replacement therapy, menopausal status, baseline
233 sion suggest that combined estrogen/androgen hormone replacement therapy might reduce the risk of bre
234 e younger at enrollment (P < 0.001) and used hormone replacement therapy more often (P < 0.003).
235 ndrome in postmenopausal US women not taking hormone replacement therapy (n=362) in a prevalent case-
236 estrogen alone (E; n = 30), and a third [non-hormone replacement therapy (NHRT; n = 62)] control grou
237 adjusted for age, body-mass index, previous hormone-replacement therapy, nodal status, tumour size,
238 ship was present among men, women not taking hormone replacement therapy, nonsmokers, and those indiv
240 e gain was present only among never users of hormone replacement therapy (odds ratio (OR) = 2.02 (95%
241 ncies regarding the effect of postmenopausal hormone replacement therapy on coronary heart disease.
242 e found that the impact of the withdrawal of hormone replacement therapy on density reduction was lar
246 r alpha (ER-alpha) may modify the effects of hormone-replacement therapy on levels of high-density li
247 rmed the putative antiatherogenic effects of hormone-replacement therapy on lipoprotein metabolism.
248 e receiving and those who had never received hormone-replacement therapy on measures of verbal memory
250 rdiovascular disease and cancer, and without hormone replacement therapy or lipid-lowering medication
251 en SLE and current use or duration of use of hormone replacement therapy or oral contraceptives, and
254 te intake), lifestyle habits (such as use of hormone replacement therapy), or biological characterist
255 djustment for age, BMI, BMD, and past use of hormone replacement therapy, or when NTx and CTx values
256 ificantly increased for women who used prior hormone replacement therapy (P = .007) or received prior
257 ynamic management, endocrine dysfunction and hormone replacement therapy, pediatric donor management,
259 model assessment of insulin resistance, and hormone replacement therapy, premature menopause was ass
260 lycystic ovarian syndrome who was undergoing hormone replacement therapy presented with a 6-month his
261 merous clinical and animal studies show that hormone replacement therapy reduces the risk of colon tu
262 en/Progestin-Replacement Study data suggests hormone-replacement therapy reduces the risk of developi
265 largely limited to women who were not taking hormone replacement therapy (relative risk, 2.60; 95% CI
266 ng information about oral contraceptive use, hormone replacement therapy, reproductive history, sun e
267 smoking, diabetes mellitus, body mass index, hormone replacement therapy, serum creatinine, and the u
270 Women's Health Initiative, however, are that hormone replacement therapy should not be used for prima
271 weight, height, menopausal status or use of hormone replacement therapy, socioeconomic status, and p
272 contraceptive pill use, surgical menopause, hormone replacement therapy, statins, acetaminophen/para
273 n increase in the HDL cholesterol level with hormone-replacement therapy that was more than twice the
274 Among the identified risks and benefits of hormone-replacement therapy, the effects of treatment on
275 vels of blood pressure, and use or nonuse of hormone-replacement therapy, the relative risks of first
277 ere seems to be little if any risk in giving hormone replacement therapy to women who have had breast
282 ness, single vitamin/mineral supplement use, hormone replacement therapy use, and smoking status.
283 ts were seen for smoking, physical activity, hormone replacement therapy use, multiparity, or hand OA
284 age at first birth, breastfeeding, menarche, hormone replacement therapy use, somatotype at age 18, b
285 ince over 90% of this group had a history of hormone replacement therapy use, the finding that years
286 fter stratification by smoking status and by hormone replacement therapy use, two factors known to in
287 ody mass index, time since menopause, use of hormone replacement therapy, use of calcium supplements,
288 t for potential confounders and exclusion of hormone replacement therapy users had little impact.
292 iteal (p < 0.05) intimal-medial thicknesses, hormone replacement therapy was associated with thinner
295 ) age of 61 +/- 11 y, who were not receiving hormone replacement therapy, were fed eucaloric diets to
296 ells would be a significant improvement over hormone replacement therapies, which incur side effects
297 pecific mortality among women who never used hormone replacement therapy, who never smoked, and who e
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。