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With the surgical improvement of congenital heart disease, Fontan operation has been applied to many complicated patients in recent years. This is the first report of a child with panhypopituitarism who underwent Fontan operation. A 5-year-old boy was scheduled for Fontan operation. He previously underwent Blalock-Taussig shunt and bidirectional Glenn operations for univentricular heart with double-outlet right ventricle and pulmonary atresia. He was receiving hydrocortisone and 1-desamino-8-D-arginine vasopressin (DDAVP) for panhypopituitarism secondary to removal of craniopharyngioma performed at the age of three years. Although urine output and serum sodium concentration were adequately controlled by adjustment of vasopressin infusion rate during surgery, massive pleural effusions and ascites developed postoperatively, which required several days for control by adjusting the dose of oral DDAVP and normalize the serum sodium level. Intraoperative management of Fontan operation for a patient with panhypopituitarism was controllable by appropriate hormone replacement. However, postoperative fluid management was complicated by the clinical features of panhypopituitarism and Fontan physiology., Author(s): Kohei Sunoki [sup.1], Yoji Otsuka [sup.1], Hidetaka Iwai [sup.1], Tatsuya Nagano [sup.1], Naoyuki Taga [sup.1], Masaaki Kawada [sup.2], Mamoru Takeuchi [sup.1] [sup.3] Author Affiliations: (1) grid.410804.9, 0000000123090000, Department of [...]

Abstract Extracts of black cohosh (Cimicifuga racemosa) are commonly used for the treatment of symptoms associated with menopause. Adverse events with black cohosh are rare, mild and reversible. A few [...]

Byline: Julie A. Pasco (1), Mark A. Kotowicz (1), Margaret J. Henry (1), Kerrie M. Sanders (1), Ego Seeman (2), Geoffrey C. Nicholson (1) Keywords: Bone mineral density; Fracture; Hormone therapy; Population-based study; Postmenopausal women Abstract: In this population-based study, we evaluated the association between exposure to hormone therapy (HT), bone mineral density (BMD) and the prevalence of non-vertebral fractures. The study was set in a region located in southeastern Australia where complete fracture ascertainment was determined from radiological reports. Current HT use for at least 6 months was ascertained in women with non-vertebral fractures [median age 70.9 years inter-quartile range (IQR) 66.5--75.9 years] and randomly selected controls (median age 70.8 years IQR 65.2--75.0 years). Current HT use was documented in 20 of 262 cases and 49 of 364 controls. The odds ratio (OR) for non-vertebral fracture associated with HT use was 0.53 (95% CI 0.31--0.92). HT use was associated with 2.6--7.5% higher BMD at axial and appendicular sites. HT use is associated with a halving of risk for non-vertebral fractures and higher BMD. Author Affiliation: (1) Department of Clinical and Biomedical Sciences: Barwon Health, The University of Melbourne, P.O. Box 281, 3220, Geelong, Australia (2) Department of Medicine, The University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia Article History: Registration Date: 10/12/2003 Received Date: 25/04/2003 Accepted Date: 08/12/2003 Online Date: 14/02/2004

Hormone replacement therapy does not slow the progression of existing coronary artery disease, according to a study of 226 postmenopausal women. This is true of both estrogen-only therapy and estrogen-progestin therapy. This study actually compared the coronary angiograms of women who took hormone replacement therapy and those who did not. There was no significant difference between the two groups during an average follow-up of 3.3 years.

While empirical research to date has generally supported positive effects of estrogen on verbal memory performance in women, the literature examining specific effects of Hormone Replacement Therapy (HRT) on cognitive [...]

Background. Sarcopenia refers to the loss of skeletal muscle mass with age. We have found a prevalence of sarcopenia of 22.6% in older postmenopausal women not receiving estrogen. The objective of this study was to determine the prevalence of sarcopenia in a population of older, nonobese, community-dwelling women who had been long-term users of estrogen replacement therapy (ERT). Methods. We measured appendicular skeletal muscle mass by dual x-ray absorptiometry (DXA) in 189 women aged 59 to 78 years old who had been using ERT for at least 2 years (mean [+ or -] SD duration, 12.7 [+ or -] 8.2 years). We defined sarcopenia as an adjusted appendicular skeletal muscle mass (ASM) (mass divided by height squared) more than 2 SDs below the mean for a young healthy reference population. Health and menopause history were obtained. Body mass index (BMI) was calculated, and physical activity and performance were measured using the Physical Activity Scale in the Elderly, the chair rise time, the 6-minute walk, and measures of lower extremity strength and power. Serum estrone, estradiol, testosterone, and sex hormone binding globulin were measured. Results. The prevalence of sarcopenia in nonobese, community-dwelling women who were long-term ERT users was 23.8%. Skeletal muscle mass correlated significantly with BMI, age at the time of starting ERT, hand grip strength, lower extremity strength and power, and testosterone level, but not with estradiol level. In linear regression analysis, BMI, leg press strength, and testosterone level contributed to adjusted ASM, accounting for 48.7% of the variance (p < .001). Conclusions. Sarcopenia is as common in nonobese women who are long-term ERT users as in community-dwelling women not using ERT, suggesting that ERT does not protect against the muscle loss of aging. BMI, strength, and testosterone level contributed to appendicular skeletal mass in women. These data suggest that interventions to target nutrition, strength training, and testosterone replacement should be further investigated for their role in preventing muscle loss with age.

We tested the hypothesis that cross-bridge mechanisms of contraction differed in early postmenopausal women who did or did not receive hormone replacement therapy (HRT). Vastus lateralis biopsies were obtained from 17 postmenopausal women (49-57 years old), 8 of whom were on HRT for the previous 24 [+ or -] 5 months and 9 of whom were never on HRT. Electrophoresis and enzyme histochemistry revealed that fiber myosin heavy chain (MHC) isoform distribution, the cross-sectional area (CSA) of slow and fast fibers, and the relative CSA occupied by each, were similar for HRT and non-HRT groups. Single permeabilized fibers containing type IIa MHC had greater [Ca.sup.2+]-activated peak specific force, unloaded shortening velocity, and peak power than fibers containing type I MHC, but in all cases the values for HRT and non-HRT groups were similar. In this cross-sectional study, we found no evidence that [Ca.sup.2+]-activated fiber function, MHC isoform distribution, or relative CSA occupied by slow and fast fibers differed between HRT and non-HRT groups.

The steady increase in female life expectancy has attracted attention to the importance of preventing cognitive aging and Alzheimer's disease (AD) in women. Evidence from randomized, controlled trials and from cross-sectional and longitudinal studies shows that estrogen-replacement therapy preferentially protects against a decline in verbal memory in healthy postmenopausal women and decreases the risk of AD. Although results are not consistent across studies, they indicate that treatment with estrogen during the postmenopausal years might protect against cognitive aging in women during the latter part of their life.

Excessive estrogen stimulation unopposed by progesterone strongly predisposes to endometrial cancer. Because the antiproliferative effect of progesterone requires the progesterone receptor (PR), which exists in two isoforms, PR-A and -B, we reasoned that variants in the PR gene may predispose to endometrial cancer. We found six variable sites, including four polymorphisms in the hPR gene and five common haplotypes. One promoter region polymorphism, +331G/A, creates a unique transcription start site. Biochemical assays showed that the +331G/A polymorphism increases transcription of the PR gene, favoring production of hPR-B in an endometrial cancer cell line. Using a case-control study nested within the Nurses' Health Study cohort, we observed a statistically significant association between the +331G/A polymorphism and the risk of endometrial cancer, which was even greater in overweight women carriers. After including a second population of controls, these associations remained intact. Our findings suggest that the +331G/A hPR gene polymorphism may contribute to endometrial cancer risk by increasing expression of the hPR-B isoform.

Hormone therapy can have different effects on HDL cholesterol in different women depending on differences in the gene for the estrogen receptor. In a study of 309 women, women with a certain gene had HDL cholesterol levels that were twice as high as other women. HDL cholesterol is 'good' cholesterol that has beneficial effects when present in large amounts.

Women with hypothyroidism who begin taking estrogen replacement therapy should have their thyroid hormones checked about 12 weeks later. Estrogen affects the concentration of thyroid hormones, so these women may need higher doses of thyroxine.

We investigated the effects of estriol (E3) on endothelial function and bone mineral density (BMD) in very elderly women. Twenty-four very elderly women (80 +/- 3.5 years old) were administered CaCl(sub 2) with or without estriol treatment (2 mg/day) for 30 weeks (hormone replacement treatment [HRT] group vs control group). Endothelium-dependent flow-mediated dilatation (FMD), endothelium-independent dilatation by nitroglycerin of the brachial artery, and BMD were assessed. Levels of plasma lipids and apoproteins were not changed; however, both plasma E3 and E2 were substantially increased (E2, 4.6 to 31.3 +/- 8.1; E3,

Background. Previous studies have demonstrated equivocal findings on the effect of chronic running on bone mass in postmenopausal women. The purpose of this study was to determine the effect of chronic running alone and in conjunction with hormone replacement therapy (HRT) on bone mineral density (BMD) in postmenopausal women. Methods. Forty-three women [15 premenopausal 48.1+/-.4 yrs(Pre); 13 postmenopausal 57.3+/-2.3 yrs(Post); and 15 HRT-treated postmenopausal 56.8+/-1.5 yrs(PostE) served as subjects. All were chronic runners (duration >5 yrs,>10 miles per week). BMD was determined by dual energy x-ray absorptiometry, VO(sub.2)max on a treadmill, body composition by hydrostatic weighing, knee strength by KinCom dynamometer, and training and menstrual history by questionnaire. Analysis of covariance with Tukey post hoc tests was utilized to compare the groups. Results. The groups were similar in body weight, VO(sub.2)max, years training, and miles run per week. Pre and PostE did not differ in total or spine BMD. However, Pre had greater hip BMD than PostE(.973+/-.03 vs .876 +/- .03g/cm(super.2),p

Physiological principles of the interrelationship of sex hormones and their regulation are the foundation of understanding appropriate treatment of the transsexual patient. While both genetic males and females have estrogens and androgens, the quantitative sex hormone production is genetically predetermined by sex hormone production both in the gonads and via peripheral conversion of hormone precursors to sex steroids. Sex hormones exert a negative feedback on the hypothalamus and pituitary gland whereby gonadotropin-releasing hormone (GnRH), pituitary luteinizing hormone (LH), and follicle-stimulating hormone (FSH) are regulated or suppressed by the endogenous levels of these hormones. Sex hormonal therapy induces attenuated GnRH stimulation of LH and FSH causing a reduction of serum sex hormone levels. It is clear that estrogen as well as androgen therapy have a dual role: (i) induction of feminization or virilization and (ii) suppression of the hypothalamic-pituitary-gonadal axis leading to a reduction of endogenous estradiol or testosterone secretion. Cross-sex hormonal treatment may have substantial medical side effects. The smallest dosage of hormonal therapy compatible with the above clinical aims should be used. KEY WORDS: transsexualism; gender identity disorders; transsexualism treatment; hormonal therapy; hormonal therapy transsexualism; hormonal complications.

Hormone replacement therapy appears to be almost as beneficial in lowering elevated cholesterol as cholesterol-lowering drugs. This was the conclusion of a study in which 58 postmenopausal women with elevated cholesterol took hormone replacement therapy with estrogen and progesterone or the cholesterol-lowering drug simvastatin for eight weeks and then switched to the other treatment after an eight-week washout period. Hormone replacement therapy lowered total and LDL cholesterol almost as much as simvastatin. Both treatments raised HDL cholesterol but only simvastatin lowered triglyceride levels.

Estrogen appears to lower blood levels of plasminogen-activator inhibitor type 1 (PAI-1), which could account for its ability to reduce a woman's risk of cardiovascular disease. PAI-1 inhibits the breakdown of blood clots, a process called fibrinolysis. Researchers measured PAI-1 in blood samples from 50 women who were on estrogen replacement therapy. Thirty women were taking oral estrogen and 20 were using an estradiol patch. Oral estrogen reduced PAI-1 levels by 50% and also increased fibrinolysis, as measured by chemicals produced during fibrinolysis. The estradiol patch had no effect on PAI-1 levels.

This report documents findings from the first 80 patients to enter our ongoing clinical trial of testosterone replacement therapy, designed for HIV+ men with low CD4 cell counts and low levels of serum testosterone, who complain of diminished sexual interest and/or sexual dysfunction. Patients were treated with testosterone for 8 weeks with biweekly intramuscular injections, starting at 200 mg. and increasing at Week 2 to 400 mg. biweekly. Week 8 responders were treated with testosterone for at least four more weeks and were then randomized to testosterone or placebo for six weeks or until relapse. Seventy-three men completed the initial eight-week phase of treatment: of the seven dropouts (19%), two men discontinued treatment because of side effects (irritability and hair loss). Of the 73 completers, 67 (92%) were rated as clearcut responders by the study doctor. Self-ratings of sexual interest, erectile functioning, and satisfaction with one's sex life revealed significant improvement in all areas. Although much of the sample was sexually abstinent both before and after treatment, sexual activity (both with partners and solitary masturbation) increased after treatment. Progressive HIV illness entails many kinds of losses; restoration of one's sexuality associated with testosterone replacement can greatly enhance quality of life and sense of vitality., We describe the effects of testosterone replacement therapy on sexual interest, function, and behavior in men with human immunodeficiency virus (HIV) infection. Endocrine abnormalities such as low testosterone are commonly [...]

Daily estrogen and progestin appear to increase bone density in postmenopausal women without increasing the risk of breast or endometrial cancer. Researchers randomly assigned 1,265 postmenopausal women to various dosages of estrogen alone or estrogen plus a progestin called norethindrone acetate (NA). The highest dosages of estrogen increased bone density significantly, but also increased the incidence of endometrial hyperplasia, which is a risk factor for endometrial cancer. There were no incidences of endometrial hyperplasia in the women who took estrogen plus NA. All hormone treatments also improved blood lipid profiles., Objective.--To compare the effect of continuous norethindrone acetate (NA)ethinyl estradiol [(EE.sub.2)] combinations with matching unopposed [EE.sub.2] or placebo. Design.--A 2-year, double-blind, placebo-controlled, parallel-group clinical trial. Setting.--Outpatients at 65 centers. Patients.--Asymptomatic or mildly symptomatic women aged 40 years or older who had undergone the onset of spontaneous menopause within the last 5 years and who had an intact uterus. Interventions.--Patients were equally randomized to placebo or 1 of 8 treatment groups: 0.2 mg of NA and 1 [micro.g] of [EE.sub.2]; 0.5 mg of NA and 2..5 [micro.g] of [EE.sub.2]; 1 mg of NA and 5 [miro.g] of [EE.sub.2]; 1 mg of NA and 10 [micro.g] of [EE.sub.2]; 1 [micro.g] of [EE.sub.2]; 2.5 [micro.g] of [EE.sub.2]; 5 [micro.g] of [EE.sub.2]; or 10 [micro.g] of [EE.sub.2]. Primary Outcome Measures.--Bone mineral density (BMD) measured by quantitative computed tomography, serum lipids, and endometrial effects as assessed by rate of hyperplasia and proliferative status. Results.--Twelve hundred sixty-five patients entered the study. Bone mineral density increased significantly from baseline (P Conclusions.--Daily treatment with NA-[EE.sub.2] was well tolerated and protected the endometrium from [EE.sub.2]-induced proliferation and hyperplasia. The NA-[EE.sub.2] treatments produced a dose-related significant increase in BMD that was not present with unopposed [EE.sub.2] treatment. The overall effect of NA-[EE.sub.2] treatments on lipid measures was favorable. JAMA. 1996;276:1397-1403

Estrogen and estrogen-progesterone combinations appear to increase bone mass in postmenopausal women. This was the conclusion of the Postmenopausal Estrogen/Progestin Interventions (PEPI) trial, which assigned 875 postmenopausal women to one of five groups: placebo, estrogen alone or estrogen in combination with various dosages of progesterone. Women in the placebo group lost almost 2% of bone mass at the spine and hip over 3 years but women taking progesterone and/or estrogen gained 3.5% to 5% bone mass during the study. Estrogen alone was just as effective as estrogen/progesterone., Objective.--To assess the effects of hormone therapy on bone mineral density (BMD) in the spine and hip of postmenopausal women. Design.--A 3-year, multicenter, randomized, double-blinded, placebo-controlled clinical trial. Participants.--A total of 875 healthy women aged 45 to 64 years recruited at 7 clinical centers. Interventions.--Treatments were (1) placebo; (2) conjugated equine estrogens (CEE), 0.625 mg/d; (3) CEE, 0.625 mg/d plus medroxyprogesterone acetate (MPA), 10 mg/d for 12 d/mo; (4) CEE, 0.625 mg/d plus MPA, 2.5 mg/d daily; or (5) CEE, 0.625 mg/d plus micronized progesterone (MP), 200 mg/d for 12 d/mo. Main Outcome Measures,--Bone mineral density at baseline, 12 months, and 36 months. Results.--Participants assigned to the placebo group lost an average of 1.8% of spine BMD and 1.7% of hip BMD by the 36-month visit, while those assigned to active regimens gained BMD at both sites, ranging from 3.5% to 5.0% mean total increases in spinal BMD and a mean total increase of 1.7% of BMD in the hip. Changes in BMD for women assigned to active regimens were significantly greater than those assigned to placebo. Women assigned to CEE plus continuous MPA had significantly greater increases in spinal BMD (increase of 5%) than those assigned to the other 3 active regimens (average increase, 3.8%). Findings were similar among those adhering to assigned therapy, although, among adherent participants, there were no significant differences in BMD changes among the 4 active treatment groups. Older women, women with low initial BMD, and those with no previous hormone use gained significantly more bone than younger women, women with higher initial BMD, and those who had used hormones previously. Conclusions.--Postmenopausal women assigned to placebo demonstrated decreased BMD at the spine and hip, whereas women assigned to estrogen therapy increased BMD during a 36-month period. These findings demonstrate that estrogen replacement therapy increases BMD at clinically important sites. JAMA. 1996;276:1389-1396

Research was conducted to determine the effect of genetic line on hormonally induced puberty. Two studies were conducted, the first to evaluate estrus response (n = 120 gilts) and the second to evaluate follicular development (n = 24 gilts), Gilts were allotted to treatments in a 2 x 2 factorial arrangement. Gilts from two genetic lines (Age at Puberty x Yorkshire [APY] and Relaxed Selection x Yorkshire [RSY]) received either P.G. 600(R) (P) or no injection (C). The percentage in estrus within 5 d after treatment was greater (P < .05) for P than for C gilts. However, no difference was detected for the percentage of P or C gilts that had ovulated within 14 d. For the APY line, P gilts had greater (P < .05) ovulation rates than C gilts. However, for the RSY line, P and C gilts did not differin ovulation rate. More P gilts than C gilts had follicular cysts (P < .05). At 48 h after onset of estrus, plasma progesterone concentration tended to be greater (P =. 13) for P gilts than for C gilts. In Exp. 2, gilts were ovariectomized 18 h after the onset of estrus. Ova were dissected from follicles on one ovary, and follicular fluid was aspirated from the other ovary. No differences were detected for the percentages of ova in various stages of meiosis. For APY gilts, follicular fluid estradiol concentration for P gilts tended to be lower (P = .12) than that for C gilts; however, no differences were detected for RSY gilts. Progesterone concentration in follicular fluid tended (P = .14) to be greater in P gilts than in C gilts. These results indicate that the effect of genetic line on age at puberty should be considered when inducing puberty. Key Words: Pigs, Genotypes, Estradiol, Progesterone, Puberty

Three trials involving 128 heifers were conducted to determine whether norgestomet implants administered during the mid- and late luteal phases after breeding could be used to synchronize a second estrus in nonpregnant, inseminated heifers without adversely affecting pregnancy in pregnant heifers. All heifers were initially synchronized with Syncro-Mate B and artificially inseminated 47 h after implant removal. On d 9 (Trial 1) or d 12 (Trial 2) after the timed AI, the heifers were randomly assigned to treated or control groups. Treated heifers received two silicone implants containing 10.0 mg of norgestomet each (Trial 1) or one silicone implant containing 3.6 mg of norgestomet (Trial 2). Silicone implants were removed on d 21 after the initial AI. In Trial 1, the calving rate to the initial AI of the control heifers was 35 vs 55% for the norgestomet-implanted heifers (P |is greater than~ .05). In Trial 2 the calving rate to the initial AI of the control heifers was 9 vs 45% in the treated heifers (P |is less than~ .01). At the return estrus 52% of the control heifers returned to estrus within a 3-d period, whereas 93% of the norgestomet-treated heifers returned to estrus within a 3-d period (P |is less than~ .01). Norgestomet treatment had no effect on serum progesterone concentrations of the pregnant heifers on d 21 after the initial AI. In Trial 3, both control and treated heifers were administered silicone implants containing 3.6 mg of norgestomet on d 12; additionally, the treated heifers received an injection containing 3.0 mg of norgestomet and 5.0 mg of estradiol valerate. Norgestomet implants were removed on d 21. The calving rate of the control heifers was 10 of 19 (53%), compared with a calving rate of 1 of 21 (5%) of the heifers that were implanted with norgestomet and injected with norgestomet and estradiol valerate on d 12. In summary, treatment with norgestomet implants on d 9 or 12, through d 21, increased calving rates of treated beef heifers and synchronized the estrus of nonpregnant, treated heifers.

Hormone-replacement therapy for postmenopausal women that combines estrogen with progestin appears to be more favorable than estrogen alone. Hormone-replacement therapy to relieve menopausal symptoms lowers women's risk of cardiovascular disease by about 50%, but the reasons for this are unclear. Of 4,958 postmenopausal women, 853 took estrogen, 173 took a combination of estrogen and progestin, 813 used to take hormones and 3,119 had never taken hormones. Women who took estrogen alone had levels of blood triglycerides significantly higher than the other three groups combined. However, they also had higher levels of high-density lipoprotein (HDL) cholesterol and lower levels of low-density lipoprotein (LDL) cholesterol than nonusers. Women who took estrogen and progestin had HDL and LDL levels similar to those of women who only took estrogen. Fibrinogen levels, which are also associated with cardiovascular disease, were lower in women who took hormones than in women who did not. There were no significant differences in blood pressure between users and non-users.