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Biomedical subjects

R L Barbieri

Publications and source records attributed to R L Barbieri.

At least 91 records · Page 5Linked to original sources
PubMed1991

Effects of growth hormone administration on dehydroepiandrosterone sulphate, androstenedione, testosterone and cortisol metabolism during nutritional repletion.

This study evaluated whether pharmacological doses of recombinant human growth hormone (hGH) influences androgen or cortisol metabolism during nutritional repletion following prolonged illness. Stable hospitalized adults (three males, seven female) receiving constant calorie and protein intake were studied. An initial control week was followed by a treatment period during which hGH (10 mg/day s.c.) was administered daily. Prior to hGH treatment, serum and 24-h urinary concentrations of dehydroepiandrosterone sulphate (DS) were below the normal range; serum androstenedione and testosterone concentrations were within the lower limit of normal. In contrast, serum cortisol (F) and 24-h urinary F excretion were normal. During hGH treatment, nitrogen balance became positive and plasma insulin-like growth factor I (IGF-I) concentrations rose five to seven-fold. However, serum DS, androstenedione, testosterone and F, and urinary F excretion did not change, while 24-h urinary DS excretion fell significantly. Growth hormone administration markedly stimulated protein anabolism but did not increase the low concentrations of circulating androgens or alter the disassociation between adrenal androgen and F release in stable hospitalized males and females. Thus, hGH does not appear to function as a cortical adrenal androgen stimulating hormone (CASH) or regulate adrenal cortisol or gonadal androgen release in this clinical setting.

Adrenal Cortex↗
PubMed1991

Polycystic ovarian disease.

Polycystic ovarian disease (PCOD) is a common endocrinopathy in women of reproductive age. Its molecular causes remain to be fully defined. Hyperinsulinemia and hyperandrogenism are positively correlated, which suggests that insulin resistance may be involved in the pathogenesis of PCOD. Point mutations in the insulin receptor gene that cause insulin resistance appear to be associated with the PCOD phenotype.

Female↗
PubMed1991

Overall body fat and regional fat distribution in young women: quantification with MR imaging.

Overall body fat and its distribution in different regions are important predispositions to known aberrations in lipid and glucose metabolism. The accuracy of MR imaging in estimating overall body fatness and regional fat distribution at individual landmarks was determined by comparing it with well-accepted measures by deuterium-oxide (D2O) dilution and bioimpedance analysis. Fourteen normal young women (athletes and control subjects) were studied. A total of 308 axial, T1-weighted, spin-echo MR images over a specific region in the trunk (21-24 scans per subject) were obtained. Morphometric computer image analysis was performed to determine the subcutaneous, internal, and total fat volumes in each image. The data were analyzed in two ways: data from all slices were summed to assess overall body fatness, and six anatomic landmarks were chosen for regional comparisons. MR-determined estimates of overall body fatness strongly correlated with total body fat measures by D2O dilution in both total fat (r = .91) and subcutaneous fat (r = .92) determinations. Athletes in both the low- and high-intensity training phases had significantly lower values of MR-determined total body fatness than did control subjects. Parallel to total body fatness, athletes had significantly lower MR-determined ratios of total fat/total volume in four of six individual landmarks compared with control subjects. Our experience suggests that MR is an accurate method to quantify overall body fatness, when compared with D2O dilution and bioimpedance analysis. MR could also discriminate regional components of subcutaneous and internal body fat at individual landmarks.

Adipose Tissue↗
PubMed1991

Hyperandrogenism: new insights into diagnosis and therapy.

Many different disease processes can result in a phenotype of hirsutism, anovulation, and oligomenorrhea or amenorrhea. An important goal of reproductive endocrinologists is to identify specific genetic diseases that can produce the hyperandrogenic phenotype. Two genetic disorders that can result in the hyperandrogenic phenotype are 1) mutations in the 21-hydroxylase gene (adrenal hyperplasia), and 2) mutations in the insulin receptor gene (the syndrome of hyperandrogenism-insulin resistance and acanthosis nigricans). The identification of these two genetic causes of hyperandrogenism provides the opportunity to investigate new approaches to prenatal diagnosis and therapy, genetic analysis of pedigrees, and innovative forms of therapy.

Acanthosis Nigricans↗
PubMed1991

Cytogenetic abnormalities in uterine leiomyomata.

Uterine leiomyomata are thought to be monoclonal tumors; however, the factors involved in the neoplastic proliferation of uterine leiomyomata are unknown. The purpose of the present study was to characterize uterine leiomyomata using cytogenetic techniques. Thirteen leiomyoma specimens were obtained by hysterectomy or myomectomy. Short-term cultures were successfully established for all specimens, and metaphase spreads were prepared by conventional techniques. Clonal chromosome rearrangements were detected in seven leiomyoma specimens (54%). These rearrangements involved chromosome bands 12q14-15 in five specimens, including three tumors with a specific translocation, t(12;14)(q14-15;q23-24). Chromosome rearrangements involving chromosome band 7q22 were identified in two specimens. A normal 46,XX karyotype was observed in six specimens. Myometrial specimens from two patients with abnormal leiomyoma karyotypes were normal cytogenetically. These results suggest that spontaneous chromosome rearrangements may be responsible for the initiation and proliferation of leiomyoma growth.

Adult↗
PubMed1990

Etiology and epidemiology of endometriosis.

The true prevalence of endometriosis remains undetermined because diagnostic laparoscopy cannot be performed on large, random, population-based samples of women. However, available evidence suggests that the disease occurs in approximately 1% to 7% of women in the United States. The cause of endometriosis is though to be associated with mechanical factors (such as retrograde menstrual flow) or estrogen production. Recent research also has suggested that regular exercise may help to protect against the disease by decreasing the rate of estrogen production.

Endometriosis↗
PubMed1990

Comparison of the pharmacology of nafarelin and danazol.

The pharmacologic profiles of danazol and nafarelin differ considerably from each other. Danazol interacts with multiple classes of proteins, whereas the gonadotropin-releasing hormone agonist nafarelin interacts only with the pituitary gonadotropin-releasing hormone receptor. Differences in the molecular, endocrine, and clinical pharmacologic properties of these agents may provide clues to their varying effects in the management of women with endometriosis.

Animals↗
PubMed1990

Gonadotropin-releasing hormone agonists and estrogen-progestogen replacement therapy.

Gonadotropin-releasing hormone agonists are effective in the treatment of endometriosis and myomas, both of which are estrogen-dependent processes, but there is a high clinical recurrence rate after therapy is discontinued. Long-term continuous therapy (2 years or more) has a cumulative effect on bone loss and causes other uncomfortable or harmful side effects. Noninvasive assessments of disease response in patients with myomas have shown that bone changes might be prevented and other side effects of long-term therapy can be alleviated by adding back small amounts of estrogen or progestin. No comparable data are available for patients with endometriosis because the need for repeated laparoscopy has made long-term studies impractical. Nevertheless, a short-term study of patients with endometriosis showed that adding small amounts of progestin during treatment with a gonadotropin-releasing hormone agonist may help prevent bone changes.

Drug Therapy, Combination↗
PubMed1990

Efficacy and safety considerations in women with uterine leiomyomas treated with gonadotropin-releasing hormone agonists: the estrogen threshold hypothesis.

Gonadotropin-releasing hormone agonists induce a reversible hypogonadotropic hypogonadal environment. Leiomyomas are common, estrogen-sensitive, benign neoplasms that decrease in size by 40% to 50% during gonadotropin-releasing hormone agonist treatment. During gonadotropin-releasing hormone agonist therapy most women are amenorrheic. After discontinuation of gonadotropin-releasing hormone agonist treatment, uterine and myoma size increase and a return to pretreatment menstrual patterns often occurs. Concerns about the safety of long-term hypoestrogenism have made long-term gonadotropin-releasing hormone agonist administration an undesirable treatment strategy. This article focuses on the use of gonadotropin-releasing hormone agonists as preoperative therapy in selected women undergoing hysterectomy or myomectomy and the combination of a gonadotropin-releasing hormone agonist with estrogen-progestin "add-back" treatment as a potential long-term medical therapy for women with symptomatic leiomyomas. Finally, an estrogen threshold hypothesis to assess the effects of circulating estrogen concentrations on different tissues, is presented.

Buserelin↗
PubMed1990

A randomized double-blind prospective trial of two doses of gestrinone in the treatment of endometriosis.

The purpose of this randomized double blind prospective trial was to study the efficacy and safety of two doses of oral gestrinone in the treatment of endometriosis. Six patients received gestrinone 1.25 mg twice weekly (group I) and six patients received gestrinone 2.5 mg twice weekly (group II). Patients underwent pretreatment and post-treatment laparoscopies and their endometriosis scores were recorded. The mean total endometriosis scores declined significantly from 20.0 +/- 5.2 (mean +/- standard error of the mean) pretreatment to 9.5 +/- 3.9 post-treatment in group I and from 19.1 +/- 4.8 pretreatment to 7.1 +/- 2.1 post-treatment in group II. A total of 67% of patients reported side effects. This study suggests that oral gestrinone 1.25 mg or 2.5 mg twice weekly is efficacious and safe in the treatment of endometriosis.

Adult↗
PubMed1990

Fasting serum growth hormone and insulin-like growth factor-I and -II concentrations in women with leiomyomata uteri treated with leuprolide acetate or placebo.

Eighteen patients with leiomyomata uteri were randomized to receive either leuprolide acetate depot (n = 9) 3.75 mg intramuscularly (IM) or placebo (n = 9) IM every 4 weeks for four injections. Leuprolide acetate treated patients demonstrated a reduction in mean uterine volume of 34% and a decrease in serum estradiol (E2) concentrations from 120 +/- 21 pg/mL (mean +/- standard error) to 16 +/- 9 pg/mL. Leuprolide acetate treated patients also demonstrated significant decreases in serum growth hormone (GH) (3.0 +/- 0.4 ng/mL versus 1.4 +/- 0.4 ng/mL) and insulin-like growth factor-I (IGF-I) concentrations (3.3 +/- 0.4 U/mL versus 1.3 +/- 0.2 U/mL) over the 12 week treatment period. Serum IGF-II levels did not change. Mean uterine volume and serum E2, GH, IGF-I, and IGF-II concentrations did not change in placebo-treated patients. These data suggest that hypoestrogenism is associated with decreases in circulating GH and IGF-I.

Adult↗
PubMed1990

Endometriosis 1990. Current treatment approaches.

Endometriosis is an extremely common gynaecological disease, affecting between 1 and 5% of women of reproductive age. Women with endometriosis typically present for medical care with one of more of the following problems: pelvic pain, infertility, or a large adnexal mass (an endometrioma). The primary treatment for an endometrioma is surgical. However, long term postoperative hormone therapy may be necessary to prevent new endometriomas from developing. There is no evidence that hormonal therapy of endometriosis will improve fecundability in women with endometriosis and infertility. Pelvic pain due to endometriosis can be successfully treated with hormonal agents in the majority of patients. Four basic hormonal regimens are currently available for the treatment of endometriosis: (a) danazol; (b) gonadotrophin-releasing hormone (GnRH) [luteinising hormone-releasing hormone (LHRH); gonadorelin] agonists; (c) progesterones (progestins); and (d) combined estrogens and progesterones. Randomised, controlled, clinical trials suggest that danazol and the GnRH agonists are equally effective in the treatment of endometriosis. However, the side effects caused by danazol and the GnRH agonists are markedly different. Danazol produces androgenic side effects including weight gain, hirsutism, acne, oily skin and deepening of the voice. GnRH agonists produce side effects due to hypoestrogenism, including hot flushes, osteoporosis and dry vagina. The ideal drug regimen for the treatment of endometriosis remains to be developed.

Endometriosis↗
PubMed1990

High dietary fiber and low saturated fat intake among oligomenorrheic undergraduates.

Numerous functional risk factors are associated with the occurrence of secondary amenorrhea in young women. Less is known regarding factors associated with the more prevalent problem of oligomenorrhea. We have evaluated nutrient intake, body composition, perceived psychological stress, 24-hour urinary cortisol, and urinary C peptide (UCP) in 35 eumenorrheic, 11 mildly oligomenorrheic, and 10 oligomenorrheic nonathletic undergraduate women. Nutrient intake was evaluated by a validated food frequency questionnaire. Oligomenorrheic women were found to consume significantly more dietary fiber, crude fiber, and polyunsaturated fat, and significantly less saturated fat than their eumenorrheic classmates. Oligomenorrheic women had significantly lower 24-hour UCP excretion than mildly oligomenorrheic women. The groups did not differ in any aspect of body composition, body weight, age of menarche, perceived psychological stress, or urinary cortisol excretion. The data suggest that higher intake of fiber and lower intake of saturated fat may be associated with oligomenorrhea among otherwise healthy undergraduate nonathletic women.

Adult↗
PubMed1989

Nicotine and cotinine inhibit rat testis androgen biosynthesis in vitro.

The effects of nicotine and cotinine, the major metabolite of nicotine, on testosterone production in rat testis were investigated. Rat Leydig cells were isolated and incubated with nicotine and cotinine. Nicotine produced a dose dependent increase in progesterone levels and a dose-dependent decrease in androstenedione and testosterone concentrations. Cotinine produced a dose-dependent increase in progesterone and androstenedione and a dose-dependent decrease in testosterone levels. The effects of nicotine and cotinine on rat testis mitochondrial cholesterol side chain cleavage enzyme and microsomal 3 beta-hydroxysteroid dehydrogenase-isomerase, 17 alpha-hydroxylase, 17,20-lyase and 17-ketosteroid reductase were examined. Nicotine competitively inhibited 17 alpha-hydroxylase (apparent Ki = 30 microM) and 17,20-lyase (apparent Ki = 18 microM). Cotinine competitively inhibited 17-ketosteroid reductase (apparent Ki = 46 microM). The addition of nicotine to preparations of rat testis microsomes yielded a Type II cytochrome P-450 binding spectrum. We conclude that nicotine and cotinine competitively inhibit multiple steps in testosterone biosynthesis.

Androgens↗
PubMed1989

Twenty-four-hour urinary-free cortisol in premenopausal cigarette smokers and nonsmokers.

Cigarette smoking has been reported to produce acute increases in plasma ACTH and cortisol, but the effect of chronic smoking on integrated adrenal steroid production has not been studied. The effects of chronic smoking on 24-hour urinary-free cortisol, 11-deoxycortisol, DHEAS, and 17-keto-steroids were studied in 10 premenopausal smokers, and their results were compared with 15 premenopausal nonsmokers. The 24-hour excretion of urinary-free cortisol (85.0 +/- 40.8 nmol/d in smokers versus 81.7 +/- 49.7 nmol/d in nonsmokers), 11-deoxycortisol (259 +/- 170 nmol/d in smokers versus 222 +/- 147 nmol/d in nonsmokers), DHEAS (3,140 +/- 2,909 nmol/d in smokers versus 2,890 +/- 1,960 nmol/d in nonsmokers), and 17-ketosteroids (17.4 +/- 8.3 mumol/d in smokers versus 23.4 +/- 19.9 mumol/d in nonsmokers) were similar in smokers and nonsmokers (all P values not significant). We conclude that chronic smoking does not result in abnormal levels of 24-hour urinary-free cortisol.

17-Ketosteroids↗