CiteULike: omalbams Miller

Growth Hormone Decreases Visceral Fat and Improves Cardiovascular Risk Markers in Women with Hypopituitarism: a Randomized, Placebo-Controlled Study

Catherine Beauregard — 2008-04-02T20:47:24-00:00

J Clin Endocrinol Metab (1 April 2008), jc.2007-2371.

Context: Data regarding gender-specific efficacy of growth hormone (GH) on critical endpoints are lacking. There are no randomized, placebo-controlled studies of physiologic GH therapy solely in women.Objective: To determine the effects of physiologic GH replacement on cardiovascular risk markers and body composition in women with GHD.Design: 6-month, randomized, placebo-controlled, double-blind studySetting: GCRCStudy Participants: 43 women with GHD due to hypopituitarismIntervention: Study participants were randomized to receive GH (goal mid-normal serum IGF-I) or placebo.Main Outcome Measures: Cardiovascular risk markers, including high sensitivity C-reactive protein, tissue plasminogen activator, and body composition, including visceral adipose tissue by cross-sectional computed tomography.Results: Mean daily GH dose was 0.67 mg. The mean IGF-I SD score increased from -2.5 +/- 0.3 to -1.4 +/- 0.9 (GH) (p<0.0001 vs. placebo). High sensitivity C-reactive protein decreased by 38.2 +/- 9.6% (GH) vs. 18.2 +/- 6.0% (placebo) (p=0.03). Tissue plasminogen activator and total cholesterol decreased and high-density lipoprotein increased. Homeostasis model assessment: insulin resistance and other markers were unchanged. Body fat decreased [-5.1 +/- 2.0 (GH) vs. 1.9 +/- 1.0% (placebo), p=0.002], as did visceral adipose tissue [-9.0 +/- 5.9 (GH) vs. 4.3 +/- 2.7% (placebo), p=0.03]. Change in IGF-I level was inversely associated with % change in visceral adipose tissue (r= -0.61, p=0.002), total body fat (r= -0.69, p<0.0001), and high sensitivity C-reactive protein (r= -0.51, p=0.003).Conclusions: Low-dose GH replacement in women with GHD decreased total and visceral adipose tissue, and improved cardiovascular markers with a relatively modest increase in IGF-I levels without worsening insulin resistance. 10.1210/jc.2007-2371

Androgen Deficiency in Women

Karen Miller — 2008-02-15T16:42:38-00:00

J Clin Endocrinol Metab, Vol. 86, No. 6. (1 June 2001), pp. 2395-2401.

Physiological and pathological processes as well as iatrogenic interventions may result in androgen deficiency compared with levels in young healthy women. Whether relative androgen deficiency results in a clinical syndrome similar to that reported in men, including osteopenia, increased fat mass, decreased libido, and diminished quality of life, has not been definitively established. However, preliminary data in postmenopausal women suggest that physiological androgen replacement therapy, which involves substantially lower doses than those used in men, may result in increased bone mineral density, increased libido, and improved quality of life. The safety of androgen preparations that result in supraphysiological levels has not been established in women and would be expected to result in hirsutism, acne, and virilization with chronic use. Androgen preparations that avoid liver metabolism and result in physiological serum androgen levels in women with androgen deficiency are not currently available, but are in development. Therefore, although widespread screening and hormone replacement for androgen deficiency cannot be recommended yet, increasing interest in this topic makes consideration of the available data important. 10.1210/jc.86.6.2395

Reversal of the hypogonadotropic hypogonadism of obese men by administration of the aromatase inhibitor testolactone.

B Zumoff — 2008-01-31T19:33:02-00:00

Metabolism, Vol. 52, No. 9. (September 2003), pp. 1126-1128.

Studies from this laboratory have shown that obese men have elevated serum estrogen levels and diminished levels of follicle-stimulating hormone (FSH) and free and total testosterone, all in proportion to their degree of obesity. The decreases in testosterone and FSH constitute a state of hypogonadotropic hypogonadism (HHG), and we have hypothesized that it results from feedback suppression of the pituitary by the elevated estrogen levels. We tested this hypothesis by lowering the serum estrogens of 6 health obese men (body mass index [BMI], 38 to 73) by administering the aromatase inhibitor testolactone (1 g daily for 6 weeks). Twenty-four-hour mean serum testosterone rose in every subject, from a mean of 290 +/- 165 ng/dL to a mean of 403 +/- 170 (P <.0003); 24-hour mean serum estradiol decreased in every subject, from a mean of 40 +/- 10.8 pg/mL to a mean of 29 +/- 6.7 (P <.004); and 24-hour mean serum luteinizing hormone (LH) increased in every subject, from a mean of 14.3 +/- 4.1 mIU/mL to a mean of 19.3 +/- 5.1 (P <.004). The rise in mean LH was due to an increase in the amplitude of the individual secretory pulses, especially at night. Twenty-four-hour mean serum estrone decreased nonsignificantly, from 48 +/- 14 pg/mL to 39 +/- 6.4, and 24-hour mean serum FSH increased nonsignificantly, from 13.5 +/- 5.3 mIU/mL to 15.0 +/- 5.4. The results are in accordance with the hypothesis, in that inhibition of estrogen biosynthesis (through administration of the aromatase inhibitor testolactone) results in alleviation of the HHG of our obese male subjects.

Underdeveloped trabecular bone microarchitecture is detected in children with cerebral palsy using high-resolution magnetic resonance imaging

C Modlesky — 2008-01-22T20:45:18-00:00

Osteoporosis International, Vol. 19, No. 2. (4 February 2008), pp. 169-176.

Abstract Summary Using high resolution magnetic resonance imaging, we detected severely underdeveloped trabecular bone microarchitecture in the distal femur of children with cerebral palsy who can not ambulate independently vs. typically developing controls. Furthermore, very good short-term reliability of trabecular bone microarchitecture measurements was observed in both groups of children. Introduction Severe forms of cerebral palsy (CP) are associated with very low areal bone mineral density and a very high incidence of fracture in the distal femur; however, the state of trabecular bone microarchitecture has not been evaluated. Furthermore, the short-term reliability of trabecular bone microarchitecture assessment in children using high-resolution magnetic resonance imaging (MRI) has not been determined. Methods Apparent bone volume to total volume (appBV/TV), trabecular number, (appTb.N), trabecular thickness (appTb.Th) and trabecular separation (appTb.Sp) were determined in the distal femur of non-ambulatory children with CP and typically developing children using MRI. Results Children with CP had a 30% lower appBV/TV, a 21% lower appTb.N, a 12% lower appTb.Th and a 48% higher appTb.Sp in the distal femur than controls (n = 10/group; P < 0.001). The short-term reliability of the trabecular bone microarchitecture measures was very good, with coefficients of variation ranging from 2.0 to 3.0% in children with CP (n = 6) and 1.8 to 3.5% in control children (n = 6). Conclusions Underdeveloped trabecular bone microarchitecture can be detected in the distal femur of children with CP who can not ambulate independently using high-resolution MRI. Furthermore, MRI can be used to assess trabecular bone microarchitecture in children with a high degree of reliability.