Final Height in Girls With Central Idiopathic Precocious Puberty Treated With Gonadotropin-Releasing Hormone Analog and Oxandrolone

Vottero, Alessandra; Pedori, S.; Verna, Marta; Pagano, Blandina; Cappa, Marco; Loche, Sandro; Bernasconi, Sergio; Ghizzoni, Lucia

doi:10.1097/01.ogx.0000234793.18257.e6

Cited by 9 publications

(12 citation statements)

References 25 publications

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“…Study has found that a mini-dose of estrogen replacement can normalize the slowdown of the growth rate during GnRHa therapy in girls with CPP (7) ; however, such treatment has the potential effect on the acceleration of bone maturation, and it is diffi cult to control the dose of estrogen because of the individual differences. The third strategy for CPP is the use of non-aromatic anabolic steroids, but currently these have only been used in some individual clinical observation studies (8) .…”

Section: Introductionmentioning

confidence: 99%

Stanozolol regulates proliferation of growth plate chondrocytes via activation of ERα in GnRHa-treated adolescent rats

Zhu¹,

et al. 2011

Journal of Pediatric Endocrinology and Metabolism

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Improving the fi nal adult height is one of the most important aims for treatment of central precocious puberty. Stanozolol (ST) is a synthetic derivative of androgen. In this study, we investigated the effects and the mechanisms of ST on the proliferation of growth plate chondrocytes isolated from adolescent rats treated with gonadotropin-releasing hormone analogue (GnRHa). Treatment with ST resulted in time-and concentration-dependent effects on proliferation as determined by MTT and proliferating cell nuclear antigen (PCNA) assays. Western blotting showed that ST increased the phosphorylation level of the estrogen receptor α (ER α ), but not the androgen receptor (AR). Pharmacological inhibition of ER α and mitogen-activated protein kinase (MAPK) attenuated the effects of ST on the proliferation of growth plate chondrocytes. A molecular dynamics simulation showed hydrophobic interactions between ST and ER α . These results suggested that ER α , but not AR, partially mediates the ST-driven proliferation of growth plate chondrocytes, and that multiple pathways may be involved in the mechanism of action of ST.

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Section: Introductionmentioning

confidence: 99%

Stanozolol regulates proliferation of growth plate chondrocytes via activation of ERα in GnRHa-treated adolescent rats

Zhu¹,

et al. 2011

Journal of Pediatric Endocrinology and Metabolism

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“…Furthermore, LHRH agonist is in clinical use for the treatment of a variety of sex steroid-exacerbated disorders such as precocious puberty (19), prostate cancer (20), endometriosis (21), and breast cancer (22). Therefore, extensive information is available regarding its pharmacokinetics, dosing, toxicity, and efficacy.…”

mentioning

confidence: 99%

Luteinizing Hormone-Releasing Hormone Enhances T Cell Recovery following Allogeneic Bone Marrow Transplantation

Goldberg

King

Nejat

et al. 2009

The Journal of Immunology

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Posttransplant immunodeficiency, specifically a lack of T cell reconstitution, is a major complication of allogeneic bone marrow transplantation. This immunosuppression results in an increase in morbidity and mortality from infections and very likely contributes to relapse. In this study, we demonstrate that sex steroid ablation using leuprolide acetate, a luteinizing hormone-releasing hormone agonist (LHRHa), increases the number of lymphoid and myeloid progenitor cells in the bone marrow and developing thymocytes in the thymus. Although few differences are observed in the peripheral myeloid compartments, the enhanced thymic reconstitution following LHRHa treatment and allogeneic bone marrow transplantation leads to enhanced peripheral T cell recovery, predominantly in the naive T cell compartment. This results in an increase in T cell function in vivo and in vitro. Graft-versus-host-disease is not exacerbated by LHRHa treatment and graft-versus-tumor activity is maintained. Because LHRHa allows for reversible (and temporary) sex steroid ablation, has a strong safety profile, and has been clinically approved for diseases such as prostate and breast cancer, this drug treatment represents a novel therapeutic approach to reversal of thymic atrophy and enhancement of immunity following immunosuppression.

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“…In addition, women with polycystic ovarian syndrome (PCOS) and low progesterone levels have been found to have increased prevalence of autoimmune thyroiditis,42 suggesting a role for progesterone in regulating immunity. Auto-antibody production has also been reported in females with PCOS43 and therefore might predispose these individuals to antibody-dependent autoimmune/inflammatory disorders, such as systemic lupus erythematosus.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of progesterone differ in dendritic cells from female and male rodents

et al. 2008

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Background-Steroid hormones, such as progesterone, are known to have immunomodulatory effects. Our research group previously reported direct effects of progesterone on dendritic cells (DCs) from female rodents. Primarily affecting mature DC function, progesterone effects included inhibition of proinflammatory cytokine secretion, downregulation of cell surface marker (major histocompatibility complex class II, CD80) expression, and decreased T-cell proliferative capacity, and were likely mediated through progesterone receptor (PR) because the PR antagonist RU486 reversed these effects.

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Final Height in Girls With Central Idiopathic Precocious Puberty Treated With Gonadotropin-Releasing Hormone Analog and Oxandrolone

Cited by 9 publications

References 25 publications

Stanozolol regulates proliferation of growth plate chondrocytes via activation of ERα in GnRHa-treated adolescent rats

Stanozolol regulates proliferation of growth plate chondrocytes via activation of ERα in GnRHa-treated adolescent rats

Luteinizing Hormone-Releasing Hormone Enhances T Cell Recovery following Allogeneic Bone Marrow Transplantation

Inhibitory effects of progesterone differ in dendritic cells from female and male rodents

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