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Your search keyword '"Kaiser, Ursula B"' showing total 12 results
Start Over Author "Kaiser, Ursula B" Journal endocrine reviews
12 results on '"Kaiser, Ursula B"'

2. The Congenital and Acquired Mechanisms Implicated in the Etiology of Central Precocious Puberty.

Author

Brito, Vinicius N, Canton, Ana P M, Seraphim, Carlos Eduardo, Abreu, Ana Paula, Macedo, Delanie B, Mendonca, Berenice B, Kaiser, Ursula B, Argente, Jesús, and Latronico, Ana Claudia

Subjects
PRECOCIOUS puberty, ETIOLOGY of diseases, ENDOCRINE disruptors
Abstract

The etiology of central precocious puberty (CPP) is multiple and heterogeneous, including congenital and acquired causes that can be associated with structural or functional brain alterations. All causes of CPP culminate in the premature pulsatile secretion of hypothalamic GnRH and, consequently, in the premature reactivation of hypothalamic-pituitary-gonadal axis. The activation of excitatory factors or suppression of inhibitory factors during childhood represent the 2 major mechanisms of CPP, revealing a delicate balance of these opposing neuronal pathways. Hypothalamic hamartoma (HH) is the most well-known congenital cause of CPP with central nervous system abnormalities. Several mechanisms by which hamartoma causes CPP have been proposed, including an anatomical connection to the anterior hypothalamus, autonomous neuroendocrine activity in GnRH neurons, trophic factors secreted by HH, and mechanical pressure applied to the hypothalamus. The importance of genetic and/or epigenetic factors in the underlying mechanisms of CPP has grown significantly in the last decade, as demonstrated by the evidence of genetic abnormalities in hypothalamic structural lesions (eg, hamartomas, gliomas), syndromic disorders associated with CPP (Temple, Prader-Willi, Silver-Russell, and Rett syndromes), and isolated CPP from monogenic defects (MKRN3 and DLK1 loss-of-function mutations). Genetic and epigenetic discoveries involving the etiology of CPP have had influence on the diagnosis and familial counseling providing bases for potential prevention of premature sexual development and new treatment targets in the future. Global preventive actions inducing healthy lifestyle habits and less exposure to endocrine-disrupting chemicals during the lifespan are desirable because they are potentially associated with CPP. [ABSTRACT FROM AUTHOR]

Published
2023
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3. Clinical Biology of the Pituitary Adenoma

Author

Melmed, Shlomo, primary, Kaiser, Ursula B, additional, Lopes, M Beatriz, additional, Bertherat, Jerome, additional, Syro, Luis V, additional, Raverot, Gerald, additional, Reincke, Martin, additional, Johannsson, Gudmundur, additional, Beckers, Albert, additional, Fleseriu, Maria, additional, Giustina, Andrea, additional, Wass, John A H, additional, and Ho, Ken K Y, additional

Published
2022
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8. Endocrine Toxicity of Cancer Immunotherapy Targeting Immune Checkpoints.

Author

Chang, Lee-Shing, Barroso-Sousa, Romualdo, Tolaney, Sara M, Hodi, F Stephen, Kaiser, Ursula B, and Min, Le

Abstract

Immune checkpoints are small molecules expressed by immune cells that play critical roles in maintaining immune homeostasis. Targeting the immune checkpoints cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed death 1 (PD-1) with inhibitory antibodies has demonstrated effective and durable antitumor activity in subgroups of patients with cancer. The US Food and Drug Administration has approved several immune checkpoint inhibitors (ICPis) for the treatment of a broad spectrum of malignancies. Endocrinopathies have emerged as one of the most common immune-related adverse events (irAEs) of ICPi therapy. Hypophysitis, thyroid dysfunction, insulin-deficient diabetes mellitus, and primary adrenal insufficiency have been reported as irAEs due to ICPi therapy. Hypophysitis is particularly associated with anti-CTLA-4 therapy, whereas thyroid dysfunction is particularly associated with anti-PD-1 therapy. Diabetes mellitus and primary adrenal insufficiency are rare endocrine toxicities associated with ICPi therapy but can be life-threatening if not promptly recognized and treated. Notably, combination anti-CTLA-4 and anti-PD-1 therapy is associated with the highest incidence of ICPi-related endocrinopathies. The precise mechanisms underlying these endocrine irAEs remain to be elucidated. Most ICPi-related endocrinopathies occur within 12 weeks after the initiation of ICPi therapy, but several have been reported to develop several months to years after ICPi initiation. Some ICPi-related endocrinopathies may resolve spontaneously, but others, such as central adrenal insufficiency and primary hypothyroidism, appear to be persistent in most cases. The mainstay of management of ICPi-related endocrinopathies is hormone replacement and symptom control. Further studies are needed to determine (i) whether high-dose corticosteroids in the treatment of ICPi-related endocrinopathies preserves endocrine function (especially in hypophysitis), and (ii) whether the development of ICPi-related endocrinopathies correlates with tumor response to ICPi therapy.

Published
2019
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10. TAC3/TACR3 Mutations Reveal Preferential Activation of GnRH Release by Neurokinin B in Neonatal Life Followed by Reversal in Adulthood

Author

Gianetti, Elena, primary, Tusset, Cintia, primary, Noel, Sekoni D., primary, Au, Margaret G., primary, Dwyer, Andrew A., primary, Hughes, Virginia A., primary, Abreu, Ana Paula, primary, Carroll, Jessica, primary, Trarbach, Ericka, primary, Silveira, Leticia FG, primary, Costa, Elaine MF, primary, de Mendonça, Berenice Bilharinho, primary, de Castro, Margaret, primary, Lofrano, Adriana, primary, Hall, Janet E., primary, Bolu, Erol, primary, Ozata, Metin, primary, Quinton, Richard, primary, Amory, John K., primary, Stewart, Susan E., primary, Arlt, Wiebke, primary, Cole, Trevor R., primary, Crowley, William F., primary, Kaiser, Ursula B., primary, Latronico, Ana Claudia, primary, and Seminara, Stephanie B., primary

Published
2010
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11. Frequency of Impaired Fibroblast Growth Factor Receptor 1 Signaling as a Cause of Normosmic Idiopathic Hypogonadotropic Hypogonadism

Author

Raivio, Taneli, primary, Sidis, Yisrael, additional, Plummer, Lacey, additional, Chen, Huaibin, additional, Ma, Jinghong, additional, Mukherjee, Abir, additional, Jacobson-Dickman, Elka, additional, Quinton, Richard, additional, Van Vliet, Guy, additional, Lavoie, Helene, additional, Hughes, Virginia A., additional, Dwyer, Andrew, additional, Hayes, Frances J., additional, Xu, Shuyun, additional, Sparks, Susan, additional, Kaiser, Ursula B., additional, Mohammadi, Moosa, additional, and Pitteloud, Nelly, additional

Published
2009
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