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Endocrine Disorders, Contraception, and Hormone Therapy during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Excess pituitary prolactin secretion can lead to symptoms of galactorrhea, menstrual irregularities, and infertility. Menstrual cycle abnormalities caused by hyperprolactinemia include primary and secondary amenorrhea, oligomenorrhea, and luteal phase defects. Hyperprolactinemia may result from a variety of different causes (pituitary adenoma, hypothyroidism, various pharmacologic agents). Etiology should be established prior to beginning therapy. Primary therapy for idiopathic hyperprolactinemia, or a small pituitary adenoma, is an ergot alkaloid compound, such as bromocriptine. Many physicians prefer to use cabergoline (Dostinex) to treat hyperprolactinemia instead of bromocriptine to avoid side effects.
Tumors of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Hyperprolactinemia Women: Infertility.Amenorrhea.Galactorrhea.Reduced libido.Delayed menarche.Men: Reduced libido.Impotence.Galactorrhea – unusual.Apathy.Weight gain.
Principles of Pathophysiology of Infertility Assessment and Treatment*
Published in Asim Kurjak, Ultrasound and Infertility, 2020
Joseph G. Schenker, Aby Lewin, Menashe Ben-David
Our early observations indicate that prolactin also exerts a direct effect on the ovaries interfering with gonadal response to exogenous gonadotropins. In addition, binding sites for prolactin were found to exist in human granulosa cells. Also, it was shown that prolactin, added to granulosa cells growing in vitro, may inhibit aromatase activity resulting in a decrease of estradiol synthesis and an accumulation of androgens. Thus, it is most likely that hyperprolactinemia induces infertility by acting on both levels: the hypothalamus-pituitary axis and the ovaries.
Relevance and therapeutic implication of macroprolactinemia detection using PEG 6000 in women of childbearing age with hyperprolactinemia: experience at a tertiary hospital
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2023
Anne Ongmeb Boli, Martine Claude Etoa Etoga, Francine Mekobe Mendane, Charly Feutseu, Eloumba Mbono Samba, Amazia Falmata, Arnaud Manga Ndi, Jean-Claude Katte, Mesmin Dehayem, Vicky Jocelyn Ama Moor, Jean Claude Mbanya, Eugène Sobngwi
Prolactin (PRL) is a single-chain protein synthesised and released by lactotroph cells of the anterior pituitary gland.1 Its secretion is regulated by dopamine, which has an inhibitory effect on lactotroph cells.1 When prolactin secretion increases in the absence of pregnancy, clinical symptoms such as galactorrhoea and irregular menstrual cycles may occur. These menstrual abnormalities include spaniomenorrhoea and amenorrhoea, which may contribute to infertility. Hyperprolactinemia is a well-recognised hormonal aetiology of infertility among women of childbearing age. It affects 30–40% of infertile women and 15–20% of women with menstrual disorders.2 Impairment of gonadal function and, ultimately, infertility result from suppression of the pulsatile secretion of gonadotrophins.3 The majority of prolactin molecules present as monomers that are biologically active, but these may also exist as macromolecules (macroPRL) known as big and big-big prolactin, which may interfere with laboratory measurements of the protein.4 According to Vilar et al., in 2019, two Brazilian series reported macroPRL as the third cause of non-physiological hyperprolactinemia after drugs and pituitary adenomas.5 All three forms of prolactin are indistinguishable by routine laboratory assays.
Pharmacological strategies for sexual recovery in men undergoing antipsychotic treatment
Published in Expert Opinion on Pharmacotherapy, 2022
Tommaso B. Jannini, Andrea Sansone, Rodolfo Rossi, Giorgio Di Lorenzo, Massimiliano Toscano, Alberto Siracusano, Emmanuele A. Jannini
A well-established treatment protocol for a different kind of hyperprolactinemia, from prolactinoma- to AP-induced hyperprolactinemia, entails the use of dopamine agonists. The rationale behind this choice lies in the above-mentioned evidence that the dopamine tone inhibits the release of Prl in the pituitary gland. However, except for scarce data on cabergoline [189], there is no evidence that dopamine agonists may have a therapeutic effect on AP-induced SD. Indeed, molecules like bromocriptine, pramipexole, or other drugs with a dopaminergic action, such as selegiline, imipramine, and the Japanese root shakuyaku-kanzo-to were not shown to improve sexual function [190]. Only mild and preliminary findings were reported from patients treated with amantadine, whose action causes a release of dopamine at neuronal terminals and, as the Authors report, an increase in sexual function [191].
Van Wyk-Grumbach syndrome and trisomy 21
Published in Baylor University Medical Center Proceedings, 2022
Aleida Rivera-Hernández, Mónica Margarita Madrigal-González, Rossana Espinosa-Peniche, Jessie Zurita-Cruz, Lourdes Balcázar-Hernández
Van Wyk-Grumbach syndrome (VWGS) is characterized by severe hypothyroidism, precocious puberty with multiple ovarian cysts with or without breast budding or early menarche, delayed bone age, elevated estradiol, prepubertal luteinizing hormone (LH), elevated follicle-stimulating hormone (FSH), and spontaneous resolution with levothyroxine treatment.1 Nontumor hyperprolactinemia may be present. Down syndrome has been associated with a high susceptibility and prevalence of thyroid disorders, including autoimmune thyroid disease (such as Hashimoto’s thyroiditis), which can lead to severe hypothyroidism.2 Despite the high prevalence of thyroid disorders, the coexistence of VWGS and trisomy 21 is rare. We present a case of a Latino patient with Down syndrome and VWGS.