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Prolactinoma
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Pituitary adenomas producing prolactin (prolactinomas, or lactotroph adenomas) are diagnosed by sustained non-pregnant elevation of serum prolactin (usually >40 μg/L × 2; normal prolactin non-pregnant: <20 μg/L) and radiographic (best is MRI) evidence of pituitary adenoma. Rule out other causes of prolactinemia (Table 8.1) [1, 2] and macroprolactinemia (a condition where more than 60% of circulating prolactin is made up of macroprolactin, a complex formed by IgG and monomeric prolactin that result in elevate serum prolactin but has low biological activity and usually requires no treatment) in all asymptomatic patients [3, 4].
Endocrine diseases and pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Prolactin levels >200ng/mL are virtually certainly due to prolactinoma; however, since physiologic hyperprolactinemia of pregnancy approaches 200ng/mL, and since lactotroph hyperplasia and hypertrophy of normal pregnancy may mimic pituitary adenoma, it is rare that prolactinoma would be suspected or confirmed during pregnancy (40).
Influence of Ovarian Hormones on the Regulation of Luteinizing Hormone and Prolactin Release by Angiotensin II
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
M.K. Steele, L.S. Myers, C.F. Deschepper, W.F. Ganong, K.N. Stephenson, R.L. Shackelford
We have investigated this phenomenon in vivo. In initial experiments, we compared the effects of intravenous LHRH (100 ng in 100 ml saline) on LH and prolactin release in intact male animals versus ovariectomized female rats that had been treated with estradiol and progesterone (Table 1; Steele, Shackelford and Ganong, unpublished data). Ten min following LHRH administration, plasma LH levels were maximally stimulated in both male and female rats. However, an increase in prolactin release was seen only in female animals, suggesting a facilitatory role for ovarian hormones in sensitizing the lactotrophs to stimulation. A similar effect has been seen in humans where estrogen treatment enhanced the prolactin-releasing effect of LHRH (Gooren et al., 1985). To assess whether pituitary AII mediates the effect of LHRH on prolactin release, we infused ovarian steroid-treated rats with Sarthran, an AII-receptor blocker (Fig. 3). In saline-infused rats, LHRH induced a significant rise in prolactin levels; however, in Sarthran-infused animals, the prolactin increase was totally abolished. When considered with the data of Denef and Andries (1983) and Jones et al. (1988), these data are consistent with the hypothesis that LHRH stimulates the release of LH and AII from pituitary gonadotrophs. The AII, then, acts on the nearby lactotrophs to stimulate prolactin secretion.
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.
Sociodemographic and clinical characteristics related with hyperprolactinaemia in psychiatric clinical population
Published in International Journal of Psychiatry in Clinical Practice, 2022
D. A. Coronel, F. R. De la Peña, L. Palacios-Cruz, D. Cuevas, S. Duran
In this research, women showed a greater proportion of hyperPRL than men and the first ones have also been proved to have PRL elevations significantly greater during the chronic antipsychotic treatment in equivalent doses (Bushe & Shaw, 2007; Holt, 2008; Smith et al., 2002). We hypothesise that these gender differences can be related with the oestrogen ability to increase the PRL levels in blood and improve the ability response of the lactotroph cells to stimuli of PRL release. In the same way, oestrogens can improve the lactotroph cells in number from the anterior pituitary and act on the hypothalamus to decrease the dopamine content (Lee & Kim, 2006; Veselinović et al., 2011). If physiologically the decrease in oestrogen that occurs in menopause decreases baseline PRL levels, it is possible to suggest that in hyperprolactinaemic patients during the reproductive stage, upon reaching menopause, levels of this hormone should decrease, but some evidence suggests that high normal circulating PRL levels may accelerate vascular ageing in this women group (Georgiopoulos et al., 2009; Santana Pérez et al., 2007).
Patients with true mixed growth hormone and prolactin-secreting pituitary adenoma: a case series of 12 patients
Published in British Journal of Neurosurgery, 2020
Daqiq Gulbadin, Zhiwei Li, Muhammad Shahbaz, Zeeshan Farhaj, Arzoo Shabbir, Qichao Qi, Kuanxiao Tang, Shilei Ni, Lei Sun
Mixed growth hormone (GH) and prolactin (PRL) pituitary adenomas are relatively rare but are the most common plurihormonal type, producing GH and PRL at the same time.1 Elevated levels of these hormones in the bloodstream result in two different syndromes: acromegaly and hyperprolactinemia.2,3 Previous studies found hyperprolactinemia in 30–40% of acromegalic patients.4,5 Such adenomas can be classified as mammosomatotrophs (GH- and PRL-producing cells) adenomas (MSA), mixed somatotrophs (GH-producing cells) and lactotrophs (PRL-producing cells) adenomas (MSLA) and acidophilic stem cell adenomas (ASCA) according to the 2017 World Health Organization classification.6 MSA were as high as 2.2% of pituitary adenomas in a recent epidemiological study.7 Almost 5% of pituitary adenomas have been found to have MSLA during immunostaining.8 Based on surgically resected samples of acromegaly patients, approximately 20–25% of acromegaly adenomas are MSLA.9 In MSA, GH and PRL are co-expressed by the same cells named mammosomatotrophs, while these hormones are secreted by somatotrophs and lactotrophs respectively in MSLA. The last type of GH-PRL adenomas, ASCA, is relatively rare accounting for 0.2% of pituitary adenomas.10 However, unlike MSA and MSLA mainly producing GH, ASCA predominantly express PRL.10