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3 results

  • Chapter 8 - Prolactin, Prolactinoma, and Pregnancy

  • from Section II - Hormones and Gestational Disorders
  • Edited by Felice Petraglia, Università degli Studi, Florence, Mariarosaria Di Tommaso, Università degli Studi, Florence, Federico Mecacci, Università degli Studi, Florence
  • Book:
    Hormones and Pregnancy
    Published online:
    09 November 2022
    Print publication:
    13 October 2022, pp 73-86

  • Summary

    Prolactin (PRL) is a key player in normal physiology and pathophysiology of reproduction. Although not indispensable to achieve gestation in humans (as opposed to rodents), PRL is essential for the development of the mammary gland and for lactation. On the other hand, hyperprolactinemia is a frequent cause of infertility and needs to be corrected in a young woman who actively seeks pregnancy. Dopamine agonists (DA) represent the first-line treatment of prolactinomas, but transsphenoidal surgery may be considered in selected cases. Among DA, preference should be given to cabergoline over bromocriptine, due to its higher efficacy and better tolerance. Both drugs are safe to use during early gestation. In most cases, however, drug withdrawal is advised as soon as the pregnancy is confirmed. Symptomatic tumor growth is a rare event in microprolactinomas (2–3 percent) but more frequent in large macroprolactinomas without previous ablative therapy (15–20 percent). Symptomatic tumor enlargement will usually be successfully treated with resumption of the DA. Breastfeeding is not contra-indicated in women with a prolactinoma. In addition, pregnancy may have a beneficial effect on further endocrine outcome, inducing early remission of hyperprolactinemia in about 40 percent of these women. Data are much less robust in men in whom PRL concentrations are less prone to increase. The male reproductive axis is also less sensitive to the effects of hyperprolactinemia. Nevertheless, significant hyperprolactinemia in men may also cause hypogonadism and infertility and must be treated as in women.

  • Plasma acetyl-l-carnitine and l-carnitine in major depressive episodes: a case–control study before and after treatment

  • Abd El Kader Ait Tayeb, Romain Colle, Khalil El-Asmar, Kenneth Chappell, Cécile Acquaviva-Bourdain, Denis J. David, Séverine Trabado, Philippe Chanson, Bruno Feve, Laurent Becquemont, Céline Verstuyft, Emmanuelle Corruble
  • Journal:
    Psychological Medicine / Volume 53 / Issue 6 / April 2023
    Published online by Cambridge University Press:
    14 October 2021, pp. 2307-2316
  • Background

    Major depressive disorder (MDD) is the main cause of disability worldwide, its outcome is poor, and its underlying mechanisms deserve a better understanding. Recently, peripheral acetyl-l-carnitine (ALC) has been shown to be lower in patients with major depressive episodes (MDEs) than in controls. l-Carnitine is involved in mitochondrial function and ALC is its short-chain acetyl-ester. Our first aim was to compare the plasma levels of l-carnitine and ALC, and the l-carnitine/ALC ratio in patients with a current MDE and healthy controls (HCs). Our second aim was to assess their changes after antidepressant treatment.

    Methods

    l-Carnitine and ALC levels and the carnitine/ALC ratio were measured in 460 patients with an MDE in a context of MDD and in 893 HCs. Depressed patients were re-assessed after 3 and 6 months of antidepressant treatment for biology and clinical outcome.

    Results

    As compared to HC, depressed patients had lower ALC levels (p < 0.00001), higher l-carnitine levels (p < 0.00001) and higher l-carnitine/ALC ratios (p < 0.00001). ALC levels increased [coefficient: 0.18; 95% confidence interval (CI) 0.12–0.24; p < 0.00001], and l-carnitine levels (coefficient: −0.58; 95% CI −0.75 to −0.41; p < 0.00001) and l-carnitine/ALC ratios (coefficient: −0.41; 95% CI −0.47 to −0.34; p < 0.00001), decreased after treatment. These parameters were completely restored after 6 months of antidepressant. Moreover, the baseline l-carnitine/ALC ratio predicted remission after 3 months of treatment (odds ratio = 1.14; 95% CI 1.03–1.27; p = 0.015).

    Conclusions

    Our data suggest a decreased mitochondrial metabolism of l-carnitine into ALC during MDE. This decreased mitochondrial metabolism is restored after a 6-month antidepressant treatment. Moreover, the magnitude of mitochondrial dysfunction may predict remission after 3 months of antidepressant treatment. New strategies targeting mitochondria should be explored to improve treatments of MDD.