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29 - Hyperprolactinemia

from PART II - INFERTILITY EVALUATION AND TREATMENT

Published online by Cambridge University Press:  04 August 2010

Botros R. M. B. Rizk
Affiliation:
University of South Alabama
Juan A. Garcia-Velasco
Affiliation:
Rey Juan Carlos University School of Medicine,
Hassan N. Sallam
Affiliation:
University of Alexandria School of Medicine
Antonis Makrigiannakis
Affiliation:
University of Crete
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Summary

INTRODUCTION

Prolactin is a polypeptide hormone that was discovered more than seventy years ago and is also known as the lactogenic hormone, lactotropin, luteotropic hormone, or luteotropin (1). It was initially thought that it is only produced by the anterior pituitary gland and is mainly involved with lactation, but now there is increasing evidence that there are many other sources of prolactin and that it is involved in diverse essential biological activities (2).

EMBRYOLOGY OF LACTOTROPHS

Prolactin is produced mainly by the pituitary lactotrophs, which normally comprise about 15–25 percent of the anterior pituitary (3). During embryologic development, the anterior pituitary (adenohypophysis) arises from Rathke's pouch (named after German embryologist and anatomist Martin Heinrich Rathke 1793–1860), which is an ectodermal out-pouching of the floor of the primitive mouth that grows upwards and later fuses with the postpituitary (neurohypophysis) that develops as a downward extension from the neuroectoderm of the diencephalon (4, 5).

Several home-domain transcription factors are released during the development of the anterior pituitary and are important in the gene activation and cell-lineage differentiation. The most important of which is Pit-1, which is necessary for the activation of prolactin (PRL), growth hormone (GH), growth hormone–releasing hormone (GHRH), and thyroid-stimulating hormone (TSH) genes. Congenital absence of Pit-1 gene causes a syndrome characterized by deficiency of lactotrophs, somatotrophs, and thyrotrophs (6–8).

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Publisher: Cambridge University Press
Print publication year: 2008

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