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Fundamento. La prolactina se puede presentar bajo varias formas moleculares siendo la forma monométrica (PRLm) la biológicamente activa. La presencia de macroprolactina (MPRL) puede originar un falso diagnóstico de hiperprolactinemia debido a la interferencia en el procedimiento de medida. El objetivo ha sido desarrollar un protocolo que permita diagnosticar la hiperprolactinemia monométrica, que además sea complementario al procedimiento que detecta MPRL. Material y métodos. La población de referencia para PRLm estaba formada por 122 mujeres y 140 hombres aparentemente sanos a los que se les extrajo sangre para la cuantificación de PRL. Además, se recogieron49 sueros (33 mujeres y 16 hombres) hiperprolactinémicos. Se cuantificó PRL en todas las muestras en un Immulite 2000. La detección de MPRL y de PRLm se realiza tras precipitación con polietilenglicol. Se confirmó el resultado por cromatografía de filtración en gel. Para la obtención de los valores de referencia se siguieron las indicaciones del Panel de Expertos de la IFCC. Resultados. Los valores de referencia de PRLm fueron 3,4-26,6 ¦Ìg/L y 4,6-16,4 ¦Ìg/L en mujeres y varones, respectivamente. De los 49 pacientes hiperprolactinémicos, en el57 % la concentración de PRLm tras PEG se encontraba fuera del intervalo de referencia previamente obtenido, confirmándosela presencia de hiperprolactinemia monométrica. Conclusiones. Se ha desarrollado e implantado un protocolo para la cuantificación de PRLm. La obtención del os valores de referencia de PRLm permite el diagnóstico de la hiperprolactinemia monométrica o activa de forma complementaria a la identificación de MPRL (AU)

Background. Prolactin can take several molecular forms of which the most biologically active is the monomericform (PRLm). The presence of macroprolactin (MPRL) can give rise to a false diagnosis of hyperprolactinemia due to interference in the measuring procedure. The aim was to develop a protocol that enables diagnosis of monomeric hyperprolactinemia, which should also be complementary to the procedure for detecting MPRL. Material and methods. The reference population for PRLm was made up of 122 healthy women and 140healthy men, from whom blood was extracted for PRL quantification. Additionally, 49 hyperprolactinemic serums (33 women and 16 men) were collected. PRL was quantified in all the samples in an Immulite 2000.The detection of MPRL and PRLm was carried out following precipitation with polyetylenglicol (PEG). The result was confirmed by gelatin filtration chromatography. The reference values were obtained following theindications of the Expert Panel of the IFCC. Results. The PRLm reference values were 3,4-26,6¦Ìg/L and 4,6-16,4 ¦Ìg/L in women and men, respectively. In 57% of the 49 hyperprolactinemic patients the concentration of PRL m following PEG fell outside the previously obtained reference interval, confirming the presence of monomeric hyperprolactinemia. Conclusions. A protocol for quantifying PRL m has been developed and implemented. Obtaining PRLm reference values makes it possible to diagnose monomeric oractive hyperprolactinemia in a complementary form to the identification of MPRL(AU)

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Around 80 years ago researchers first established that the pituitary gland regulates mammary gland function as demonstrated by the ability of its extracts to promote both mammogenesis and lactogenesis in animal models. Little did they realize that in fact two hormones, prolactin (PRL) and growth hormone (GH), were contributing to these effects. By the mid 1930s PRL had been purified as a distinct lactogen, while the galactopoietic effect of GH was confirmed after its purification in the 1940s. Interest in these hormones initially centered about their potential for increasing milk production, while in the latter half of the twentieth century it became obvious that these hormones also had the potential to influence mammary cancer development. During the past 50 years large strides have been made into understanding how these hormones signal to, and within, cells of the mammary gland, paralleling rapid developments in the fields of cellular and molecular biology. In compiling this review we have summarized the progress that has been made to date regarding roles for these hormones in the mammary gland, with a goal of ensuring that some of the seminal literature is not diluted or forgotten. In doing so it is clear that there are lessons to be learned from past experiences, where new methods and technologies will continue to present exciting new opportunities to revisit lingering questions regarding these fascinating hormones and this fascinating organ.

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When I was a beginning graduate student 41 yr ago it had been established that estrogen caused mammary duct growth; a combination of estrogen and progesterone was required for lobule-alveolar development of the mammary glands; and prolactin and growth hormone were essential for mammary growth. In laboratory species exogenous prolactin, glucocorticoids, and estrogen would initiate secretion of milk provided the mammary glands had a well-developed lobule-alveolar system. It was not known with certainty that progesterone inhibited the process. For some species, prolactin and thyroxine had been shown to stimulate lactation, while glucocorticoids suppressed lactation. Definitive roles for growth hormone and insulin during lactation had not been established. Studies of hormonal control of mammary growth and function in cattle were few. In vitro methods to study hormonal regulation of the mammary glands were in their infancy. Quantitative measures of changes in mammary cell numbers and specific components of milk in response to hormones were rare. The concepts for quantification of hormone concentrations, hormone receptors, growth factors, and binding proteins in blood; hormonal regulation of nutrient partitioning; and hormonally induced mechanisms of action within mammary cells were waiting to be discovered. And eventually they were. However, lest we become too enamored with our current understanding of the hormones that control mammary growth and lactation, it remains a fact that the greatest physiological stimulus for milk yield is pregnancy, not some cocktail of exogenous hormones, growth factors, receptor agonists/antagonists, or gene therapies. Viva la mom!

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Although prolactin was discovered in the early 1930's in sheep, cows, birds etc., no human form had been because it was thought to be identical to human growth hormone (HGH). In fact, prior to 1970, most endocrinologists doubted human prolactin even existed. Prolactin-like effects could be demonstrated from a homogenate of human pituitary but attempting to purify it identified only growth hormone. Independent histological studies had identified prolactin-secreting "pregnancy cells" fuelling the conviction that prolactin was a distinct and separate pituitary hormone. A search was begun for prolactin through protein synthesis studies using pituitaries from pregnant and postpartum monkeys. Proteins obtained in a radioactive peak were similar to, but not identical with, growth hormone by molecular weight and electrophoretic mobility. The hypothesis that the unknown protein peak represented synthesis of prolactin rather than growth hormone proved correct. Evidence was then obtained confirming that in the human pituitary prolactin and growth hormone synthesis could be distinguished using antibodies to human growth hormone or to sheep prolactin. Human prolactin purified from pituitary glands using immunological tools capable of distinguishing between the two hormones provided ultimate proof of a separate and distinct human prolactin, a hormone which has its major impact today in endocrinology and reproductive medicine. This discovery represented an exciting and truly international collaborative effort.

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