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International Journal of Molecular... Jul 2020The hair cycle and hair follicle structure are highly affected by various hormones. Androgens-such as testosterone (T); dihydrotestosterone (DHT); and their prohormones,... (Review)
Review
The hair cycle and hair follicle structure are highly affected by various hormones. Androgens-such as testosterone (T); dihydrotestosterone (DHT); and their prohormones, dehydroepiandrosterone sulfate (DHEAS) and androstendione (A)-are the key factors in terminal hair growth. They act on sex-specific areas of the body, converting small, straight, fair vellus hairs into larger darker terminal hairs. They bind to intracellular androgen receptors in the dermal papilla cells of the hair follicle. The majority of hair follicles also require the intracellular enzyme 5-alpha reductase to convert testosterone into DHT. Apart from androgens, the role of other hormones is also currently being researched-e.g., estradiol can significantly alter the hair follicle growth and cycle by binding to estrogen receptors and influencing aromatase activity, which is responsible for converting androgen into estrogen (E2). Progesterone, at the level of the hair follicle, decreases the conversion of testosterone into DHT. The influence of prolactin (PRL) on hair growth has also been intensively investigated, and PRL and PRL receptors were detected in human scalp skin. Our review includes results from many analyses and provides a comprehensive up-to-date understanding of the subject of the effects of hormonal changes on the hair follicle.
Topics: Androgens; Estradiol; Female; Hair Follicle; Humans; Male; Prolactin; Sex Characteristics
PubMed: 32731328
DOI: 10.3390/ijms21155342 -
Orphanet Journal of Rare Diseases Jan 2017Aromatic L-amino acid decarboxylase deficiency (AADCD) is a rare, autosomal recessive neurometabolic disorder that leads to a severe combined deficiency of serotonin,... (Review)
Review
Aromatic L-amino acid decarboxylase deficiency (AADCD) is a rare, autosomal recessive neurometabolic disorder that leads to a severe combined deficiency of serotonin, dopamine, norepinephrine and epinephrine. Onset is early in life, and key clinical symptoms are hypotonia, movement disorders (oculogyric crisis, dystonia, and hypokinesia), developmental delay, and autonomic symptoms.In this consensus guideline, representatives of the International Working Group on Neurotransmitter Related Disorders (iNTD) and patient representatives evaluated all available evidence for diagnosis and treatment of AADCD and made recommendations using SIGN and GRADE methodology. In the face of limited definitive evidence, we constructed practical recommendations on clinical diagnosis, laboratory diagnosis, imaging and electroencephalograpy, medical treatments and non-medical treatments. Furthermore, we identified topics for further research. We believe this guideline will improve the care for AADCD patients around the world whilst promoting general awareness of this rare disease.
Topics: Age of Onset; Amino Acid Metabolism, Inborn Errors; Aromatic-L-Amino-Acid Decarboxylases; Cholinergic Antagonists; Dopamine Agonists; Guidelines as Topic; Humans; Monoamine Oxidase Inhibitors; Prolactin; Pyridoxal Phosphate
PubMed: 28100251
DOI: 10.1186/s13023-016-0522-z -
American Journal of Health-system... May 2021This article aims to evaluate management options for antipsychotic-induced hyperprolactinemia and associated treatment considerations such as efficacy, tolerability,...
PURPOSE
This article aims to evaluate management options for antipsychotic-induced hyperprolactinemia and associated treatment considerations such as efficacy, tolerability, drug interactions, contraindications, and dosing regimens.
SUMMARY
Hyperprolactinemia is a common adverse effect of antipsychotics. First-line management includes reducing the dose of the offending antipsychotic, discontinuing the antipsychotic, or switching to another antipsychotic associated with a lower risk of hyperprolactinemia. However, these options are not always practical and are associated with a risk of relapse of the psychiatric illness. Other management options include adjunctive aripiprazole, dopamine agonists (cabergoline and bromocriptine), metformin, and herbal supplements. A search of Embase, PubMed, and Google Scholar using key terms such as hyperprolactinemia, prolactin, antipsychotic, treatment guidelines, aripiprazole, dopamine agonist, cabergoline, bromocriptine, metformin, herbals, supplements, and medications was conducted for literature retrieval. Upon evaluation of the available literature we found the following: (1) aripiprazole is safe and effective in lowering prolactin levels within normal limits; (2) adjunctive cabergoline and bromocriptine decrease elevated prolactin levels, while cabergoline may be more effective in reducing prolactin but can also be associated with a more serious adverse effect of cardiac valvular abnormalities; (3) metformin causes a mild reduction of prolactin levels; and (4) there are limited data to support use of herbal medications (chamomile, Peony-Glycyrrhiza decoction, and shakuyaku-kanzo-to) in antipsychotic-induced hyperprolactinemia.
CONCLUSION
There are treatments available for antipsychotic-induced hyperprolactinemia in patients who are unable to alter their current antipsychotic regimen. However, there remains a need for additional short- and long-term studies to determine the efficacy and safety of these treatment strategies, given that patients taking antipsychotics typically require chronic, life-long treatment for their illnesses.
Topics: Antipsychotic Agents; Aripiprazole; Humans; Hyperprolactinemia; Mental Disorders; Prolactin
PubMed: 33954421
DOI: 10.1093/ajhp/zxab065 -
Frontiers in Immunology 2018The great asymmetry of autoimmune diseases between genders represents one of the most enigmatic observations among the mosaic of autoimmunity. Sex hormones are believed... (Review)
Review
The great asymmetry of autoimmune diseases between genders represents one of the most enigmatic observations among the mosaic of autoimmunity. Sex hormones are believed to play a crucial role on this dimorphism. The higher prevalence of autoimmunity among women at childbearing ages, disease onset/relapses during pregnancy, and post-partum are some of the arguments that support this hypothesis. Certainly, motherhood represents one of the most remarkable challenges for the immune system, which not only has to allow for the conceptus, but also has to deal with complex endocrine alterations. Hormonal homeostasis is known to exert a crucial influence in achieving a competent and healthy immune system. Prolactin (PRL) has a bioactive function acting as a hormone and a cytokine. It interferes with immune system modulation, mainly inhibiting the negative selection of autoreactive B lymphocytes. Likewise, hyperprolactinemia has been described in relation to the pathogenesis and activity of several autoimmune disorders. Dopamine is an effective inhibitor of PRL secretion due to either a direct influence on the hypophysis or stimulation of postsynaptic dopamine receptors in the hypothalamus, arousing the release of the PRL inhibitory factor. Hence, dopamine agonists have proven to offer clinical benefits among autoimmune patients and represent a promising therapy to be explored. In this review, we attempt to provide a critical overview of the link between PRL, autoimmune diseases, and motherhood.
Topics: Animals; Autoantibodies; Autoimmune Diseases; Autoimmunity; Cytokines; Female; Gonadal Steroid Hormones; Humans; Hyperprolactinemia; Pregnancy; Prolactin; Sex Factors
PubMed: 29483903
DOI: 10.3389/fimmu.2018.00073 -
Journal of Experimental Zoology. Part... Dec 2022In most animals, annual rhythms in environmental cues and internal programs regulate seasonal physiology and behavior. Prolactin, an evolutionarily ancient hormone,... (Review)
Review
In most animals, annual rhythms in environmental cues and internal programs regulate seasonal physiology and behavior. Prolactin, an evolutionarily ancient hormone, serves as a molecular correlate of seasonal timing in most species. Prolactin is highly pleiotropic with a wide variety of well-documented physiological effects; in a seasonal context prolactin is known to regulate annual changes in pelage and molt. While short-term homeostatic variation of prolactin secretion is under the control of the hypothalamus, long-term seasonal rhythms of prolactin are programmed by endogenous timers that reside in the pituitary gland. The molecular basis of these rhythms is generally understood to be melatonin dependent in mammals. Prolactin rhythmicity persists for several years in many species, in the absence of hypothalamic signaling. Such evidence in mammals has supported the hypothesis that seasonal rhythms in prolactin derive from an endogenous timer within the pituitary gland that is entrained by external photoperiod. In this review, we describe the conserved nature of prolactin signaling in birds and mammals and highlight its role in regulating multiple diverse physiological systems. The review will cover the current understanding of the molecular control of prolactin seasonality and propose a mechanism by which long-term rhythms may be generated in amniotes.
Topics: Animals; Prolactin; Seasons; Photoperiod; Birds; Mammals
PubMed: 35686456
DOI: 10.1002/jez.2634 -
The Journal of Headache and Pain Apr 2024Sexual dimorphism has been revealed for many neurological disorders including chronic pain. Prelicinal studies and post-mortem analyses from male and female human donors... (Review)
Review
Sexual dimorphism has been revealed for many neurological disorders including chronic pain. Prelicinal studies and post-mortem analyses from male and female human donors reveal sexual dimorphism of nociceptors at transcript, protein and functional levels suggesting different mechanisms that may promote pain in men and women. Migraine is a common female-prevalent neurological disorder that is characterized by painful and debilitating headache. Prolactin is a neurohormone that circulates at higher levels in females and that has been implicated clinically in migraine. Prolactin sensitizes sensory neurons from female mice, non-human primates and humans revealing a female-selective pain mechanism that is conserved evolutionarily and likely translationally relevant. Prolactin produces female-selective migraine-like pain behaviors in rodents and enhances the release of calcitonin gene-related peptide (CGRP), a neurotransmitter that is causal in promoting migraine in many patients. CGRP, like prolactin, produces female-selective migraine-like pain behaviors. Consistent with these observations, publicly available clinical data indicate that small molecule CGRP-receptor antagonists are preferentially effective in treatment of acute migraine therapy in women. Collectively, these observations support the conclusion of qualitative sex differences promoting migraine pain providing the opportunity to tailor therapies based on patient sex for improved outcomes. Additionally, patient sex should be considered in design of clinical trials for migraine as well as for pain and reassessment of past trials may be warranted.
Topics: Migraine Disorders; Humans; Female; Animals; Sex Characteristics; Calcitonin Gene-Related Peptide; Prolactin; Male
PubMed: 38658853
DOI: 10.1186/s10194-024-01771-w -
Nature Communications May 2020The genetic basis and corresponding clinical relevance of prolactinomas remain poorly understood. Here, we perform whole genome sequencing (WGS) on 21 patients with...
The genetic basis and corresponding clinical relevance of prolactinomas remain poorly understood. Here, we perform whole genome sequencing (WGS) on 21 patients with prolactinomas to detect somatic mutations and then validate the mutations with digital polymerase chain reaction (PCR) analysis of tissue samples from 227 prolactinomas. We identify the same hotspot somatic mutation in splicing factor 3 subunit B1 (SF3B1) in 19.8% of prolactinomas. These patients with mutant prolactinomas display higher prolactin (PRL) levels (p = 0.02) and shorter progression-free survival (PFS) (p = 0.02) compared to patients without the mutation. Moreover, we identify that the SF3B1 mutation causes aberrant splicing of estrogen related receptor gamma (ESRRG), which results in stronger binding of pituitary-specific positive transcription factor 1 (Pit-1), leading to excessive PRL secretion. Thus our study validates an important mutation and elucidates a potential mechanism underlying the pathogenesis of prolactinomas that may lead to the development of targeted therapeutics.
Topics: Adult; Female; Humans; Male; Mutation; Phosphoproteins; Progression-Free Survival; Prolactin; Prolactinoma; RNA Splicing Factors; Receptors, Estrogen; Transcription Factor Pit-1; Young Adult
PubMed: 32427851
DOI: 10.1038/s41467-020-16052-8 -
Frontiers in Endocrinology 2022Prolactin coordinates with the ovarian steroids to orchestrate mammary development and lactation, culminating in nourishment and an increasingly appreciated array of... (Review)
Review
Prolactin coordinates with the ovarian steroids to orchestrate mammary development and lactation, culminating in nourishment and an increasingly appreciated array of other benefits for neonates. Its central activities in mammary epithelial growth and differentiation suggest that it plays a role(s) in breast cancer, but it has been challenging to identify its contributions, essential for incorporation into prevention and treatment approaches. Large prospective epidemiologic studies have linked higher prolactin exposure to increased risk, particularly for ER+ breast cancer in postmenopausal women. However, it has been more difficult to determine its actions and clinical consequences in established tumors. Here we review experimental data implicating multiple mechanisms by which prolactin may increase the risk of breast cancer. We then consider the evidence for role(s) of prolactin and its downstream signaling cascades in disease progression and treatment responses, and discuss how new approaches are beginning to illuminate the biology behind the seemingly conflicting epidemiologic and experimental studies of prolactin actions across diverse breast cancers.
Topics: Breast Neoplasms; Disease Progression; Female; Humans; Infant, Newborn; Lactation; Prolactin; Prospective Studies
PubMed: 35784527
DOI: 10.3389/fendo.2022.910978 -
The Primary Care Companion For CNS... May 2019To examine the role of permeability glycoprotein (P-gp) and its substrates in the mechanism of hyperprolactinemia. (Review)
Review
OBJECTIVE
To examine the role of permeability glycoprotein (P-gp) and its substrates in the mechanism of hyperprolactinemia.
DATA SOURCES
PubMed and Google Scholar were queried with the search term permeability glycoprotein crossed with antipsychotic, neuroleptic, prolactin, risperidone, paliperidone, and amisulpride. The searches were performed in early 2018 with no date restrictions.
STUDY SELECTION
All references cited in PubMed were examined (108), but only the first 40 references of each search in Google Scholar (total of approximately 30,000 hits) for a total of 240 were examined. Approximately 100 references were felt to be relevant.
DATA EXTRACTION
Information regarding mechanism of action and clinical relevance was extracted as appropriate for the discussion.
RESULTS
Risperidone, paliperidone, and amisulpride are associated with higher prolactin levels than would be anticipated from striatal dopamine receptor occupancy studies. This elevation occurs because the levels of these antipsychotics are higher in the anterior pituitary than in parts of the brain protected by the blood-brain barrier and P-gp. P-gp has high affinity to all these antipsychotics and selectively removes them from the brain and concentrates them in the blood draining the hypothalamus, allowing greater dopamine receptor blockade in the cells in the anterior pituitary that produce prolactin.
CONCLUSIONS
The anatomy of the portal circulation, the presence of P-gp, and the high affinity of this protein to risperidone, paliperidone, and amisulpride all conspire to concentrate the antipsychotic concentration in the anterior pituitary to levels higher than in other parts of the brain, with consequent increase of prolactin above expectations.
Topics: Antipsychotic Agents; Capillary Permeability; Glycoproteins; Humans; Prolactin
PubMed: 31106995
DOI: 10.4088/PCC.18nr02412 -
Endokrynologia Polska 2022Hyperprolactinaemia is the most common dysfunction of the hypothalamic-pituitary axis and occurs more commonly in women. The prevalence of hyperprolactinaemia ranges... (Review)
Review
Hyperprolactinaemia is the most common dysfunction of the hypothalamic-pituitary axis and occurs more commonly in women. The prevalence of hyperprolactinaemia ranges from 0.4% in the general adult population to as high as 9-17% in women with reproductive diseases. It is accompanied by the phenomenon of insulin resistance (IR), which is also a significant clinical problem nowadays. The prevalence of IR is increasing, particularly in developing countries and in younger populations, with estimates of prevalence ranging from 20 to 40% in different populations. The aim of our review is to summarize recent data on the possible association between IR and hyperprolactinaemia. This review is based on an electronic search of the literature in the PubMed database published from 2000 to 2022 using combinations of the following keywords: IR, hyperprolactinemia or IR and hyperprolactinemia. The references included in previously published review articles were also checked, and any relevant papers were also included. Numerous scientific studies have shown a relationship between IR and hyperprolactinaemia. Increased plasma prolactin (PRL) levels are often associated with an increase in tissue resistance to insulin. There are many scientific theories explaining the probable mechanisms of this phenomenon. One is the finding that glucose and PRL act synergistically in inducing the transcription of insulin genes. It is also suggested that PRL may act as a regulator of insulin sensitivity and metabolic homeostasis in adipose tissue. The topic of the mutual correlation of hyperprolactinaemia and IR is important, and it certainly requires further research and observation.
Topics: Adult; Humans; Female; Hyperprolactinemia; Insulin Resistance; Prolactin; Insulin
PubMed: 36621922
DOI: 10.5603/EP.a2022.0075