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Principles of the prolactin/vasoinhibin axis

Prolactin - Wikipedia

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Prolactin (PRL), also known as ..

Tobacco use in combination with estrogen therapy is associated with an increased risk of . All transgender women who smoke should be counselled on tobacco risks and cessation options at every visit. Many transgender women may be unable or unwilling to quit smoking; this should not represent an absolute contraindication to estrogen therapy. After an in depth and careful informed consent discussion, it is reasonable to prescribe estrogen using a harm reduction approach, with a preferred route of transdermal estrogen. 81mg/day can be considered as an additional preventive measure in smokers, though no evidence exists to allow and informed assessment of the risk/benefit ratio between VTE prevention and gastrointestinal hemorrhage (Grading: X C W). Transdermal estrogens are preferred to minimize risk (Grading: T O S).

however prolactin is the only adenohypophyseal hormone whose principal control is inhibitory

While hormones may contribute to mood disorders (such as in premenstrual dysphoric disorder or postpartum depression), there is no clear evidence that estrogen therapy is directly associated with the onset of or worsening of mental health conditions. In fact one study found that transgender women experience improvements in social functioning and reduced anxiety and depression once estrogen therapy is begun.[56] Mental health conditions in transgender women should be approached with a broad differential diagnosis as in any other patient. It may be advisable to avoid injected estrogen due to the potentially cyclic levels, which could bring about or worsen existing mood symptoms.

Prolactin in the Immune System | InTechOpen

Prolactin in the Immune System ..

The goal of feminizing hormone therapy is the development of female secondary sex characteristics, and suppression/minimization of male secondary sex characteristics. General effects include breast development (usually to Tanner stage 2 or 3), a redistribution of facial and body subcutaneous fat, reduction of muscle mass, reduction of body hair (and to a lesser extent, facial hair), change in sweat and odor patterns, and arrest and possible reversal of scalp hair loss. Sexual and gonadal effects include reduction in erectile function, changes in libido, reduced or absent sperm count and ejaculatory fluid, and reduced testicular size. Feminizing hormone therapy also brings about changes in emotional and social functioning. The general approach of therapy is to combine an estrogen with an androgen blocker, and in some cases a progestagen.

5-alpha reductase inhibitors include finasteride and dutasteride. Finasteride blocks 5-alpha reductase type 2 and 3 mediated conversion of testosterone to the potent androgen dihydrotestosterone.[8] Finasteride 1mg daily is FDA-approved for male pattern baldness, while the 5mg dose is approved for management of prostatic hypertrophy.[9] Dutasteride 0.5mg more effectively blocks the type 1 isozyme, which is present in the pilosebaceous unit and therefore may have more dramatic feminizing effects. Since these medications block neither the production nor action of testosterone, their antiandrogen effect is less than that encountered with full blockade. 5-alpha reductase inhibitors may be a good choice for those unable to tolerate, or with contraindications to the use of spironolactone. 5-alpha reductase inhibitors may also be an option for use as a single agent in patients seeking partial feminization, or for those who continue to exhibit virilized features or hair loss after complete androgen blockade or orchiectomy.

Human Reproduction, Lectures: Prolactin - EHSL

Prolactin is a hormone produced in the pituitary gland, named because of its role in lactation

Many patients are eager to begin maximal feminizing hormone therapy and are opposed to the idea of a slow upward titration. Weak evidence suggests that initiation of estrogen therapy at lower doses and titrating up over time may result in enhanced breast development in transgender women. The estrogen receptor agonist activity of spironolactone may play a role in reduced breast development due to premature breast bud fusion. As such an escalating regimen beginning with low dose estrogen only, and titrating up over several months, and then adding spironolactone may be an alternative approach,[17] consistent with management practices in children with delayed pubertal onset (Grading: T O W). Upward titration of spironolactone can also help minimize side effects such as orthostasis or polyuria. It is recommended that providers discuss these considerations with patients before initiation of hormones in order to make an informed decision.

Calcium is central to all aspects of exocytosis, including rapid fusion and unloading of the vesicles as well as recruitment and translocation of loaded vesicles.
Calcium influx occurs through voltage-gated calcium channels and leads to fusion of the synaptic vesicles with the plasma membrane and release of their content to the extracellular space. This is a much faster process than the relatively slow release of peptide or protein hormones from endocrine cells.
In most neurons, dopamine is released into the synaptic cleft and binds to postsynaptic receptors. In contrast, the dopaminergic neurons of the hypothalamo-pituitary unit (with the exception of the dopaminergic neurons innervating the intermediate lobe of the pituitary) lack true synaptic contacts and are classified as secretory neurons .
In this case, dopamine diffuses away from the terminals through the perivascular space and is transported by portal blood to distal pituitary target cells. The rate of dopamine release from secretory neurons appears to be slower than that from classical neurons.
It has been argued that the speed of neurotransmitter release is reciprocally related to the distance of its site of action, but the mechanism responsible for this feature is unclear.
It is assumed that only a small fraction of docked vesicles can instantaneously release their cargo in response to calcium influx. These vesicles comprise the “fusion-ready” pool that undergoes a very rapid -dependent fusion. The slower release phase is carried out by docked vesicles that exist in a different biochemical state and require priming to promote fusion.
These vesicles constitute a precursor pool that replenishes the rapid release pool. Priming is dependent, involves the proteins, and is associated with production of phosphoinositides and protein phosphorylation. An even slower pool is composed of vesicles that are anchored to the cytoskeleton via actin-binding synapsins but are not docked to the membrane .
When synapsins become phosphorylated in response to an influx of calcium, the vesicles detach from the cytoskeletal elements and can translocate to the active zone of the presynaptic membrane. However, vesicular trans location is too slow to account for the immediate calciumdependent exocytosis.

Dopamine is the primary neuroendocrine inhibitor of the secretion of prolactin ..
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  • TRH stimulates prolactin synthesis through the activation of ERK, ..

    In this group the principal ..

  • 15/11/2015 · Principles of the prolactin ..


  • results in the synthesis of vasoinhibins of ..

    Dopamine - Wikipedia

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Dopamine as a Prolactin (PRL) Inhibitor 2002

Since estrogen dosing should be based on physiologic female levels, no reduction in estrogen dosing is required after gonadectomy. Some patients may choose to use a lower dose, which is appropriate as long as dosing is adequate to maintain bone density. Adequacy of dosing in those on low estrogen replacement post gonadectomy may be assessed by following LH and FSH levels (Grading: T O W).[11]

inhibits prolactin synthesis at ..

Sildenafil (Viagra) and tadalafil (Cialis) can be used for preservation of erectile function at any stage or with any feminizing hormone regimen, in consideration of the typical contraindications and precautions when using this class of medication. Individual results may vary. It is reasonable check both total and bioavailable testosterone levels, and consider reduction of androgen blockade to allow an increase in testosterone, depending on patient goals.

serine protease inhibitor that by inhibiting tissue ..

Prolactin elevations and growth of pituitary prolactinomas are theoretical risks associated with estrogen therapy; several cases have been reported.[42] However, with the administration of physiologic doses of estrogen, there is no clear basis for an increased risk of prolactinomas in comparison to the population background rate in non-transgender women. Furthermore, Endocrine Society guidelines for the management of incidental prolactinomas are expectant management only, in the absence of suggestive visual or other symptoms (significant galactorrhea, headaches).[43] Routine screening with serum prolactin levels in asymptomatic transgender women would not have an impact on management, and could result in costs or harm if further workup if pursued. As such it is recommended that prolactin be checked only in cases of visual disturbances, excessive galactorrhea, and be considered in cases of new onset headaches. It is noted that some transgender women experience a minimal amount of galactorrhea early in their hormone therapy course. The presence of non-bloody minimal galactorrhea from more than one duct and/or bilateral is almost certainly physiologic and would not warrant further evaluation.

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