The problem here is that many people seem to think that it should be a general rule to take bromo/cabergoline while on deca/tren which is wrong.
I agree that gyno is a result of a combination of factors, but high estrogen/androgen (test-DHT) ratio is usually noticed in gynecomastia.
Even when PRL is considered a factor, elevated PRL will lead to high estrogen/androgen ratio which can contribute to gyno..
If someone does experience symptoms like lactation for whatever reason, he should use bromo or similar drug...
The problem with PRL is that its regulation is affected by many factors so people may attribute the PRL rise while ON to a certain AS, while it could be caused by another factor:
Causes of hyperprolactinemia :
PHYSIOLOGIC HYPERPROLACTINEMIA — Serum prolactin concentrations normally increase substantially during pregnancy and to a lesser degree in response to nipple stimulation and stress. The upper normal value for serum prolactin in most laboratories is 20 ng/mL.
Pregnancy — Serum prolactin increases throughout pregnancy, reaching a peak at delivery (show figure 1) [1]. The magnitude of the increase, however, is quite variable; in one study the mean value at term was 207 ng/mL, but the range was from 35 to 600 ng/mL [1]. The probable cause of the hyperprolactinemia is the increasing serum estradiol concentrations during pregnancy. By six weeks after delivery, estradiol secretion has decreased and the basal serum prolactin concentration is usually normal.
Nipple stimulation — Nipple stimulation increases serum prolactin concentrations, presumably via a neural pathway. The magnitude of the increase is directly proportional to the degree of preexisting lactotroph hyperplasia due to estrogen. In the first weeks postpartum, for example, the serum prolactin concentration increases up to a few hundred ng/mL above baseline in response to suckling; in contrast, several months after delivery the increase is usually less than 10 ng/mL above baseline (show figure 2) [1].
Stress — Stress of any kind, physical or psychologic, can cause an increase in the serum prolactin concentration. As with all stimuli of prolactin secretion, women have greater increases than men, presumably due to the effect of their higher serum estradiol concentrations on the lactotroph cells. The magnitude of the increase in prolactin in response to stress is small, the values rarely exceeding 40 ng/mL.
PATHOLOGIC HYPERPROLACTINEMIA — Pathologic hyperprolactinemia can be caused by the following:
• Lactotroph adenomas (prolactinomas), which are benign tumors of the lactotroph cell.
• Lactotroph hyperplasia, which can be caused by a decrease in dopaminergic inhibition of prolactin secretion and other mechanisms.
• Other conditions, including decreased clearance of prolactin.
Serum prolactin concentrations in patients who have lactotroph adenomas can range from minimally elevated to 50,000 ng/mL; in comparison, in hyperprolactinemia due to other causes, the concentrations rarely exceed 200 ng/mL [3] (show figure 3).
LACTOTROPH ADENOMAS — Lactotroph adenomas, like other pituitary adenomas, arise from monoclonal expansion of a single cell which has presumably undergone somatic mutation [4, 5]. Most adenomas that secrete prolactin and cause hyperprolactinemia are comprised solely of lactotroph cells; however, about 10 percent are comprised of both lactotroph and either somatotroph or somatomammotroph cells and therefore secrete growth hormone as well as prolactin [6].
Lactotroph adenomas are relatively common, accounting for approximately 30 to 40 percent of all clinically recognized pituitary adenomas. The diagnosis is made more frequently in women than in men, especially between the ages of 20 and 40 years [7], presumably because of the sensitivity of menses to disruption by hyperprolactinemia. However, the adenomas that occur in men are usually larger, in part due to the lack of symptoms or delay in seeking medical attention for symptoms such as erectile dysfunction [8]. In addition, the tumors in men may have an inherently greater rate of growth [8].
Most lactotroph adenomas are sporadic, but they can rarely occur as part of the multiple endocrine neoplasia type 1 syndrome [9]. Almost all lactotroph tumors are benign but a rare tumor can be malignant and metastasize [10].
Prolactin secretion by lactotroph adenomas is generally characterized by both efficiency and proportionality.
• As a result of their efficiency, even microadenomas (<1 cm in diameter) typically secrete sufficient prolactin to cause hyperprolactinemia.
• As a result of their proportionality, serum prolactin concentrations tend to vary with adenoma size. Adenomas <1 cm in diameter are typically associated with serum prolactin values below 200 ng/mL; those approximately 1.0-2.0 cm in diameter with values between 200 and 1000 ng/mL; and those greater than 2.0 cm in diameter with values above 1000 ng/mL (show figure 3).
There are exceptions to both generalizations. As an example, occasional patients have a large adenoma but only modest hyperprolactinemia. Such adenomas are generally less well differentiated and respond less well to dopamine agonists than the more typical tumors. (See "Treatment of hyperprolactinemia due to lactotroph adenoma and other causes"
. In other patients who have macroadenomas but only modest elevation of the reported serum prolactin concentration, the reason for the discrepancy between the large size of the adenoma and modest elevation of the prolactin concentration is due to an artefact in the immunoradiometric assay for prolactin. This artefact, called the "hook effect", can be obviated by dilution of the sera, which will allow a true assessment of the prolactin concentration [11, 12, 13].
LACTOTROPH HYPERPLASIA — Continuous stimulation or decreased inhibition of the lactotroph cells can lead to lactotroph hyperplasia, prolactin hypersecretion, and hyperprolactinemia. The best recognized mechanism by which hyperprolactinemia due to lactotroph hyperplasia occurs is interference with normal dopamine inhibition of prolactin secretion. This may occur as a result of damage to the dopaminergic neurons of the hypothalamus, pituitary stalk section, or drugs that block dopamine receptors on lactotroph cells.
Hypothalamic and pituitary disease — Any disease in or near the hypothalamus or pituitary that interferes with the secretion of dopamine or its delivery to the hypothalamus can cause hyperprolactinemia [3]. These include:
• Tumors of the hypothalamus, both benign (eg, craniopharyngiomas) and malignant (eg, metastatic breast carcinoma)
• Infiltrative diseases of the hypothalamus (eg, sarcoidosis)
• Section of the hypothalamic-pituitary stalk (eg, due to head trauma)
• Adenomas of the pituitary other than lactotroph adenomas
Drug use — Several drugs are known dopamine D2 receptor antagonists, and raise serum prolactin by that mechanism. These include antipsychotic drugs such as risperidone, phenothiazines, haloperidol [14], butyrophenones [15], metoclopramide [16], sulpiride [17], and domperidone [18]. Serum prolactin concentrations increase within hours after acute administration of these drugs and return to normal within two to four days after cessation of chronic therapy [15]. The magnitude of the elevation varies with the drug. Haloperidol, for example, raises the serum prolactin concentration by an average of 17 ng/mL, whereas risperidone may raise it by 45 to 80 ng/mL [14].
The antihypertensive drugs, methyldopa and reserpine, neither of which is commonly used now, increase prolactin secretion by a similar mechanism. Methyldopa inhibits dopamine synthesis [19], while reserpine inhibits dopamine storage [20].
Verapamil may raise serum prolactin concentrations [21], but other calcium channel blockers do not [22]. The mechanism of this verapamil-induced increase is not known. Hyperprolactinemia occurred in 8.6 percent of 449 men taking verapamil in one report, as compared with only 3 percent of control men [23]. The elevated serum prolactin concentration persisted during continued drug administration in 14 of 15 men, and returned to normal in all 9 after the drug was stopped.
Estrogen — Estrogen increases prolactin secretion proportionate to the degree of estrogenization. Amounts of estrogen that are physiologic for a woman increase the basal serum prolactin concentration minimally, but explain the greater prolactin response of women (compared with men) to almost all physiologic stimuli [24]. Greater amounts of estrogen, such as occur in pregnancy, increase basal serum prolactin concentrations, as described above.
The mechanism by which estrogen stimulates prolactin secretion appears to involve binding of estrogen to the estrogen receptor, which then binds to an estrogen response element on the prolactin gene, in the lactotroph cell of the pituitary [25, 26].
Hypothyroidism — Hypothyroidism predisposes to hyperprolactinemia. However, basal serum prolactin concentrations are normal in most hypothyroid patients [27], and only the serum prolactin response to stimuli, such as TRH (thyrotropin-releasing hormone), is increased [28]. In the few hypothyroid patients who have elevated basal serum prolactin concentrations, the values return to normal when the hypothyroidism is corrected [29, 30]. It is important to recognize hypothyroidism as a potential cause of an enlarged pituitary gland (due to thyrotroph hyperplasia, lactotroph hyperplasia, or both) and hyperprolactinemia, and not to confuse this entity with a lactotroph adenoma.
The mechanism of hyperprolactinemia in hypothyroidism is not known. Both enhanced hypothalamic synthesis of TRH and increased pituitary responsiveness to TRH have been described [28].
Chest wall injury — Chest wall injuries, such as severe burns, increase prolactin secretion, presumably due to a neural mechanism similar to that of suckling [31].
Chronic renal failure — The serum prolactin concentration is high in patients who have chronic renal failure and returns to normal after renal transplantation [32]. The major mechanism is a three-fold increase in prolactin secretion, and there is a one-third decrease in metabolic clearance rate [33].
OTHER CAUSES OF HYPERPROLACTINEMIA
Idiopathic hyperprolactinemia — In a substantial number of patients whose serum prolactin concentration is between 20 and 100 ng/mL, no cause can be found. Although many of these patients may have undetectable lactotroph microadenomas, in most of them the serum prolactin concentrations change little during follow-up for several years [34, 35, 36]. In one report, for example, only 1 of 59 patients who were followed for an average of 6.5 years developed a detectable pituitary adenoma and about 20 percent had a normal serum prolactin concentration when it was last measured [36].
Decreased clearance of prolactin — There are two settings in which hyperprolactinemia is caused by decreased clearance of prolactin:
• Chronic renal failure — Hyperprolactinemia is common in patients with end-stage renal failure and improves after renal transplantation [32, 33].
• Big prolactin — The most common form of prolactin in serum is 23 kD in size and is not glycosylated, but a small amount of a 25 kD glycosylated form can also be detected. In rare cases, glycosylated prolactin, which appears to circulate in aggregates, accounts for most of the prolactin [37]. In this situation the prolactin has been called "big prolactin" and the condition referred to as "macroprolactinemia." The elevated serum prolactin concentration in these patients can be distinguished from hyperprolactinemia of other causes by gel filtration or polyethylene glycol precipitation [38]. In one series of 1,106 patients with hyperprolactinemia, approximately 10 percent had macroprolactinemia [39].
The clinical manifestations of macroprolactinemia were described in a series of 55 women ages 18 to 55. None had a history of amenorrhea, eight had oligomenorrhea before age 40, and one had galactorrhea. All subjects had pituitary imaging; no macroadenomas and four microadenomas were seen (consistent with the prevalence of incidentalomas in the normal population). Thus, macroprolactinemia appears to be a benign clinical condition [40].
Equally rare is a raised serum prolactin level due to complexing of normal-sized prolactin with circulating prolactin antibodies [41]. In this situation, the free prolactin concentration is normal and causes no biologic abnormalities.
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References
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2 Jarrell, J, Franks, S, McInnes, R, et al. Breast examination does not elevate serum prolactin. Fertil Steril 1980; 33:49.
3 Kleinberg, DL, Noel, GL, Frantz, AG. Galactorrhea: A study of 235 cases, including 48 with pituitary tumors. N Engl J Med 1977; 296:589.
4 Alexander, JM, Biller, BMK, Bikkal, H, et al. Clinically nonfunctioning pituitary tumors are monoclonal in origin. J Clin Invest 1990; 86:336.
5 Herman, V, Fagin, J, Gonsky, R, et al. Clonal origin of pituitary adenomas. J Clin Endocrinol Metab 1990; 71:1427.
6 Corenblum, B, Sirek, AMT, Horvath, E, et al. Human mixed somatotrophic and lactotrophic pituitary adenomas. J Clin Endocrinol Metab 1976; 42:857.
7 Mindermann, T, Wilson, CB. Age-related and gender-related occurrence of pituitary adenomas. Clin Endocrinol 1994; 41:359.
8 Delgrange, E, Trouillas, J, Maiter, D, et al. Sex-related difference in the growth of prolactinomas: A clinical and proliferation marker study. J Clin Endocrinol Metab 1997; 82:2102.
9 Prosser, PR, Karam, JH, Townsend, JJ, et al. Prolactin-secreting pituitary adenomas in multiple endocrine adenomatosis, type I. Ann Intern Med 1979; 91:41.
10 Walker, JD, Grossman, A, Anderson, JV, et al. Malignant prolactinoma with extracranial metastases: A report of three cases. Clin Endocrinol 1993; 38:411.
11 Petakov, MS, Damjanovic, SS, Nikolic-Durovic, MM, et al. Pituitary adenomas secreting large amounts of prolactin may give false low values in immunoradiometric assays. The hook effect. J Endocrinol Invest 1998; 21:184.
12 St-Jean, E, Blain, F, Comtois, R. High prolactin levels may be missed by immunoradiometric assay in patients with macroprolactinomas. Clin Endocrinol (Oxf) 1996; 44:305.
13 Barkan, AL, Chandler, WF. Giant pituitary prolactinoma with falsely low serum prolactin: The pitfall of the "high-dose hook effect." Neurosurgery 1998; 42:913.
14 David, SR, Taylor, CC, Kinon, BJ, Breier, A. The effects of olanzapine, rispiridone, and haloperiodol on plasma prolactin levels in patients with schizophrenia. Clin Ther 2000; 22:1085.
15 De Rivera, JL, Lal, S, Ettigi, P, et al. Effect of acute and chronic neuroleptic therapy on serum prolactin levels in men and women of different age groups. Clin Endocrinol 1976; 5:273.
16 McCallum, RW, Sowers, JR, Hershman, JM, et al. Metoclopramide stimulates prolactin secretion in man. J Clin Endocrinol Metab 1976; 42:1148.
17 Mancini, AM, Guitelman, A, Vargas, CA, et al. Effect of sulpiride on serum prolactin levels in humans. J Clin Endocrinol Metab 1976; 42:181.
18 Sowers, JR, Sharp, B, McCallum, RW. Effect of domperidone, an extracerebral inhibitor of dopamine receptors, on thyrotropin, prolactin, renin, aldosterone, and 18-hydroxycorticosterone secretion in man. J Clin Endocrinol Metab 1982; 54:869.
19 Steiner, J, Cassar, J, Mashiter, K, et al. Effect of methyldopa on prolactin and growth hormone. Br Med J 1976; 1:1186.
20 Lee, PA, Kelly, MR, Wallin, JD. Increased prolactin levels during reserpine treatment of hypertensive patients. JAMA 1976; 235:2316.
21 Fearrington, EL, Rand, CH, Rose, JD. Hyperprolactinemia-galactorrhea induced by verapamil. Am J Cardiol 1983; 51:1466.
22 Veldhuis, JD, Borges, JLC, Drake, CR. Divergent influences of the structurally dissimilar calcium entry blockers, diltiazem and verapamil, on the thyrotropin- and gonadotropin-releasing hormone-stimulated anterior pituitary hormone secretion in man. J Clin Endocrinol Metab 1985; 60:144.
23 Romeo, JH, Dombrowski, R, Kwak, YS, et al. Hyperprolactinemia and verapamil: Prevalence and potential association with hypogonadism in men. Clin Endocrinol 1996; 45:571.
24 Frantz, AG. Prolactin. N Engl J Med 1978; 298:201.
25 Murdoch, FE, Byrne, LM, Ariazi, EA, et al. Estrogen receptor binding to DNA: affinity for nonpalindromic elements from the rat prolactin gene. Biochemistry 1995; 34:9144.
26 Malayer, JR, Gorski, J. The role of estrogen receptor in modulation of chromatin conformation in the 5' flanking region of the rat prolactin gene. Mol Cell Endocrinol 1995; 113:145.
27 Honbo, KS, Van Herle, AJ, Kellett, KA. Serum prolactin levels in untreated primary hypothyroidism. Am J Med 1978; 64:782.
28 Snyder, PJ, Jacobs, LS, Utiger, RD, Daughaday, WH. Thyroid hormone inhibition of the prolactin response to thyrotropin releasing hormone. J Clin Invest 1973; 52:2324.
29 Groff, TR, Shulkin, BL, Utiger, RD, Talbert, LM. Amenorrhea-galactorrhea, hyperprolactinemia, and suprasellar pituitary enlargement as presenting features of primary hypothyroidism. Obstet Gynecol 1984; 63:86S.
30 Grubb, MR, Chakeres, D, Malarkey, WB. Patients with primary hypothyroidism presenting as prolactinomas. Am J Med 1987; 83:765.
31 Morley, JE, Hodgkinson, DH, Kalk, WJ. Galactorrhea and hyperprolactinemia associated with chest wall injury. J Clin Endocrinol Metab 1977; 45:931.
32 Lim, VS, Kathpalia, SC, Frohman, LA. Hyperprolactinemia and impaired pituitary response to suppression and stimulation in chronic renal failure: Reversal after transplantation. J Clin Endocrinol Metab 1979; 48:101.
33 Sievertsen, GD, Lim, VS, Nakawatase, C, Frohman, LA. Metabolic clearance and secretion rates of human prolactin in normal subjects and patients with chronic renal failure. J Clin Endocrinol Metab 1980; 50:846.
34 Schlechte, J, Dolan, K, Sherman, B, et al. The natural history of untreated hyperprolactinemia: A prospective analysis. J Clin Endocrinol Metab 1989; 68:412.
35 Martin, TL, Kim, M, Malarkey, WB. The natural history of idiopathic hyperprolactinemia. J Clin Endocrinol Metab 1985; 60:855.
36 Sluijmer, AV, Lappöhn, RE. Clinical history and outcome of 59 patients with idiopathic hyperprolactinemia. Fertil Steril 1992; 58:72.
37 Carlson, HE, Markoff, E, Lee, DW. On the nature of serum prolactin in two patients with macroprolactinemia. Fertil Steril 1992; 58:78.
38 Olukoga, AO, Kane, JW. Macroprolactinaemia: validation and application of the polyethylene glycol precipitation test and clinical characterization of the condition. Clin Endocrinol (Oxf) 1999; 51:119.
39 Vallette-Kasic, S, Morange-Ramos, I, Selim, A, et al. Macroprolactinemia revisited: a study on 106 patients. J Clin Endocrinol Metab 2002; 87:581.
40 Leslie, H, Courtney, CH, Bell, PM, et al. Laboratory and clinical experience in 55 patients with macroprolactinemia identified by a simple polyethylene glycol precipitation method. J Clin Endocrinol Metab 2001; 86:2743.
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Here's some info from:
GYNECOMASTIA: ETIOLOGY, DIAGNOSIS, AND TREATMENT
Chapter 14 - Gladys E. Palomeno, MD, and Ronald S. Swerdloff, MD
ESTROGEN, GH AND IGF-1, PROGESTERONE, & PROLACTIN
Estrogen and progesterone act in an integrative fashion to stimulate normal adult female breast development. Estrogen, acting through its ER a receptor, promotes duct growth, while progesterone, also acting through its receptor (PR), supports alveolar development (13). This is demonstrated by experiments in ER a knockout mice which display grossly impaired ductal development, whereas the PR knockout mice possess significant ductal development, but lack alveolar differentiation (25,6).
Although estrogens and progestogens are vital to mammary growth, they are ineffective in the absence of anterior pituitary hormones (13). Thus, neither estrogen alone nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1, as confirmed by studies involving the administration of estrogen and GH to hypophysectomized and oophorectomized female rats, which resulted in breast ductal development. The GH effects on ductal growth are mediated through stimulation of IGF-1. This is demonstrated by studies of estrogen and GH administration to IGF-1 knockout rats that showed significantly decreased mammary development when compared to age-matched IGF-1- intact controls. Combined estrogen and IGF-1 treatment in these IGF-1 knockout rats restored mammary growth. (21, 36). In addition, Walden et al. demonstrated that GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development (43). Furthermore, other data indicates that estrogen promotes GH secretion and increased GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development.
Like estrogen, progesterone has minimal effects in breast development without concomitant anterior pituitary hormones; again indicating that progesterone interacts closely with pituitary hormones. For example, prolonged treatment of dogs with progestogens such as depot medroxyprogesterone acetate or with proligestone caused increased GH and IGF-1 levels, suggesting that progesterone may also have an effect on GH secretion (29). In addition, clinical studies have correlated maximal cell proliferation to specific phases in the female menstrual cycle. For example, maximal proliferation occurs not during the follicular phase when estrogens reach peak levels and progesterone is low (less than 1 ng/mL[3.1nmol}), but rather, it occurs during the luteal phase when progesterone reaches levels of 10-20 ng/mL (31- 62nmol) and estrogen levels are two to three times lower than in the follicular phase (38). Furthermore, immunohistochemical studies of ER and PR showed that the highest percentage of proliferating cells, found almost exclusively in the type 1 lobules, contained the highest percentage of ER and PR positive cells (38). Similarly, there is immunocytological presence of ER, PR, and androgen receptors (AR) in gynecomastia and male breast carcinoma. ER, PR and AR expression was observed in 100% (30/30) of gynecomastia cases (37). Given these data and the fact that PR knockout mice lack alveolar development in breast tissue, it appears as if progesterone, analogous to estrogen, may increase GH secretion and act through its receptor on mammary tissue to enhance breast development, specifically alveolar differentiation (25, 16).
Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. (39, 23). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.
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