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2006.03.04 12:46
3.4. Alcohol, estrogen and prolactinomas

Alcohol consumption has often been shown to be associated with increased plasma levels of estrogen in humans (15,41). The increased plasma levels of estrogen are believed to be due to an alcohol-induced increase in adrenal steroid production and conversion of these weak adrenal androgens to estrogen (15) or abnormal conversion of estrogen from androgen in the liver due to cirrhosis (42). Recently phytoestrogen, a biologically active substance of plant origin, has been identified in alcoholic beverages. These phytoestrogens cause reproductive disorders in animals and may cause clinically significant effects in human. Two phytoestrogens ß-sitosterol and biochanin A have been found in bourbon (43,44). De-ethanolized bourbon extracts have been shown to be estrogenic both in vivo and in vitro (45) and also in normal postmenopausal women (46). Recently it has been reported that beer, the most common alcoholic beverage, contains two phytoestrogens, diadzein and genistein (47). Both diadzein and genistein are biologically active and are associated with either uterine hypertrophy or infertility in animals (48). These phytoestrogens are capable of eliciting an estrogenic response in vitro by competing with estradiol for uterine cytosolic estrogen receptor binding sites (49-51). Thus, alcoholics are exposed to high levels of estrogen due to increased endogenous production of estrogen or ingestion of phytoestrogen often present in beer.

There are several reports showing evidence for the existence of high levels of prolactin in chronic alcoholic men and women (41, 52-55). In a study conducted by European scientists, persistent hyperprolactinemia was observed in 16 alcoholic women during a 6-week treatment trial (52). These patients reported daily alcohol intake of 170 g for a 2-16 year period, but had no clinical evidence of alcoholic liver cirrhosis. In a study reported by Japanese scientists, 22 of 23 women admitted for alcoholism treatment had prolactin levels above normal, ranging between 27-184 ng/ml. These women reported drinking an average of 84.1 g of alcohol each day for at least 7 years. None of these patients showed liver cirrhosis but 10 had hepatitis and the rest had fatty liver (53,54). Studies conducted in a Massachusetts hospital reported hyperprolactinemia (22-87 ng/ml) in 6 of 12 alcohol-dependent women who had a history of drinking 75-247 g of alcohol per day for a minimum period of 7 years (55). Alcohol-induced hyperprolactinemia is also reported in healthy, well-nourished women during residence for 35 days in a clinical research ward (56). Sixty percent of women in the heavy drinker category (blood alcohol level, BAC, 109-199 mg/dl) and 50% of moderate drinkers (BAC, 48-87 mg/dl) showed elevated prolactin levels, and many of these drinkers had elevated prolactin levels several days after cessation of drinking. Alcohol-induced hyperprolactinemia was also evident in 66 postmenopausal women (42). The increase in prolactin levels in these patients, however, was associated with increased androgen conversion to estrogen, possibly due to liver cirrhosis.

Alcoholic men also showed elevated plasma levels of prolactin (57-59). Male alcoholic patients frequently show evidence of feminization that is manifested by gynecomastia, spider angiomata, palmar erytherma and changes in body hair patterns (15). Several studies now indicate a potential role for prolactin and estrogen in the pathogenesis for the observed feminization (15). Alcoholic men show a positive association between the presence of clinically apparent gynecomastia and elevated circulating levels of prolactin. These patients also show an elevation of plasma levels of estrogen, which is believed to be due to peripheral conversion of weak adrenal androgens to estrogen. The gynecomastia found in alcoholic patients is characterized by a proliferation of the stroma and ducts that are known to be estrogen-positive. Prolactin also may act synergistically with estrogen and adrenal steroids and may, therefore, contribute to enhanced breast hypertrophy in alcoholic men. Thus, it appears that chronic alcohol administration in humans causes increased estrogen production and prolactin elevation. Alcohol-induced hyperprolactinemia has also been demonstrated in non-human primates (60-62) and laboratory animals (63,64). Some of the macaque female monkeys showed elevated prolactin levels after chronic self-administration of high doses of alcohol (3.4g/kg/day). Interestingly, in one of these monkeys, immunocytochemical examination of the pituitary gland showed apparent pituitary hyperplasia (60). Recently we have shown that alcohol promotes estrogen-induced increases in pituitary weight and protein, and potentiates estrogen-induced lactotropic cell proliferation in ovariectomized female rats (65). Therefore, the clinical data as well as the animal data suggest that alcohol consumption is a positive risk factor for prolactinomas and hyperprolactinemia.

참고 링크:
http://www.bioscience.org/1998/v3/d/sarkar/list.htm [영문/full text]
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