Aromatase inhibitor after steroids

Research suggests the common table mushroom has anti- aromatase [17] properties and therefore possible anti-estrogen activity. In 2009, a case-control study of the eating habits of 2,018 women in southeast China revealed that women who consumed greater than 10 grams of fresh mushrooms or greater than 4 grams of dried mushrooms per day had an approximately 50% lower incidence of breast cancer. Chinese women who consumed mushrooms and green tea had a 90% lower incidence of breast cancer. [18] However the study was relatively small (2,018 patients participating) and limited to Chinese women of southeast China.

A number of investigators have reported on a rather rare syndrome of excess aromatase activity. In boys, it can lead to gynecomastia , and in girls to precocious puberty and gigantomastia . In both sexes, early epiphyseal closure leads to short stature. This condition is due to mutations in the CYP19A1 gene which encodes aromatase. [16] It is inherited in an autosomal dominant fashion. [17] It has been suggested that the pharaoh Akhenaten and other members of his family may have suffered from this disorder, [18] but more recent genetic tests suggest otherwise. [19] It is one of the causes of familial precocious puberty—a condition first described in 1937. [20]

Clinical and endocrinological effects of exemestane (6-methylenandrosta-1,4-diene-3,17-dione; PNU 155971) were evaluated in an open Phase I study. Thirteen postmenopausal women suffering from advanced breast cancer received exemestane in escalating doses over a 12-week period. Starting on 5 mg once daily (.), exemestane was subsequently escalated at 2-week intervals to 10, 25, 50, 100, and 200 mg . Each patient subsequently continued treatment on the highest tolerated dose until time of progression. One patient terminated treatment after 6 days due to diarrhea that was probably not related to drug therapy, although a relationship could not be excluded. Apart from this, no serious side effects were seen during the dose escalation period. Exemestane (10 mg .) caused maximal suppression of plasma estradiol (E2) and estrone (E1) to a mean of and % of pretreatment levels, respectively, whereas 25 mg of exemestane . suppressed estrone sulfate (E1S) to % of pretreatment levels. No fall in adrenal steroid levels was recorded. Exemestane (5 mg .) suppressed urinary E2 and E1 to a mean of and % of pretreatment levels, respectively. Administering exemestane at doses of 50-200 mg . caused no further suppression of urinary E1, whereas urinary E2 fell to 6-7% of pretreatment levels. Median time to progression was 63 weeks. We conclude that exemestane is a well-tolerated aromatase inhibitor that effectively suppresses plasma and urinary estrogens in postmenopausal patients with breast cancer.

Aromatase inhibitor after steroids

aromatase inhibitor after steroids


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