After completion of this educational activity, the participant should be better able to identify cutaneous manifestations of gynecologic malignancies, evaluate patients with a thorough workup to screen those who have dermatoses suggestive of malignancy and assess patients with malignancy for the opportunity of early diagnosis and appropriate treatment.
The metabolite of dihydrotestosterone, 5α-androstane-3α,17β-diol (3α-Diol), is a potent inhibitor of estrogen-induced gonadotropin and prolactin secretion and lordosis behavior in the female rat. This study examined whether 3α-Diol can counteract the ultrastructural changes which are known to occur in the ventromedial nucleus (VMN) of the hypothalamus following estrogen treatment. Ovariectomized rats were treated with estradiol (E2; n = 7), 3α-Diol (n = 5), E2 and 3α-Diol (n = 6), or received control (n = 6) treatments. E2 was administered in subcutaneous capsules for two discontinuous 2-hour periods separated by 5 h, a ‘pulsed’ treatment regimen known to mimic the timing of endogenous E2 action and to influence neuronal ultrastructure in the VMN. Animals given 3α-Diol received subcutaneous injections (6 mg/kg) 3 h prior to each implantation of E2 or empty capsules. Control animals received vehicle 3 h prior to implantation of blank capsules. Animals were perfused 24 h after initial hormone treatment and neurons from the ventrolateral portion of the VMN were examined using electron microscopy. Separately, both E2 and 3α-Diol treatment increased somal and nuclear size, altered somal and nuclear shape, and increased the numbers of lysosomes present in the cytoplasm above control levels. E2 treatment resulted in increased stacking of the rough endoplasmic reticulum while 3α-Diol treatment resulted in an unusual plexiform rough endoplasmic reticulum distribution. In contrast, combined treatment with E2 and 3α-Diol resulted in cells which were similar to ovariectomized control cells on these measures. All steroid treatments decreased the amount of heterochromatin present within the nucleus compared to that seen in controls. Thus, 3α-Diol influences the ultrastructural characteristics of neurons within the VMN in a manner somewhat though not altogether similar to E2. However, 3α-Diol given in combination with E2 counteracts or prevents the actions of E2 within these same neurons.
Women with breast cancer (n = 78) had a higher excretion of total fecal steroids in mg/gm of dry weight (56 + 37) compared to controls (45 + 29; n = 71) (P = 0.03). Increases in both total neutral steroids and total bile acids in cases contributed to this significant difference. Lean women (Quetelet's index less than 3.5) with breast cancer seemed to have inappropriately high excretion of total fecal steroids (56 +/- 35), which was significantly higher than that of controls (41 +/- 27) (P = 0.03). Obesity resulted in higher excretion of fecal steroids only in controls. The differences persisted, even after pairing control cases for race-ethnicity and menopausal status. In 59 such pairs, cases had higher values (56 +/- 33), compared to controls (41 +/- 26) (P = 0.008). Significant differences (P = 0.005) were also present in 24 postmenopausal pairs, while in 35 premenopausal pairs a similar trend, but no significant differences were noted. Women with benign breast disease had higher total fecal steroids (51 +/- 34) compared to other controls (38 +/- 21) (P = 0.05). This observation suggests a common etiology between benign breast disease and breast cancer. There were no significant differences in dietary intake of total calories, total fat or dietary cholesterol between controls and cases suggesting that the observed differences in fecal steroids could be attributed to higher endogenous synthesis of cholesterol in cases.
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