Bloody nipple discharge.

Bloody nipple discharge is a complaint that worries both the patient and the physician. Unlike other types of nipple discharge, it signals intrinsic breast disease. A benign etiology is the rule rather than the exception, but this symptom warrants careful evaluation. If there is no palpable mass or mammographic abnormality, bloody discharge from a single duct in a nonpregnant young woman is usually due to a benign intraductal papilloma.

Retarded development of castration cells after adrenalectomy or sham adrenalectomy.

Castration produces hypertrophy of gonadotropes, stimulates a shift in storage patterns to cells that store LH and FSH together, and results in a significant rise in serum LH and FSH within 12 h. Adrenalectomy retards and attenuates this postcastration rise for 24 h (1, 2). In this study, we examined the effect of adrenalectomy on castration cell morphological development. The increased percentages of LH and FSH cells that are seen normally 24 h after castration were not seen if adrenalectomy or sham adrenalectomy was performed simultaneously. In fact, the percentages of LH cells were below control values. The expansion in the average area of LH and FSH cells was also retarded after simultaneous castration and adrenalectomy or sham adrenalectomy. The corticotrope population responded as expected to adrenalectomy and the surgical stress of castration, with an increase in the percentage and area of stained cells as well as partial degranulation. The serial sections showed no ACTH staining in gonadotropes after any of the surgical treatments. The gonadotropic storage patterns were altered, however. In castrated rats exposed to simultaneous adrenalectomy or sham adrenalectomy, the percentage of LH/FSH cells was reduced from 70% of gonadotropes in intact rats to 30%. Over 60% of the serially sectioned gonadotropes stored only one hormone, and these monohormonal cells tended to occur in clusters. Our experiments thus show that the gonadotropin storage pattern can be shifted with experimental manipulation. This may also reflect shifts in the site of hormone storage within a given cell. We suggest that adrenalectomy or sham adrenalectomy retards the postcastration rise in gonadotropins by preventing the immediate expansion of the granulated cell population and causing an apparent loss in the numbers of certain types of gonadotropes.

Ontogeny of sex differences in LH and FSH levels 48 h after castration in the rat.

Serum gonadotropin levels were measured 12, 24, and 48 h after gonadectomy in male and female rats (ages, 22--60 days) to assess when during development the rate of rise of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) after castration approximates that seen in the gonadectomized adult. In females serum LH levels 48 h after ovariectomy were increased above sham levels only when the ovaries were removed prior to vaginal opening. Ovariectomy on the day of vaginal opening or at older ages resulted in no increase in LH levels by 48 h after surgery. Serum FSH levels at 24 and 48 h after ovariectomy declined with increasing age at the time of ovariectomy. In males serum LH levels at 48 h after castration increased with increasing age at the time of gonadectomy. Serum FSH levels at either 12, 24, or 48 h after orchidectomy did not change appreciably with age at the time of surgery. It is concluded that the acute pituitary secretion of gonadotropins after removal of testes in the immature male resembles that seen in the mature male early in the course of the development of sexual maturity. In contrast, the acute pituitary secretion of gonadotropins after removal of the ovaries in the immature female does not resemble that seen in the ovariectomized adult until she is mature and capable of ovulating. Thus, the observed delay in the rise of LH seen in ovariectomized adults may be a function of some aspect of the hormonal changes associated with the estrous cycle.

Specific FSH suppression in male rat by porcine follicular fluid.

A variety of protocols using intact, castrated, and sham-castrated adult male rats was used to test the ability of porcine follicular fluid to selectively suppress serum follicle-stimulating hormone (FSH). A total dose of 500 microliters follicular fluid injected intraperitoneally will suppress FSH in the rat with testes within 5 h of injection. This is more than is necessary to suppress FSH in the intact or ovariectomized female. A total dose of 1 ml of follicular fluid is needed to suppress FSH reliably in the castrated male rat. Serum FSH is suppressed significantly beginning between 4 and 5.5 h after intraperitoneal injection of 1 ml of follicular fluid and 3 h after intravenous injection. The suppression continues until 10 h postinjection and is abated by 26 h postinjection. Serum luteinizing hormone (LH) is unaffected by follicular fluid in any protocol tested. It is concluded that 1) follicular fluid can suppress serum FSH in the male if large enough doses are given, 2) follicular fluid has no effect on serum LH, and 3) follicular fluid suppresses serum FSH levels in the male as well as previously tried testicular sources. These results suggest that the delay in demonstrating the existence of inhibin may be due to the use of males as both source and test subject.

Selective suppression of the primary surge of follicle-stimulating hormone in the rat: further evidence for folliculostatin in porcine follicular fluid.

Charcoal-extracted porcine follicular fluid (PFF), when injected at 1200 h on proestrus, blocked the primary FSH surge seen at 1700 and at 1830 h without affecting the LH surge. In contrast, if the injection was withheld until 1330 h, the FSH surge occurred in the normal way at 1700 h but was suppressed at the 1830 h autopsy. The suppression of FSH by 0.5 ml PFF at 1200 h had abated by 0400 h of estrus. The blockade of the primary surge of FSH at 1700 and 1830 h did not prevent ovulation, nor did it prevent the expected rise in serum progesterone or fall of estradiol levels. There appears to be a latency of at least 3.5 h, when PFF is administered ip, before FSH can be suppressed. This latency occurs whether the injection is carried out in intact proestrous rats or in acutely or chronically ovariectomized females.