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Biomedical subjects

A E Boyd

Publications and source records attributed to A E Boyd.

At least 91 records · Page 5Linked to original sources
PubMed1978

The relationship of changes in serum estradiol and progesterone during the menstrual cycle to the thyrotropin and prolactin responses to thyrotropin-releasing hormone.

The responses of serum TSH and PRL to TRH (500 microgram) were studied in normal young women in the early follicular, periovulatory, and midluteal phases of the menstrual cycle in order to examine the relationship of these responses to the levels of estradiol relationship of these responses to the levels of estradiol (E2) and progesterone. Each woman was studied twice in each phase in order to assess intraindividual variability. There was no significant difference in either the TSH or PRL responses among the phases of the menstrual cycle nor was either response affected by the periovulatory rise in E2 or by the luteal rise in both E2 and progesterone. Thus, the interpretation of the TSH and PRL responses to TRH in normal women is not affected by the menstrual cycle although both responses are greater in women that in men. Both the peak TSH and peak PRL after TRH were highly correlated with the basal levels of TSH (r = 0.85; P less than 0.01) and PRL (r = 0.67; P less than 0.01), respectively, indicating that the TSH and PRL responses to TRH in women are directly proportionate to the basal levels of the respective hormones, as previously shown for the TSH response in men. The mean intraindividual variability (coefficient of variation) of the TSH response to TRH was 18%, but ranged as high as 56%, while that of the PRL response was 16% and ranged up to 31%; variability was not affected by the phase of the menstrual cycle. The normal range of the peak TSH after TRH in women is 7-33 microU/ml (mean +/- 2 SD); however, because of the variability, a normal woman may sometimes have a peak TSH after TRH as low as 4 microU/ml. Repeating the test will result in a normal value if the woman is truly normal. Similarly, the normal peak PRL after TRH in women is 22-111 ng/ml (mean +/- 2 SD); usually, however, the lower limit is 30 ng/ml with lower values due to intraindividual variation. The data suggest that the higher average level of E2 in women compared to women, but that the cyclic changes in serum E2 or progesterone in women have little or no additional effect.

Adult↗
PubMed1978

L-dopa absorption and the pituitary-hypothalamic axis.

Administration of oral L-dopa is often used as a neuropharmacological probe to evaluate the pituitary hypothalamic axis. The effect of gastrointestinal absorption of L-dopa on the changes in plasma GH, PRL, and body temperature which occur after ingestion of this amino acid is unknown. Plasma L-dopa, GH, PRL, and rectal and skin temperatures were measured in 14 male volunteers after oral administration of 1.0 g measured in 24 men after random administration of L-dopa and a placebo. L-Dopa levels rose to 1.85 +/- 1.33 microgram/ml (mean +/- SD), but maximum plasma levels occurred at variable times from 30-230 min after drug administration. Plasma GH levels increased to 23.7 +/- 14.7 ng/ml, while PRL levels fell to 46.7 +/- 12.3% of the mean basal values. Rectal temperature decreased significantly in 3 of the men after L-dopa ingestion. Plasma GH levels after L-dopa correlated with the absorption of the drug (P less than 0.05) and inversely with the basal level of GH before L-dopa administration. There was no correlation between the basal PRL level or basal body temperature and the magnitude of the fall in PRL or body temperature after L-dopa administration. The variability of responses in GH, PRL, and body temperature after oral L-dopa ingestion is not the result of differences in absorption in the amino acid alone, and indicate either that there is a different sensitivity in the mechanisms that stimulate GH secretion and lower plasma PRL and body temperature, or that L-dopa acts at different sites to bring about each of these changes.

Adolescent↗
PubMed1978

Neurogenic galactorrhea-amenorrhea.

Neuroendocrine function in two women with galactorrhea-amenorrhea arising from abnormalities in the PRL reflex arc was compared to that of normal women. Basal gonadotropins were lower than normal, and one patient lacked episodic secretion of LH; however, the serum gonadotropin rise after iv LRH was in the normal range in both patients. Mean basal PRL levels were slightly elevated in one patient and were normal in the other, and the PRL levels after TRH, chlorpromazine, and levodopa testing were similar to those seen in normal women. Breast stimulation did not increase PRL levels in either patient. PRL levels fell with bromergocryptine therapy, galactorrhea ceased, and normal menses resumed. These studies indicate that chronic afferent impulses originating in the PRL reflex arc can result in galactorrhea and amenorrhea and that bromergocryptine therapy in such patients can restore normal menses.

Adult↗
PubMed1978

Pituitary apoplexy following chlorpromazine stimulation.

Chlorpromazine is frequently administered to patients with hyperprolactinemia to stimulate an increase in the serum levels of prolactin. A patient with a prolactin secreting adenoma is described in whom pituitary apoplexy developed in association with a hypotensive episode following the administration of 25 mg of chlorpromazine. Prolactin levels fell from more than 2,000 ng/ml to 340 ng/ml following infarction of the pituitary tumor. Pituitary apoplexy should be considered as a rare complication of chlorpromazine stimulation in a patient with a pituitary tumor.

Adenoma, Chromophobe↗
PubMed1977

Changes in the prolactin response to thyrotropin-releasing hormone (TRH) during the menstrual cycle of normal women.

Serum prolactin (PRL) and thyrotropin (TSH) levels were measured after iv administration of 200 microng of synthetic thyrotropin-releasing hormone (TRH) in 20 normal women ages 18 to 34. Ten women received TRH on days 7 to 8 of the menstrual cycle and 10 women received TRH on days 21-22. Although there was no difference in the dose of TRH relative to body weight in the two groups of women, the peak PRL level after TRH stimulation was greater in the women studied on day 21-22 (48.5+/-5.7 ng/ml, mean+/-SE) than on day 7-8 (35.2+/-4.2 ng/ml) of the cycle (P less than 0.05). In contrast, TSH rose to a greater degree in the preovulatory phase (13.8+/-1.8 micronU/ml) than the luteal phase (7.7+/-0.7 micronU/ml of the cycle (P less than .01). Studies of the PRL and TSH response after TRH administration should take the phase of the menstrual cycle into account.

Adult↗
PubMed1977

Galactorrhea-amenorrhea syndrome: diagnosis and therapy.

Tests of prolactin regulation in the galactorrhea-amenorrhea syndrome were compared in 18 patients with normal pituitary fossae, seven patients with prolactin-secreting adenomas, and eight normal women. Mean basal prolactin was highest in patients with adenomas and was elevated in those with normal fossae when compared with normal subjects (278 versus 73 versus 10.2 ng/ml). Levodopa, water loading, or luteinizing hormone-releasing hormone testing were of no predictive value in the diagnosis of adenoma. Some patients with adenomas show a greater prolactin response after administration of thyrotrophin hormone-releasing hormone (TRH) than of chlorpromazine, whereas these responses are usually similar in patients with normal fossae. A mean basal prolactin level above 150 ng/ml or an increase of more than 100 ng/ml after TRH administration in a patient with hyperprolactinemia unresponsive to chlorpromazine stimulation strongly suggests a prolactin-secreting tumor. However, because some patients with tumor have prolactin levels below 150 ng/ml, or do not respond to TRH stimulation, or both, functional studies alone cannot permit the diagnosis of all adenomas before the appearance of radiographic changes.

Adenoma↗
PubMed1976

Prolactin-releasing factor (PRF) in porcine hypothalamic extract distinct from TRH.

Extracts of porcine hypothalamic fragments (HF) bring about the release of prolactin when injected into estrogen-progesterone pretreated male rats. To determine the extent to which this prolactin-releasing activity (PRA) is attributable to thyrotropin-releasing hormone (TRH) and/or vasopressin (VP), (both hormones capable of releasing prolactin in this preparation), PRA was assayed following destruction of TRH and VP by incubation in rat serum, and after separation on Sephadex G-25 columns. Acetic acid (2N) extracts of HF contain 22 to 27 ng TRH and 650 to 1000 ng of VP per HF as determined by immunoassay. Incubation for 1 h in fresh rat serum degraded 91 to 99% of both TRH and VP. PRA fell after incubation, but was still detectable, indicating residual activity that resisted degradation. Prolactin release responses to HF extracts and to TRH were log-dose dependent, but had different activity slopes. The minimal detected dose of TRH which released prolactin was 10 ng, while minimal effective doses of serum inactivated HF extract contained only 0.6 ng of TRH. Maximum effects with serum-inactivated HF extract were achieved with 2 HF equivalents containing 2.6 ng of TRH. More than 400 ng of TRH were required to give an equivalent PRA response. Sephadex G-25 chromatography of hypothalamic extracts using 2.0 N acetic acid separated a fraction which after treatment with serum to inactivate most TRH present caused marked prolactin release and contained only 0.7 ng of TRH and 0.3 ng of VP per dose. Evidence for a PIF was the demonstration that retarded fractions from the column significantly decreased plasma prolactin levels. The finding of PRA in hypothalamic extracts separate from both TRH and VP is evidence for the existence of a distinct prolactin-releasing factor.

Animals↗