Therapy of endometriosis--avoidance of confounders!
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Endometriosis↗
Biomedical subjects
M P Platia
Publications and source records attributed to M P Platia.
Midluteal phase endometrial biopsy does not accurately predict luteal function.
OBJECTIVE: To investigate whether a midluteal phase endometrial biopsy accurately predicts luteal function. DESIGN: One nonpregnant menstrual cycle was evaluated in a prospective fashion. SETTING: Outpatient Clinic of the Clinical Center of the National Institutes of Health. PARTICIPANTS: Fifty healthy, normally cycling women. INTERVENTIONS: Serum progesterone (P) was measured daily throughout the luteal phase. An endometrial biopsy was performed 7 to 9 days after the luteinizing hormone (LH) surge, as detected by rapid plasma assays, and dated histologically according to Noyes' criteria. MAIN OUTCOME MEASURE: To correlate endometrial maturation with luteal P secretion. RESULTS: Mean integrated P measurements were reduced only when the lag between histologic and chronological dating was > or = 3 days or > or = 4 days, depending on whether chronological dates were assigned prospectively from the LH surge or retrospectively from the onset of next menses, respectively. However, these lags did not consistently predict deficient luteal function because subnormal integrated P secretion was seen in only 14% of women with these delays in endometrial maturation. CONCLUSIONS: Midluteal phase endometrial biopsy provides a crude test of luteal function that does not precisely distinguish luteal insufficiency.
Adult↗
Elevation of plasma immunoreactive luteinizing hormone releasing hormone in hyperprolactinemic-amenorrheic women on bromocriptine therapy.
There is evidence to suggest that abnormalities in the secretion of prolactin (PRL) in patients with the hyperprolactinemia-amenorrhea syndrome are due to hypothalamic dysfunction. In an attempt to further define the inhibitory effect of excessive PRL release on luteinizing hormone releasing hormone (LHRH) and luteinizing hormone (LH) secretory patterns in human plasma, four amenorrheic women with known hyperprolactinemia were studied before and during bromocriptine (BRCR) therapy. Ten-minute blood samples collected with a continuous withdrawal pump for two hours were analyzed for immunoreactive LHRH (IR-LHRH), LH and PRL using previously established radioimmunoassay procedures. Three patients showed a significant rise in mean IR-LHRH plasma levels coincident with a significant decrease in mean PRL concentrations five days to two weeks following BRCR therapy, whereas mean LH titers increased significantly in only one patient. One patient showed no increase in IR-LHRH or LH with BRCR therapy and failed to show a decrease in serum PRL to normal levels after five days of this treatment. A defect in the control of PRL release in these patients seemed to result from the inability of dopaminergic inhibition to be mediated effectively and seemed to be associated with altered secretion of LHRH.
Adult↗
Regulation of primate angiotensin II receptors during altered sodium intake.
In the rat, angiotensin II receptors of the adrenal glomerulosa and smooth muscle undergo reciprocal regulatory changes that parallel the changes in target cell sensitivity to angiotensin II during altered sodium intake. In primates, the relative importance of angiotensin II receptor regulation during sodium-induced changes in angiotensin II sensitivity is not clear. To evaluate the role of angiotensin II receptor regulation in the primate, we analyzed the changes in angiotensin II receptors of adrenal and bladder membrane-rich particles after 4 to 6 days of high or low sodium intake in the monkey (Macaca fascicularis). Consistent with the decreased pressor response to angiotensin II, smooth muscle angiotensin II receptors were fewer in sodium-restricted monkeys (93 +/- 17 fmol/mg) than in sodium-loaded monkeys (171 +/- 6 fmol/mg). However, in contrast to the rat, changes in zona glomerulosa angiotensin II receptors in monkey adrenal were similar to those in smooth muscle, decreasing with sodium restriction and increasing with sodium loading (344 +/- 64 and 660 +/- 68 fmol/mg, respectively). There was no change in angiotensin II receptor affinity in either smooth muscle or adrenal particles during altered sodium intake. Concomitant with the decrease in adrenal angiotensin II receptors, 18-hydroxylase activity was increased twofold in adrenal mitochondria from sodium-restricted monkeys (74 +/- 8 fmol/mg/min) compared with sodium-loaded animals (28 +/- 11 fmol/mg/min). The increased sensitivity of the primate adrenal to angiotensin II despite a fall in angiotensin II receptors indicates that full activation of steroidogenesis by angiotensin II can be maintained with partial receptor occupancy.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Cortex↗
Effects of 17 beta-estradiol on angiotensin II receptors and prolactin release in cultured pituitary cells.
Angiotensin II (AII) binds to specific receptors in the lactotroph and stimulates PRL secretion from isolated rat pituitary cells. Since estrogens exert major regulatory actions on PRL secretion, the effects of estradiol (E2) on pituitary AII receptors and PRL responses were studied in vivo and in cultured rat anterior pituitary cells. In female rats, treatment with E2-containing Silastic capsules for 4 days caused a significant increase in PRA from 1.3 to 3 ng/ml X min and a 38% decrease in the binding of [125I]AII to anterior pituitary membrane-rich fractions (P less than 0.01). In vitro studies showed that treatment of cultured anterior pituitary cells with 1 nM E2 for 4 days caused a 57 +/- 6% decrease in AII receptor concentration with no change in binding affinity. Reduction of AII receptors by E2 in 4-day cultures was dose dependent and was demonstrable with E2 concentrations that occur in plasma during the estrous cycle (0.01-1 nM). The decrease in AII receptors in cells incubated with 1 nM E2 was near maximum after 24 h of culture, and results were similar when receptor concentrations were calculated per unit protein or per cell. Despite the substantial decrease in AII receptors, E2 treatment did not specifically decrease the responsiveness of the pituitary cells to AII stimulation. Thus, PRL responses to AII (10 nM) or TRH (100 nM) were unchanged after 1 day of E2 treatment and were increased after 4 days of treatment. These findings demonstrate that E2 has a direct inhibitory action on expression of pituitary AII receptors that is not accompanied by a decrease in AII-stimulated PRL secretion. In the rat pituitary, estrogen modulation of postreceptor events is the predominant determinant of lactotroph responsiveness during stimulation of PRL release by AII.
Animals↗
Transvaginal fluoroscopic recanalization of a proximally occluded oviduct.
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Adult↗
Estrone sulfatase activity in the human brain and estrone sulfate levels in the normal menstrual cycle.
When the plasma concentrations of estrone sulfate (E1S) were measured in five menstrual cycles, the highest concentrations were found on the day of LH peak (14.25 nmol/l +/- 2.94 [SE]). Peak levels of E1S were 20 times higher than the highest E2 levels measured (0.769 +/- 0.276 nmol/l). To determine whether E1S can be metabolized by adult and fetal tissues we examined estrone (E1) sulfatase activity in brain and other tissues. E1 Sulfatase activity was present in all tissues studied including adult endometrium, fat and skin. When the rate of sulfatase activity was measured in homogenates of fetal hypothalamus, frontal cortex and pituitary (n = 4), the hypothalamic activity (306.0 +/- 39.1 [SE] pmol/min/mg protein) was significantly higher than that of the frontal cortex (127.4 +/- 19.4, P less than 0.002) or pituitary (193.7 +/- 43.3, P less than 0.03). This was not apparent in the adult (n = 2) where the enzyme activity was similar in the hypothalamus (413.9 +/- 27.3) and frontal cortex (446.3 +/- 82.2) and lower in the pituitary (98.2 +/- 19.2). The Km for E1 sulfatase in the fetal frontal cortex was 28.9 microM. The high E1 sulfatase activity in estrogen responsive target tissues, particularly fetal hypothalamus, accompanied by a large circulating reservoir of E1S, suggest that this enzyme could possibly have a regulatory role in controlling the level of intracellular estrogens and in modulating their intracellular function.
Adult↗
Refractoriness to gonadotropin therapy: how to distinguish ovarian failure versus pseudoovarian resistance caused by neutralizing antibodies.
Ovarian resistance to exogenously administered gonadotropins and elevated serum gonadotropins, especially follicle-stimulating hormone (FSH), are considered virtually diagnostic of ovarian failure. However, similar clinical findings can be caused by circulating antibodies to gonadotropins which can neutralize the biologic activity of exogenously administered gonadotropins and can also cause falsely high gonadotropin determinations by routine double-antibody radioimmunoassay (RIA). We have used a primate model with anti-FSH antibodies to demonstrate that an acute course of combined estrogen-progestin therapy will suppress the pituitary secretion of FSH, which is markedly elevated in ovarian failure, while the false FSH elevations caused by circulating anti-FSH antibodies are not reduced by steroid negative feedback. Thus, gonadotropin (RIA) determinations before versus during an acute course of estrogen and progesterone therapy can distinguish true ovarian failure from the presence of circulating anti-gonadotropin antibodies.
Animals↗
Isolation, radioimmunoassay and physiologic secretion of rat neurophysins.
Rat posterior pituitaries were extracted in acid and total rat neurophysins were isolated. Preparative disc gel electrophoresis separated the total neurophysins into three main peptides of differing electrophoretic mobility. Antisera raised in rabbits recognized a common antigenic site in the three peptides and identical radioimmunoassay standard curves were obtained with each of the isolated rat neurophysins. A homologous rat neurophysin radioimmunoassay was utilized to measure neurophysin in samples of unextracted rat plasma. Basal neurophysin levels, 3.7 +/- 0.2 ng/ml (mean +/- SEM), did not differ in samples collected by decapitation, carotid artery cannulation, or tail vein bleeding. Water-loading caused a significant reduction in neurophysin, 2.8 +/- 0.1 ng/ml, while hypertonic saline and dehydration caused a significant elevation, 10.4 +/- 2.1 and 8.0 +/- 1.4 ng/ml, respectively. A step-wise decrease in blood volume caused a step-wise increase in plasma neurophysin concentrations which returned to baseline with reinfusion of the withdrawn blood. A second hemorrhage caused an even greater release of neurophysin indicating large neurophysin reserve in the pituitary. In periodic tail vein samples over 23 days of pregnancy a rise in plasma neurophysin was found from day 14 continuing to parturition with a peak value of greater than 13 ng/ml by day 21. Two days postpartum the value was 4.6 +/- 0.3 ng/ml. With this homologous assay, the basal levels of plasma neurophysin are lower and the stimulated values higher than with previously reported heterologous assays. Therefore, the relative change with physiologic maneuvers is distinctly increased.
Animals↗