Dissociated response of thyrotropin and prolactin to dopamine receptor blockade with domperidone in hypothyroid subjects.

To investigate the hypothesis of an altered hypothalamic dopaminergic activity in primary hypothyroidism, eight patients with hypothyroidism and seven normal subjects, all female, were studied. All of them were submitted to two tests: TRH stimulation and after the administration of dopamine receptor-blocking drug, Domperidone. The hypothyroid patients with basal TSH values less than or equal to 60 mU/L (4 cases--group 1) had lower PRL levels than the remaining 4 subjects with TSH greater than 60 mU/L (group 2) (p less than 0.001), despite all patients presenting the PRL levels within the normal range. A significant increase occurred for both TSH and PRL after the administration of TRH and Domperidone in normal as well as in the hypothyroid subjects, except for TSH in group 1 after the administration of Domperidone. The area under the curve for PRL response to THR was not different between the normal subjects and both hypothyroid groups, while that under the curve for TSH was greater in the hypothyroidism as a whole than in the normal subjects (p = 0.006) and between the hypothyroid groups, being greater in group 2 than in 1 (p less than 0.009). In relation to Domperidone, the area under the curve for TSH was significantly higher in group 2 when compared to the normal controls (p less than 0.001), while for PRL it was not different between hypothyroid groups in relation to normal controls and when groups I and II were compared. These results suggest that the hypothalamic dopamine activity is not altered in primary hypothyroidism and favor the small relevance of dopamine on the control of TSH secretion.     

Possible thyrotrophs insensitivity to dopamine in hyperprolactinaemic amenorrhoeic patients

The study assessed the sensitivity of the thyrotrophs of hyperprolactinaemic patients to a physiological dose of dopamine (DA). Eight hyperprolactinaemic amenorrhoeic patients received 4-hour infusions of either DA (0.4 micrograms/kg x min) or glucose. Twelve normal women served as controls. In normal women the mean thyrotrophin (TSH) concentration declined significantly (P less than 0.05) from 81 +/- 6.6% of basal levels during glucose infusion to 59 +/- 5.8% of basal levels during DA infusion. In contrast DA infusion to hyperprolactinaemic patients caused no significant reduction in TSH levels compared to glucose infusion (DA infusion 68 +/- 4.7% of basal levels; glucose infusion 73 +/- 4.9% of basal levels). DA infusion caused a significant reduction in serum prolactin (PRL) levels both in hyperprolactinaemic patients (P less than 0.001) and normal women (P less than 0.02), but the PRL suppression was significantly (P less than 0.05) less pronounced in the hyperprolactinaemic patients, compared to normal women. We propose that the abnormal PRL as well as TSH secretion in hyperprolactinaemic amenorrhoeic patients may be due to a common defect. Both the lactotrophs and the thyrotrophs may be relatively insensitive to dopaminergic inhibition.     

Impaired LH-RH release by estrogen in women with sulpiride-induced hyperprolactinemia

The effects of hyperprolactinemia on the release of immunoreactive luteinizing hormone-releasing hormone (LH-RH) and luteinizing hormone (LH) in response to iv injection of 20 mg conjugated estrogens (Premarin) were studied. Five normal cycling women were injected with Premarin on the morning of the 7th day of the first cycle (control cycle), and then the plasma levels of LH-RH, LH, and prolactin (PRL) were determined every 8 to 16 hours for 72 h. Two months later, the same women received 200 mg of oral sulpiride daily for 8 days from the 3rd day of the cycle (sulpiride treated cycle), and then the same protocol as in the control cycle was applied. Mean (+/- SE) plasma levels of PRL on day 7 in the sulpiride treated cycle were significantly higher than those in the control cycle (118 +/- 24 ng/ml vs. 14 +/- 4 ng/ml, p less than 0.001). After estrogen injection, the mean percent increases in immunoreactive LH-RH at 32 h (control: 71 +/- 38% vs. sulpiride: 6 +/- 36%) and 40 h (154 +/- 38% vs. -5 +/- 21%) and in LH at the 48 h (175 +/- 89% vs. 57 +/- 57%) and 56 h (99 +/- 32% vs. 7 +/- 21%) were significantly (p less than 0.01 or p less than 0.05) suppressed in the sulpiride cycle. These data suggest that the impaired positive feedback effect of estrogen on LH-release in hyperprolactinemic anovulatory women may be caused, at least in part, by disturbed LH-RH release.     

Dopaminergic regulation of gonadotropin and thyrotropin hormone secretion is altered with age.

To determine if age-related changes in glycoprotein pituitary hormone secretion are associated with alterations in dopaminergic regulation, plasma gonadotropins and TSH were measured before and after L-dopa administration in 44 young (31-44 years of age) and 42 old (64-88 years of age) healthy male participants. Plasma GH and PRL were also determined in order to examine the somatotroph and lactotrope response. In the young, following L-dopa, plasma FSH, LH and TSH were unchanged from baseline. However, in older subjects, plasma FSH was significantly increased (p less than 0.001) and a similar trend was noted for LH. Plasma TSH was significantly depressed (p less than 0.002) in older subjects only. Following L-dopa, increases in plasma GH and decreases in plasma PRL were of similar magnitude in each group. These data indicate that dopaminergic modulation of gonadotropins and TSH is altered with age.     

Effect of luteal metoclopramide-induced hyperprolactinemia on pituitary and luteal responsiveness to gonadotropin-releasing hormone

The pituitary and corpus luteum responses to acute gonadotropin-releasing hormone (GnRH) administration at the mid-luteal phase (LP) were studied in 24 infertile women. Patients were randomly divided into two groups. In one group (n = 12) metoclopramide (MCP, 10 mg orally 3 times daily) was administered from day 0 or 1 of the LP for 7 days. On day 7 or 8 of LP blood samples were taken every 15 min for 180 min; then 25 micrograms GnRH were acutely administered intravenously and blood samples taken at 185, 195, 210, 225, 240, 255, 270, 285 and 300 min. In the other 12 patients the same experimental design was performed on day 7 or 8 of an untreated LP. Plasma prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone and estradiol (E2) were assayed. The responsiveness of the different hormones to GnRH was evaluated as the integrated secretory area for 120 min after injection (sISA = stimulated integrated secretory area) and as the percentage increase (delta A) with respect to the area under basal conditions before GnRH administration (bISA = basal integrated secretory area). MCP-treated women showed higher basal PRL levels (p less than 0.01) and lower basal plasma concentrations and bISA (p less than 0.01) values of LH than controls. After GnRH a more marked response of LH secretion was observed in the treated group (p less than 0.01), so that the absolute values of sISA were superimposable in both groups. Basal and stimulated FSH secretion did not differ significantly in the study groups. Basal plasma and bISA values of progesterone were also decreased in MCP-treated subjects. After GnRH injection the absolute values of progesterone sISA were greater in controls (p less than 0.01), but delta A values were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolactin and thyrotropin response to thyrotropin-releasing hormone in premenopausal women with fibrocystic disease of the breast

Plasma PRL, TSH, total and free T4, total and free T3, and 17 beta-estradiol were evaluated in 29 premenopausal women with well-documented fibrocystic disease of the breast and in 29 healthy matched controls. Plasma PRL and TSH dynamics after acute TRH injection (200 micrograms i.v.) were also determined. All hormonal measurements were performed in the follicular phase of the menstrual cycle. Neither patients nor controls showed any thyroid function impairment. Basal plasma levels of the examined hormones were in the normal range in both groups. When considering data pertinent to PRL and TSH secretory patterns after TRH stimulation, no difference was recorded between patients and controls for TSH secretion, evaluated in terms of maximum peak, net (delta) and percent (delta %) increase above the baseline level and integrated area of response. On the contrary, the response of PRL was significantly higher in patients than controls (maximum peak at 20 min, mean +/- SE, 119.9 +/- 14.1 vs. 60.8 +/- 5.5 ng/ml, p less than 0.001; integrated area of response, 5,725 +/- 908 vs. 3,243 +/- 266 ng/ml/120 min, p less than 0.01). The results are compatible with the view that, in most patients with fibrocystic disease of the breast, there are abnormalities in the control of PRL secretion, which lead to enhanced release of the hormone after stimulation. In such cases the control of TSH appears to be operating normally.     

Simultaneous administration of TRH and sulpiride caused additive but not synergistic PRL responses in normal subjects.

In order to study the mode of action of TRH and sulpiride in man, we administered TRH (500 micrograms, iv) and sulpiride (DA D2 receptor antagonist, 100 mg, im) simultaneously to 6 normal females (20-21 yr). Normal females showed significantly greater PRL increments and AUC in response to the combined administration compared to a single administration of each agent (P < 0.05-0.01), while the increment and AUC in response to the combination did not exceed the sum of those responses to a single administration. In contrast, the combined administration of TRH and sulpiride did not elicit an enhanced response of plasma TSH. These results indicate that the sites of action of TRH and sulpiride might be different from each other, and these agents work additively with no interaction in human lactotrophs.     

Plasma aldosterone response to metoclopramide is unmodified by hyperprolactinemia

It has been previously demonstrated that patients with hyperprolactinemia have impaired PRL response to dopaminergic blockade and increased TSH response. Since inhibitory dopaminergic modulation of aldosterone is well established, we have examined whether prolactinoma patients have an altered aldosterone response to dopaminergic blockade. To investigate this possibility we compared the plasma PRL, TSH and aldosterone responses to the dopamine (DA) antagonist metoclopramide (MCP; 10 mg i.v.) in 10 women with prolactinomas and 7 healthy female controls. Basal PRL levels in prolactinoma patients were elevated and showed a blunted rise following MCP. Although basal TSH levels were similar in the 2 groups of subjects, they significantly increased (p = 0.017) in prolactinoma patients while in contrast they did not significantly change in control subjects. Basal supine plasma aldosterone was similar in patients with prolactinomas (0.23 +/- 0.03 nmol/l) and in healthy subjects (0.25 +/- 0.04 nmol/l) and the increased aldosterone concentrations from 15 to 120 min following MCP were not significantly different in prolactinoma patients and in control subjects. It is concluded that in patients with prolactinomas, the alteration in the dopaminergic regulation is specifically related to the lactotroph.     

Gonadotropin, prolactin and thyrotropin pituitary secretion after exogenous dehydroepiandrosterone-sulfate administration in normal women.

The effect of exogenous dehydroepiandrosterone-sulfate (DHAS) on luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL) and thyroid-stimulating hormone (TSH) pituitary secretion was studied in 8 normal women during the early follicular phase. The plasma levels of these hormones were evaluated after gonadotropin-releasing hormone (GnRH)/thyrotropin-releasing hormone (TRH) stimulation performed after placebo or after 30 mg DHAS i.v. administration. The half-life of DHAS was also calculated on two subjects; two main components of decay were detected with half-times of 0.73-1.08 and 23.1-28.8 h. The results show an adequate response of all hormones to GnRH or TRH tests which was not significantly modified, in the case of LH, FSH and PRL, when performed in the presence of high levels of DHAS. However, the TSH response to TRH was significantly less suppressed (p less than 0.05) (39%) after DHAS administration than during repeated TRH stimulation without DHAS (51%). The data support the hypothesis that DHAS does not affect LH, FSH and PRL secretion, while TSH seemed to be partially influenced.     

The role of estrogen in the TSH and prolactin responses to thyrotropin-releasing hormone in postmenopausal as compared to premenopausal women.

The basal and TRH (Thyrotropin-Releasing Hormone) stimulated TSH (Thyrotropin) and PRL (Prolactin) responses (incremental area; IA) to 200 micrograms TRH was studied in 13 pre- and 13 postmenopausal women of 60 years of age. Both groups consisted of healthy women, none had goiter and all were negative for thyroid autoantibodies. The serum levels of TSH, T3, T4 and SHBG (sex hormone-binding globuline) were in the normal range and did not differ significantly between the groups. There were no differences in basal TSH (1.3 +/- 0.5 vs 1.4 +/- 0.5 mIU/l) or PRL (6.4 +/- 2.7 vs 6.6 +/- 2.5 micrograms/l) or for PRL IA (498 +/- 126 vs 584 +/- 165) between pre- and postmenopausal women. However, for TSH IA there was a slight decrease (15%), but not significant, in the postmenopausal group compared to the premenopausal group (1630 +/- 598 vs 2067 +/- 893). In conclusion, a weak but not significant decrease in the TSH response to TRH in postmenopausal women may be explained by the lower endogenous estradiol level.     

Effect of sulpiride on serum growth hormone and prolactin concentrations following L-DOPA administration in man.

The effect of chronic administration of sulpiride on serum human growth hormone (hGH), prolactin and thyroid stimulating hormone (TSH) was examined in 6 normal subjects. Sulpiride was given orally at a dose of 300 mg (t.i.d.) for 30 days. Sulpiride raised serum prolactin levels in all subjects examined. In addition, sulpiride suppressed hGH release induced by L-dopa, although the basal hGH level was not changed. Sulpiride treatment appeared to antagonize partially the inhibitory effect of L-dopa on prolactin release. Following thyrotropin-releasing hormone (TRH) injection, the percent increment in prolactin levels from the baseline in sulpiride-treated subjects was less than in controls without sulpiride. In contrast, both the basal and TRH-stimulated TSH levels were not influenced by sulpiride. These observations suggest that sulpiride suppresses L-dopa-induced hGH release and stimulates prolactin release, presumably by acting against the dopaminergic mechanism either on the hypothalamus or on the pituitary. The decreased prolactin response to TRH after sulpiride treatment may indicate a diminished reserve capacity in pituitary prolactin release.     

Influence of central dopaminergic activity on thyrotropin responsiveness to thyrotropin-releasing hormone in normal and thyrotoxic subjects

To study whether central dopaminergic activity influences TSH responsiveness to TRH in normal individuals and in patients with hyperthyroidism, three experiments (A, B and C) were carried out in 8 normal subjects, and two experiments (A and B) in 8 patients with untreated thyrotoxicosis. In experiment A oral placebo (PBO) preceded iv administration of 200 micrograms TRH by 90 min. In experiment B dopamine receptor blockade with 15 mg oral metoclopramide (MET) was given 90 min before iv administration of 200 micrograms TRH. In experiment C two oral doses (each dose 2.5 mg) of bromocriptine (BCT), known for dopamine agonistic properties, were given 9 and 1 hour before ingestion of 15 mg MET which, in turn, preceded iv injection of 200 micrograms TRH by 90 min. In the healthy subjects experiment A revealed a TSH responsiveness, as reflected by the TSH incremental area, which was 430 +/- 74. The corresponding TSH responsiveness was significantly larger in experiment B (661 +/- 138; P less than 0.02). In experiment C the TSH incremental area (332 +/- 102) did not differ significantly from the one obtained in experiment A. The thyrotrophs responded quite different to TRH in the group of thyrotoxic patients, where the TSH incremental area was zero regardless of whether PBO or MET were given as oral pretreatments. These results imply that central dopaminergic activity inhibits the pituitary thyrotrophs and modulates the TSH response to TRH in healthy subjects, but does not contribute significantly to the blocked TSH responsiveness in patients with untreated hyperthyroidism.     

Episodic thyrotropin (TSH) and prolactin (PRL) secretion during aging in postmenopausal women.

While aging is known to decrease episodic thyrotropin (TSH) secretion in men, no detailed information is available as to age-related alterations in the TSH and prolactin (PRL) release patterns in postmenopausal women (PMW). Accordingly, we compared the TSH and prolactin (PRL) secretory profiles of 6 euthyroid younger PMW (mean age: 53.0 years) with those of 7 euthyroid older PMW (mean age: 80.4 years). In all PMW, blood samples were obtained at 10 minute intervals for 10 hours for serial determinations of TSH and PRL by RIA. While thyroxine (T4) serum concentrations were not different in younger from older PMW, triiodothyronine (T3) levels markedly (p less than 0.05) decreased in older PMW. In both younger and older PMW, TSH and PRL were secreted episodically (by Cluster pulse algorithm), with considerable inter-individual variabilities in either study group. TSH and PRL pulse attributes (interpulse intervals, frequencies, amplitudes) were comparable in younger and older PMW, although a tendency of mean TSH to increase (p = 0.18) was noted for older PMW. Mean TSH and PRL serum concentrations were positively (r = 0.94, p less than 0.01) correlated in older, whereas not in younger PMW. These observations demonstrate that the pulse characteristics of episodic TSH and PRL secretion are preserved in PMW even of old age. However, in view of markedly decreased circulating T3 concentrations and of no substantial change in the TSH pulsatile secretion in older PMW, the negative feedback on the hypothalamic-pituitary unit may be impaired in elderly women.     

Twenty-four hour secretory pattern of thyroid-stimulating hormone in hyperprolactinemic women with pituitary microadenoma

In order to determine whether endogenous dopaminergic tone has any role in the diurnal variation in TSH secretion, the 24-h secretory pattern of TSH and the TSH response to a dopamine antagonist, metoclopramide (MCP), were evaluated in normal women (n = 4) and in hyperprolactinemic-amenorrheic women with pituitary microadenoma (n = 6). TSH concentrations expressed as percent deviation from the 24-h mean significantly differed with respect to time of day in normal women and hyperprolactinemic women. They were significantly higher during the night (2000-0700 h) than during the daytime (0800-1900 h). Whereas MCP administration induced no significant changes in serum TSH levels in normal women, it significantly increased serum TSH levels in hyperprolactinemic women. Thus, the diurnal variation in TSH secretion was demonstrated in hyperprolactinemic women with pituitary microadenoma in the face of an increased dopaminergic inhibition of TSH secretion. The present study did not provide evidence that the diurnal pattern of TSH secretion is related to the endogenous dopaminergic tone.     

Prolactin as a marker of dopaminergic activity at different levels of thyroid function in man

To investigate the hypothesis of an altered dopaminergic activity in hypothyroidism, seven patients without thyroid tissue were studied by means of three consecutive tests: an iv bolus of TRH (200 micrograms); a continuous iv infusion (5 mg during 30 min) of metoclopramide (MCP); and a second, post-MCP, iv bolus of TRH (200 micrograms). The study was performed three times: (A) without treatment; (B) on the 15th day while on L-T4 (150 micrograms i.d.); and (C) on the 30th day with the same treatment. Each time was a different situation of thyroid function; on the basis of basal serum TSH (P less than 0.001, A vs B vs C). The response of PRL to the first (non-primed) TRH, expressed as the sum of increments in ng/ml (mean +/- SE), was significantly higher in A (659 +/- 155) than in C (185 +/- 61). Individual PRL responses correlated with circulating T3 (P less than 0.02), but not with T4. A significant increase of PRL occurred after MCP in the three situations, but there were no differences among them. Likewise, the responses to the second (MCP-primed) TRH showed no differences. Although there was an expected high correlation (P less than 0.001) between basal TSH and circulating thyroid hormones, the maximal response of TSH to both non-primed and MCP-primed TRH was in B. After MCP, no measurable increase of TSH could be demonstrated at any of the three levels of thyroid function. These results do not support the hypothesis of an altered dopaminergic activity in hypothyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Response of thyrotropin, prolactin and free thyroid hormones to graded exercise in normal male subjects

Serum levels of thyrotrophin (TSH), prolactin (PRL), free thyroxine (FT4) and free triiodothyronine (FT3) were determined before and after physical exercise in 21 normal male subjects. The subjects were divided into 3 groups as follows: group I--light exercise (exercise on the Mijnhardt bicycle ergometer at 100 Watts for 15 min); group II--moderate exercise (a 5 km marathon); group III--heavy exercise (a 10 km marathon). In group I, TSH level rose from 1.96 +/- 0.42 mu u/ml (mean +/- SEM) to 2.52 +/- 0.30 mu u/ml (p less than 0.01), and PRL levels rose from 11.0 +/- 2.0 ng/ml to 19.0 +/- 5.2 ng/ml (p less than 0.01). In group II, TSH rose from 2.11 +/- 0.51 mu u/ml to 2.62 +/- 0.56 mu u/ml (p less than 0.05), and PRL rose from 11.2 +/- 1.6 ng/ml to 24.0 +/- 5.2 ng/ml (p less than 0.01). In group III, TSH rose from 2.01 +/- 0.41 mu u/ml to 2.36 +/- 0.45 mu u/ml (p less than 0.02), and PRL rose from 12.1 +/- 2.0 ng/ml to 47.7 +/- 9.3 ng/ml (p less than 0.01). The serum levels of FT4 showed different results among the three groups: Group I showed an increased response from 1.60 +/- 0.12 ng/dl to 1.72 +/- 0.12 ng/dl (p less than 0.01); Group II showed no significant difference; and group III demonstrated a diminished response from 1.61 +/- 0.14 ng/dl to 1.45 +/- 0.16 ng/dl (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of tartrate thyrotropin-releasing hormone treatment on serum thyrotropin, free triiodothyronine, free thyroxine and prolactin levels in patients with spinocerebellar degeneration.

The aim of the present study was to investigate the pituitary-thyroid axis function during the long-term (30 days) intramuscular administration of 4 mg/day of thyrotropin-releasing hormone tartrate (TRH-T) in 15 patients with spinocerebellar degeneration. The study was performed as follows: (1) acute 4 mg TRH-T test with hourly prolactin (PRL) and thyroid-stimulating hormone (TSH) level evaluations for 6 h; (2) placebo; and (3) 4 mg/day of TRH-T administration for 30 days with TSH, PRL, and free T3 and T4 (FT3 and FT4) levels evaluated on days 1, 15 and 30. Hormone determination was performed just before and 1 h after placebo or TRH-T administration. The acute administration of TRH-T caused a sustained rise of TSH which lasted until the 6th hour and of PRL which declined after 1 h (p < 0.01). During placebo administration, no change of TSH, PRL, FT3 or FT4 was observed. On the 1st day of treatment, 1 h after the TRH-T injection, a significant increase of both TSH and PRL levels occurred (p < 0.01). As compared to the 1st day, a significant decrease of the TSH (p < 0.01) levels occurred on the 15th and 30th days before TRH-T: the TSH response to TRH-T administration was present although less than on the 1st day (p < 0.01). Moreover, throughout the whole period of treatment, no difference was recorded for PRL levels before or after TRH-T administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dopamine control of aldosterone secretion in end-stage renal failure

The role of the tonic inhibitory effect of dopamine on aldosterone secretion has been investigated in 10 patients with chronic renal failure (CRF) on hemodialysis, in 8 normotensive renal transplant recipients (Tx) with normal renal function and in 8 normotensive volunteers (NV). The following tests were performed: the response of plasma aldosterone (PA) to metoclopramide administration; the response of plasma prolactin (PRL) to TRH administration, and the changes induced by Lisuride (a dopaminergic agonist, on the values of PA and PRL). The basal values of PA and PRL were higher in CRF than in NV and Tx. The inverse was true for plasma renin activity (PRA) values. The response of PA and PRL to metoclopramide showed blunted increases in CRF when compared to NV, in the absence of changes of PRA, cortisol and potassium. After TRH administration, PRL increase in CRF was also inferior. Lisuride induced a decrease of both PA and PRL both in CRF and NV. In Tx, basal values of PA and PRL were similar to NV. Nevertheless, the response to metoclopramide and TRH were partially blunted when compared to that of NV. These results point to the existence of a deranged dopaminergic regulation of aldosterone secretion in end-stage renal failure patients. The alterations are partially corrected by a well-functioning kidney graft.     

Effect of alpha-human atrial natriuretic polypeptide on anterior pituitary function in men

In order to examine the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on the basal plasma concentrations of GH, TSH, LH, FSH and PRL in humans, synthetic alpha-hANP was infused into 10 normotensive, euvolemic, healthy volunteers. There were observed marked hypotensive, diuretic and natriuretic effects during the alpha-hANP infusion. The basal plasma concentrations of GH, TSH, LH and FSH, showed no significant change following the alpha-hANP infusion. However, significant suppression of the plasma PRL concentration was observed with the alpha-hANP administration. The mean plasma PRL concentration tended to be decreased during 20 min of alpha-hANP infusion, however, there the differences were not statistically significant. A significant reduction in the mean plasma PRL concentration (-20%, P less than 0.5) was observed 10 min after the end of infusion, following the reversion to the preinfusion level at 70 min after the end of infusion. Such a significant and delayed suppression was not seen in the case of placebo infusion. The data suggest that the circulating hANP may reduce the release of PRL.     

Functional evaluation of the adenohypophysis with metoclopramide in hyperprolactinemic-amenorrheic women in relation to radiological findings on the sella turcica

The responses of the adenohypophyseal hormones to metoclopramide (MCP) were evaluated in hyperprolactinemic women with various radiological findings on the sella turcica. Serum PRL concentrations significantly increased after MCP administration in normal women, hyperprolactinemic patients with normal sella and patients with microadenoma, but not in macroadenoma patients with and without suprasellar expansion (SSE). The PRL response to MCP administration was significantly lower in hyperprolactinemic patients than in normal women. Serum TSH concentrations significantly increased after MCP administration in each group of subjects. The TSH response to MCP was significantly higher in patients with normal sella and patients with microadenoma than in normal women. However, the responses of PRL and TSH to MCP were not significantly different between patients with normal sella and patients with microadenoma. Therefore, they were not considered useful in distinguishing tumorous from nontumorous hyperprolactinemia. Serum LH concentrations significantly increased after MCP administration in patients with normal sella, patients with microadenoma and macroadenoma patients without SSE, but not in normal women or macroadenoma patients with SSE. The LH response to MCP was significantly higher in patients with microadenoma than in patients with normal sella. Serum FSH concentrations significantly increased after MCP administration only in patients with microadenoma. The different responses of the adenohypophyseal hormones to MCP in hyperprolactinemic women with various radiological findings on the sella turcica may be explained by the difference in the hypothalamic dopamine activity and in the impairment of the hypothalamic-pituitary system due to pituitary tumor.