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Life-threatening hypoglycemia following insulin administration to assess growth hormone secretory capacity in children with hypopituitarism is well known. We report hypoglycemic convulsions in a child with congenital hypopituitarism after the administration of clonidine to assess growth hormone reserve.
While bromocriptine is effective in controlling hyperprolactinemia, it is not known if bromocriptine therapy can restore the abnormal regulation of prolactin (PRL) release found in patients with pathological hyperprolactinemia. We report 15 hyperprolactinemic patients treated for a mean duration of 5.5 +/- 0.6 years (mean +/- SE) in whom stimulation tests to assess PRL control mechanisms [thyrotropin releasing hormone (TRH) and metoclopramide] were performed before and at least one month after withdrawal of bromocriptine therapy. The basal PRL level after withdrawal of bromocriptine therapy was significantly lower (p less than 0.001) than that before therapy. All patients had blunted PRL stimulatory responses to TRH and metoclopramide (% delta 16.0 +/- 5.6%) before treatment. After withdrawal of bromocriptine, PRL responses to stimulatory tests were significantly improved in seven patients (termed 'responders', % delta 376 +/- 55%) but remained unchanged in eight patients (termed 'non-responders', % delta 9.2 +/- 3.0%). Basal PRL levels were significantly lower (p less than 0.01) in responders (290 +/- 35 mIU/l) than in non-responders (10360 +/- 6790 mIU/l). Four of the responders have maintained normoprolactinemia and normal stimulated PRL responses for 15 months to three years following cessation of bromocriptine therapy and appear to be in remission. Favourable factors amongst the responders were the female sex, absence of a macroadenoma, and a pre-treatment PRL level below 3000 mlU/l. PRL stimulation tests performed before therapy could not predict which patients would respond. No relationship was found between duration of therapy, or age at presentation, and improvement after bromocriptine.(ABSTRACT TRUNCATED AT 250 WORDS)
Anterior pituitary function tests were performed in 33 patients in the vegetative state, and the results were assessed for correlation with various clinical factors. Radioimmunoassays were employed to measure the secretion of growth hormone and cortisol during insulin tolerance testing (regular insulin, 0.15 to 0.20 U/kg), luteinizing hormone and follicle stimulating hormone under administration of luteinizing hormone-releasing hormone (100 micrograms), and thyroid stimulating hormone and prolactin under administration of thyroid-releasing hormone (500 micrograms). Impairment rate, defined as number of abnormal hormone secretions divided by number of hormones examined, was calculated for each patient. The data were statistically assessed by analysis of variance in terms of disease, sex, age, site of lesion, etiology of vegetative state, duration of illness, brain atrophy as demonstrated by computed tomography, and Hockaday's electroencephalographic (EEG) grade. The results were as follows. 1) The levels of growth hormone, luteinizing hormone, follicle stimulating hormone, cortisol, thyroid stimulating hormone, and prolactin were abnormal in 70%, 67%, 45%, 39%, 36%, and 15% of cases, respectively. 2) Anterior pituitary hormone secretion was impaired in all 33 patients, severely in 52%. 3) The impairement rate was significantly increased in patients with ruptured cerebral aneurysms, primary coma, severe brain atrophy, and abnormal EEGs. 4) The impairment rate tended to be higher in long-term vegetative patients. These results suggest that, in the vegetative state, impairment of anterior pituitary function frequently occurs at the onset of disease and worsens over time.
An acquired partial pituitary insufficiency with selective ACTH and GH deficiency was demonstrated in two men aged 47 and 54, for which the clinical course over many years corresponds to Addison's disease. In one of the 2 cases, antibodies to anterior pituitary cell membrane, assayed by an immunofluorescence method with GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse ACTH secreting cell) as antigens, were positive. We also present a 55-year-old man with isolated ACTH deficiency associated with transient GH deficiency. In this case, hydrocortisone replacement corrected his subnormal, pre-therapy GH response to insulin tolerance and glucagon propranolol tests, although there was no response of serum GH to L-dops and arginine stimulation test before therapy. Selective ACTH and GH deficiency are very rare and the finding of transient GH insufficiency in a patient with isolated ACTH deficiency suggests that repeated testing while on hydrocortisone replacement therapy is of great diagnostic importance in order to distinguish between selective ACTH and GH deficiency and isolated ACTH deficiency accompanied by transient GH insufficiency.
We determined 293 plasma-ACTH levels out of 49 patients. In 12 patients with various pituitary diseases 168 samples were collected during a standardized pituitary stimulation test. For this purpose we used the following kits: the DYNOtest ACTH and LUMItest ACTH and Allegro HS-ACTH test. Additionally, morning ACTH levels were analyzed from 49 patients using Allegro HS ACTH test and DYNOtest ACTH. Regarding ACTH concentrations during pituitary stimulation the clinical usefulness of the 3 named tests were comparable. Pair differences of morning ACTH levels were not statistically significant. In a setting of a wide range of ACTH levels all 3 trials proved appropriate for making a diagnosis. Practicability of all 3 tests was similar. For all 3 methods incubation can be done overnight which saves time. Reagents can be reused when frozen immediately after reconstitution.
Plasma ACTH (normal value: 0.16 plus or minus mU/100 ml) was measured in 116 patients with Cushing's syndrome, using a bioassay including dynamic tests and sequential determinations. In 10 patients with adrenal tumors ACTH levels were nondetectable (ND) or low, and usually nonstimulatable. In 10 patients with ectopic ACTH secretion high levels (0.42 plus or minus 0.07 mU/100 ml) were measured. The extracts of 6 tumors yielded an ACTH-like substance. Forty-three patients with Cushing's disease (without pituitary tumor) had, before treatment, a mean ACTH level of 0.18 plus or minus 0.01 mU/100 ml, accompanied by high levels of plasma cortisol (32.1 plus or minus 1.9 mug/100 ml). Irregular nycthemeral variations occurred. ACTH rose to 0.30 mU/100 ml after incomplete adrenalectomy (20 patients) and to 1.14 mU/100 ml after total adrenalectomy (21 patients). Dexamethasone (8 mg per day) suppressed ACTH levels. Metyrapone induced a normal ACTH rise, but at abnormal times. Lysine-vasopressin (LVP) induced an ACTH mean relative increase of 120% before, and of 140% after adrenalectomy (i.e., within the normal range). Six nonadrenalectomized patients with pituitary tumors showed similar abnormalities of ACTH regulation. However, the ACTH rise after LVP was above 500%. When pituitary tumors occurred after adrenalectomy (12 patients) the mean basal ACTH level was 18 mU/100 ml. Dexamethasone induced a 90% decrease, and LVP a 416% increase in ACTH levels. In 6 patients with nodular adrenal hyperplasia, ACTH was undetectable before treatment. After adrenalectomy, ACTH rose to 0.4 mU/100 ml (11 patients) and the increase after LVP was 90%. Five additional patients developed pituitary tumors. These data confirm the abnormalities of ACTH feedback regulation in Cushing's disease. However, even when pituitary tumors occur, ACTH levels can be altered by metyrapone, dexamethasone and LVP. This last test is of particular interest for the detection of pituitary tumors. The follow-up pattern of treated nodular adrenal hyperplasia appears to be very similar to that of Cushing's disease.
The studies aimed at evaluation of pituitary reserve of growth hormone following stimulation with GRF have been carried out in a group of 33 patients (11 women and 22 men, of age between 25 and 62 years) with pituitary tumors. The studied material included cases with pituitary adenoma characterized by excessive secretion of growth hormone (somatotropinoma), prolactin (prolactinoma) or alpha subunits of glycoprotein hormones (alphoma), and those with hormonally inactive adenoma. The GRF stimulation tests were carried out in hospitalized patients after overnight fast between 8.00 and 10.00 a.m. Blood samples for hormonal determinations were taken before the test, and after 15, 30, 60, 90 and 120 minutes following intravenous administration of 100 micrograms of GRF 1-29. Besides growth hormone, also the blood serum concentrations of other pituitary hormones were determined in the patients studied, both in the basal state and during the dynamic tests. In patients with acromegaly the results of the determinations of growth hormone following stimulation with GRF showed considerable individual variability. In 5 cases there was an increase in blood serum growth hormone concentration. No response to GRF was noted in the remaining 8 cases. In adenoma cases of prolactinoma type, growth hormone concentration began to rise already at the 15-th minute of the test in most cases. In three cases of prolactinoma associated with acromegaly no response to GRF was observed. The cases of alphoma-type adenoma were usually characterized by the secretion of pituitary hormones other than growth hormone.(ABSTRACT TRUNCATED AT 250 WORDS)
Prolactin response to various pharmacologic agents was tested and hypocycloidal polytomograms of pituitary sellae were performed in 77 women with galactorrhea. Polytomographic findings of pituitary sellae and the results of hypothalamic-pituitary tests were analyzed retrospectively in 18 patients with pituitary adenoma. Of the patients with pituitary tumor, 94% had abnormal polytomograms of sellae turcica, 89% had serum prolactin levels greater than 160 ng/ml (range, 170 to 264 ng/ml), and 78% showed abnormal response to thyrotropin-releasing hormone (TRH) stimulation test. Transsphenoidal excision of the tumor was complete in all 14 patients with microadenoma (10 mm or less in diameter) but was incomplete in 4 patients with macroadenoma and evidence of extrasellar extension. Galactorrhea ceased and normal ovulatory menses resumed after surgery in all patients with microadenoma. Twenty-five patients received bromocriptine. Twenty-three of them had hyperprolactinemia and 21 had normal sellar polytomograms. Galactorrhea ceased and normal menses occurred in 18; 6 patients conceived. Two patients with abnormal polytomography and euprolactinemia responded to bromocriptine treatment and 1 of them conceived. The findings suggest that serial prolactin levels and hypocycloidal polytomography of sella turcica are helpful in diagnosis of pituitary prolactinomas. The TRH stimulation test is also useful in evaluating these patients. Because the natural course of the prolactinomas and the long-term results of the surgical and pharmacologic treatments are unknown, ideal management has yet to be established.
The time course of the basal level of the thyrotropic hormone (b TSH) and its concentration after thyroliberin (TRH) stimulation was studied in 28 patients with diffuse toxic goiter suffering from severe thyrotoxicosis before the onset of drug therapy, directly before operation, early and long after the operation. The TRH test was shown as a diagnostic test of efficacy of drug therapy. A higher level of b TTH with a lowered reaction to TRH in the first 6 mos. after operation was of compensatory nature requiring no substitution therapy. The restoration of the endocrine axis hypothalamus-pituitary gland-thyroid was noted 1 year after the operation.
The prolactin (PRL) response to thyrotropin-releasing hormone (TRH) was evaluated in 686 patients over a 4-year period. Of the 170 control subjects tested, none had a blunted PRL response to TRH. Eighty patients with prolactinomas documented by surgery were tested. Ninety-five percent (76 of 80) of these patients had an abnormally blunted PRL response to TRH. Of the 87 patients with a prolactinoma who did not undergo surgery, 98% (85 of 87) had a blunted PRL response to TRH. Many patients with other pituitary and hypothalamic diseases (pituitary tumors other than prolactinomas [Cushing's disease, acromegaly, chromophobe adenoma], craniopharyngioma) also had an abnormal PRL response to TRH (79 of 153, 52%). In the majority of patients with hyperprolactinemia due to dopamine antagonist medications, TRH stimulation did not produce a normal rise in PRL. The TRH test may be helpful in confirming the diagnosis of prolactinoma, but it is not a decisive factor in the diagnosis or management of this entity.
Thermoregulation was investigated pre and postoperatively in 5 and only preoperatively in 7 patients with suprasellar pituitary adenomas by exposing them to external cold and heat in a climatic chamber. Five healthy subjects served as controls. Body core and skin temperatures, oxygen consumption, electromyographic activity, skin blood flow and local sweating rates were continuously measured. Threshold temperatures for activation of heat production and heat loss were calculated from these data. Hormone analysis was performed before and after stimulation with releasing factors. In the patients, core temperatures as well as threshold temperatures for heat production and heat loss were elevated by about 0.5 degrees C as compared with controls. This elevation of core and threshold temperatures was achieved, despite a reduced resting metabolic rate, by a reduction of skin blood flow indicated by a low mean skin temperature. After successful operation the thermoregulatory alterations normalized. Serum levels of growth hormone were reduced preoperatively and stimulation by GHRF did not cause an appropriate increase. Prolactin was elevated in 6 patients with prolactinomas, but there was no correlation with changes in thermoregulatory threshold temperatures. Stimulation of the other hypophyseal hormones by the combined anterior pituitary function test revealed a normal hormonal response. Apart from prolactin there were no significant hormonal changes postoperatively. It is concluded that disturbances of temperature regulation are present in patients with suprasellar adenomas, but that they are not detectable by routine clinical methods. These alterations probably depend on a disturbance of hypothalamic function and are reversible by surgery.
OBJECTIVE: Secreting pituitary adenomas are usually not considered a disease of older people. However, in male patients, prolactin-secreting pituitary tumours occur at a similar frequency throughout the entire life span, giving the opportunity to study in this gender the influence of age on the clinical presentation and response to treatment of these tumours. METHODS: We conducted a retrospective study including 9 male patients aged >/=60 (range 60-73) years and 10 aged </=30 (range 17-30) years presenting with a prolactinoma in order to compare clinical presentation, results of pituitary function tests, and response to dopamine agonist therapy between older and younger patients. RESULTS: Four of the 9 elderly as well as the 10 younger patients came to medical attention for typical features of male prolactinomas including visual field defect in 5 (2 elderly), headaches in 2 (1 elderly), impotence in 3 (1 elderly), gynaecomastia and/or galactorrhoea in 2, and arrested puberty in 2. The remaining 5 older people presented for other various reasons: symptoms related to cortisol deficiency in 2, lethargy with clinical signs of hypopituitarism in 1, spontaneous multiple vertebral fractures in 1, and incidental discovery of a pituitary mass in 1. Basal prolactin levels (3,051+/-4,151 vs. 3,365 +/- 4,949 microg/l) and mean tumour diameter (30 +/- 16 vs. 25 +/- 13 mm) were similar in old and young patients. Cortisol deficiency was significantly more frequent in the elderly (n = 6) than in the young (n = 1) patients (p 0.02, Fisher's exact test). Secondary hypothyroidism was found in 2 elderly only, but not in young patients. Sixteen patients (8 elderly) received bromocriptine therapy for at least 6 months with a good tolerance. Normalization of the prolactin levels was achieved in 6 older (75%) and 4 younger patients (50%). CONCLUSIONS: The presentation of a prolactinoma in the elderly man is very heterogeneous and can be misleading. At the time of diagnosis, hypopituitarism is more frequent among older than younger patients despite a similar tumour size. We found dopamine agonists equally effective in the elderly.
A case of a 14-year-old boy with optic hypoplasia and pituitary dwarfism was presented. Eye Examination showed typical hypoplasia of the left optic nerve and mild hypoplasia of the right optic nerve. Except for dwarfism and nystagmus, the appearance of the patient was not unusual. Computed tomography revealed an enlargement of the suprachiasmatic cistern, and the presence of the septum pellucidum. The pituitary function tests revealed complete deficiency in GH, and poor or intermediate secretion in ACTH, TSH, PRL, LH and FSH. Urine volume and specific gravity were normal. Therapy with human growth hormone has been successful. It was indicated that hypopituitarism was probably of hypothalamic origin and early recognition of the syndrome is important in view of the possibility of treating growth retardation in some blind, or near blind children.
The endocrine effect of SMS 201-995, an octapeptide analogue of somatostatin, was assessed during a combined anterior pituitary function test. There was no effect on the extent of hypoglycaemia after intravenous insulin infusion or on the subsequent rate of recovery of plasma glucose. SMS 201-995 administration, however, resulted in a profound and selective suppression of the GH response to hypoglycaemia without affecting the ACTH or cortisol responses. There was also a marked reduction of TSH release in response to intravenous TRH; the prolactin response was unimpaired. The LH response to LHRH was blunted and the FSH response unaffected. SMS 201-995 does not significantly impair the counterregulatory mechanisms in response to hypoglycaemia, and, in particular, the hypothalamic-pituitary-adrenal axis remains intact.
The serum gonadotropin response to LH-RH (100 mug e.v.) in a group of women with various types of amenorrhea was critically evaluated. Most patients responded to rapid LH-RH injection with a significant rise in plasma LH and FSH. In the authors' opinion this response is observed in healthy women as well as in those with lesions, even severe ones, of the pituitary, so that quantification of the response does not supply reliable information on diagnosis and prognosis. On the other hand, a negative response to the injection of 100 mug LH-RH does not necessarily imply a pituitary lesion but is often a sign of altered hypothalamic function which can be diagnosed and in some instances restored by clomiphene administration.
The concentration of luteinizing hormone (LH), of follicle stimulating hormone (FSH), of thyroid stimulating hormone (TSH), of prolactin (Prl) and of growth hormone (GH) was evaluated, in basal conditions and during stimulation tests, in serum of 32 patients with benign prostatic hypertrophy (BPH), of 29 patients suffering from prostatic carcinoma and of a control group of similar age. Significant difference in pituitary Prl secretion was found between the prostatic patients and the control group.
Thyroid and pituitary function tests using hypothalamic releasing factors were performed in seven patients with thalassaemia and secondary haemosiderosis and in a control group of seven healthy subjects. The TSH level in the thalassaemic patients (18.07 +/- 1.10 microU/ml) was higher than in the controls (1.01 +/- 0.14 microU/ml, P less than 0.001). After TRH administration the TSH values increased less than in controls. Serum thyroxine and FT41 values were lower in the group of patients with thalassaemia (76.7 +/- 7.8 nmol/l and 19.3 +/- 2.2) compared to the controls (116.1 +/- 6.9 nmol/l, P less than 0.005 and 38.6 +/- 3.6, P less than 0.001). The basal prolactin values did not differ significantly between the two groups, but after TRH administration the increment was significantly lower in thalassaemics than in controls (P less than 0.005). The basal LH values were lower in the thalassaemic patients (1.37 +/- 0.24 ng/ml) than in the controls (3.23 +/- 0.50 ng/ml) and did not increase significantly after LHRH administration. The FSH values were also lower in the thalassaemic group (0.46 +/- 0.15 ng/ml) compared to the controls (2.06 +/- 0.08 ng/ml, P less than 0.001), and increased only slightly after LHRH administration. We conclude that in thalassaemia pituitary deficiency exists, mostly of gonadotrophs, but possibly also for the thyrotrophs and the lactotrophs. Latent primary hypothyroidism has also been found in the thalassaemic group. The functional abnormalities found in both endocrine glands are best explained as a consequence of coexisting haemosiderosis.
Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. Over the 3 years before the dog's death, the combination of specific pituitary function tests, peptide hormone radioimmunoassays, and visualization of the tumor by use of x-ray computed tomography of the skull, allowed an etiologic diagnosis. Because initial signs of glucocorticoid excess were questionable and adrenolytic therapy was not allowed by the owners, treatment consisted only of administration of synthetic vasopressin, which was successful in the management of the diabetes insipidus.