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Biomedical subjects

B Ambrosi

Publications and source records attributed to B Ambrosi.

At least 73 records · Page 4Linked to original sources
PubMed1988

Addison's disease and empty sella.

A 47-year-old woman affected by Addison's disease, inadequately treated with corticosteroids for 14 yr, was referred to our clinic. As a x-ray of skull revealed an enlarged sella turcica, a more thorough study of hypothalamic-pituitary function and of the sellar region was performed. The normal suppression of high plasma ACTH levels induced by hydrocortisone infusion and the normal pattern of ACTH, TSH, PRL, LH and FSH to appropriate stimuli (CRH, TRH, GnRH) excluded the possible existence of an ACTH-secreting adenoma; the CT scan images showed the presence of an empty sella. The impaired GH rise after GHRH may be attributed to either the empty sella or the adrenal failure. This is the first patient with Addison's disease and empty sella, in whom the hypothalamic-pituitary function has been studied by the administration of four releasing hormones.

Addison Disease↗
PubMed1988

Dopaminergic control of aldosterone secretion is not mediated by atrial natriuretic factor in patients with essential hypertension.

Both dopamine and atrial natriuretic factor (ANF) are known to suppress aldosterone secretion. Since it is possible that dopaminergic mechanisms facilitate ANF release, we investigated the relationship between these two inhibitory systems by comparing the increases in aldosterone induced by metoclopramide, a dopaminergic antagonist, with decreases in ANF. Aldosterone, ANF, prolactin, plasma renin activity, cortisol and potassium were measured before and after the intravenous injection of 10 mg metoclopramide, blood samples being collected at 15-min intervals up to 2 h after the injection. These studies were performed in patients with essential hypertension who were maintained on a constant sodium intake (100 mmol/day), before and after 5 days of treatment with ibopamine, an orally active dopamine analogue. Before ibopamine metoclopramide induced the expected, marked increases in aldosterone and in prolactin, but only minimal, non-significant decreases in ANF. All other humoral parameters, as well as blood pressure and heart rate, were unaffected by metoclopramide. After ibopamine treatment, which caused a transient natriuretic effect, the responses of aldosterone and of ANF to metoclopramide were similar to those observed in control studies, whereas that of prolactin was enhanced. Thus, it appears that the suppressive effect exerted by the dopaminergic tone on aldosterone secretion is independent of ANF both before and after dopaminergic stimulation.

Aldosterone↗
PubMed1988

Loperamide, an opiate analog, differently modifies the adrenocorticotropin responses to corticotropin-releasing hormone and lysine vasopressin in patients with Addison's disease.

Loperamide is a peripheral opiate agonist able to inhibit ACTH secretion. In this work, the interactions between loperamide and two ACTH secretagogues, lysine vasopressin (LVP) and corticotropin-releasing hormone (CRH), were investigated in patients with Addison's disease. After loperamide (16 mg orally) or placebo administration, 5 patients received LVP (0.06 IU/kg i.v. over 1 h) and 6 patients received oCRH (1 micrograms/kg i.v. as bolus). In all patients loperamide induced a significant fall in plasma ACTH levels. LVP increased ACTH levels after both loperamide (from 48 +/- 17.3 to a peak of 95 +/- 21 pmol/l) and placebo (from 231 +/- 59.5 to 365 +/- 86.6 pmol/l): the interaction between treatments and time was not significant. CRH caused a rise in plasma ACTH after both loperamide (from 30 +/- 16.6 to a peak of 108 +/- 31 pmol/l) and placebo (from 98.5 +/- 47 to 211 +/- 61.7 pmol/l): the interaction between treatments and time was significant, and the first phase of CRH-induced ACTH secretion was significantly lower after loperamide. These data demonstrate that loperamide differently modifies the stimulatory action of LVP and CRH on ACTH secretion: namely, LVP and loperamide act in an additive manner, while CRH and loperamide interact in a non additive way. Although these findings might be explained by the involvement of different intracellular ACTH-secreting mechanisms, an influence of loperamide on some suprapituitary factors modulating the ACTH response is suggested.

Addison Disease↗
PubMed1987

Effects of angiotensin II blockade on the responses of the pituitary-adrenal axis to corticotropin-releasing factor in humans.

We investigated the possibility that angiotensin II (ANGII) augments the sensitivity of the pituitary to corticotropin releasing factor (CRF) by comparing, in patients with essential hypertension, the responses of plasma adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin activity to a bolus injection of either 0.5 or 1.0 microgram/kg of synthetic ovine CRF in control conditions and after chronic treatment with the converting enzyme inhibitor captopril to block the formation of ANGII; the effects of CRF were examined up to 4 h after its administration. In control studies, we found that the two doses of CRF induced similar increments in ACTH and cortisol, the levels of which remained elevated throughout the studies; these changes were associated with increments in plasma aldosterone that were dose dependent, less pronounced, and of shorter duration and with a slight decrease in plasma renin activity. Captopril treatment increased basal plasma renin activity and lowered plasma aldosterone while leaving basal ACTH and cortisol unchanged. During converting enzyme inhibition, the responses of ACTH and cortisol to CRF were similar to those observed in control studies, whereas the changes in plasma aldosterone and plasma renin activity were, respectively, smaller and greater. From these results, it appears that during ANGII blockade the sensitivity of ACTH to CRF stimulation is unaffected, whereas that of the adrenals to ACTH is selectively reduced at the level of the zona glomerulosa.

Angiotensin II↗
PubMed1987

Vasoactive intestinal polypeptide enhances ACTH levels in some patients with adrenocorticotropin-secreting pituitary adenomas.

Vasoactive intestinal polypeptide (VIP) was administered (75 micrograms iv over 12 min) to 14 patients with Cushing's disease, 1 patient with Nelson's syndrome, and 8 normal subjects. VIP induced a significant rise of plasma ACTH levels in 6 patients with Cushing's disease, from a baseline of 13.2 pmol/l (9.9-18.5 pmol/l) to a peak of 24.5 pmol/l (7.7-18.9 pmol/l), median and range (P less than 0.05), and in the patient with Nelson's syndrome, from a baseline of 260.9 to 461.3 pmol/l. A significant elevation of cortisol levels was also observed, from a baseline of 567 nmol/l (185-842 nmol/l) to a peak of 727 nmol/l (364-1029 nmol/l); P less than 0.05. No modifications in plasma ACTH and cortisol levels were noticed in the other 8 patients with Cushing's disease, or in the normal subjects. In the responsive patients, the median plasma ACTH level reached after VIP was found to be less than that induced by CRH administration. In 2 of the responsive patients, VIP was injected again after successful microadenomectomy and did not then cause changes in ACTH and cortisol concentration. These data demonstrate that VIP specifically stimulates ACTH release in some patients with corticotropinomas but not in normal subjects; the disappearance of such abnormal ACTH responses after successful adenomectomy suggests the presence of specific VIP receptors only on the adenomatous corticotropes.

Adenoma↗
PubMed1987

Loperamide modifies but does not block the corticotropin-releasing hormone-induced ACTH response in patients with Addison's disease.

The effect of loperamide - a peripheral opiate agonist - on plasma ACTH response to Corticotropin-releasing Hormone (CRH) has been investigated in 6 patients with Addison's disease. After placebo administration CRH induced a marked ACTH increase. After loperamide administration ACTH levels fell to a nadir of 135 +/- 76 pg/ml, and then CRH was still able to induce an ACTH increase; the pattern of ACTH response to CRH was slightly delayed. There was a significant difference between the two ACTH curves after CRH only in the early phase of the response. These data suggest that the inhibitory role of loperamide on ACTH secretion is exerted at supra-pituitary level, although a pituitary site of action can not be excluded.

Addison Disease↗
PubMed1986

Loperamide, an opiate analogue, inhibits plasma ACTH levels in patients with Addison's disease.

The effects of loperamide, an opiate analogue of the piperidine class on pituitary hormone secretion were evaluated in eight patients with Addison's disease. In all patients loperamide administration (16 mg orally) induced a marked fall in plasma ACTH levels (P less than 0.01), without affecting GH, PRL and LH levels. Plasma ACTH concentration fell significantly from 854 +/- 167 pg/ml (mean +/- SEM) to 460 +/- 123 pg/ml at 60 min (P less than 0.01). The inhibition persisted throughout the whole test period, the nadir being reached at 300 min. Low dose naloxone infusion 180 min after loperamide administration caused plasma ACTH to rise from 181 +/- 61 pg/ml to 539 +/- 99 pg/ml (P less than 0.01). The present data suggest that the opiate analogue loperamide is a potent inhibitor of ACTH secretion in patients with Addison's disease, which may be acting on mu receptors, since its effect is blocked by low doses of naloxone.

Addison Disease↗
PubMed1985

Abnormalities of sex hormones in men with systemic lupus erythematosus.

Sex hormone concentrations were studied in 10 men with systemic lupus erythematosus (SLE) before and after HCG stimulation and compared with those of 10 healthy volunteers. The SLE men had significantly lower testosterone/estradiol ratios (before HCG test) and significantly lower mean increases in testosterone after HCG stimulation than the normals. Our findings confirm that there are sexual hormone abnormalities in SLE and suggest that these abnormal patterns may be important in the modulation of immune responses in SLE.

Adult↗
PubMed1985

Persistence of a circadian rhythmicity of glucocorticoid secretion in a patient with Cushing's syndrome: study before and after unilateral adrenalectomy.

A 47-year-old woman affected by Cushing's syndrome due to an adrenal adenoma is described. An altered but rhythmometrically apparent cortisol secretory rhythm was detected using the single-cosinor computation. In fact serum cortisol levels and urinary excretion of 17-OHCS were elevated in the PM hours, particularly between 14:00-18.00 h and 18:00-22:00 h, and normal between 02:00-10:00 h. The patient was cured by unilateral adrenalectomy and one year later the circadian rhythm of corticosteroids secretion was investigated again. A normal rhythm of cortisol secretion and of 17-OHCS urinary excretion was found. Though it may be hypothesized that factors intrinsic to the tumoral adrenal cells were responsible for the rhythmic, but phase-shifted, hormonal release, the cause of the persistent and abnormal cortisol secretory rhythm is unknown.

17-Hydroxycorticosteroids↗
PubMed1985

Human pancreatic growth hormone-releasing factor (hpGRF-44) in acromegaly before and after adenomectomy. Modifications induced by somatostatin (GHRIH) infusion.

The influence of human pancreatic growth hormone-releasing factor (hpGRF-44) on GH secretion was investigated in 15 patients with active acromegaly. Following the administration of hpGRF-44 (1 microgram/kg, iv) mean (+/- SE) serum GH level increased from 22.4 +/- 6.3 ng/ml to 42.9 +/- 8.2. ng/ml (peak, p less than 0.01). The pattern and the magnitude of the GH rises were widely variable and it was possible to identify three types of responses: in fact in 2 cases a very large serum GH rise, eight folds over baseline, was observed, in 7 patients a clear GH stimulation, two-three fold over baseline was noticed and in 6 patients no significant GH modifications were seen. No correlation was found between the response to hpGRF-44 and the existence of abnormal GH responses to dopamine infusion, TRH and dopamine-sulpiride test. In 5 acromegalic patients hpGRF-44 was injected again after transsphenoidal adenomectomy. The magnitude of serum GH response decreased in one hyperresponsive patient, increased in 2 previously unresponsive cases and did not change in the remaining cases. In 6 GH responsive patients hpGRF-44 was injected at 120 min during a 4 hour infusion of somatostatin (GHRIH, 3.33 micrograms/min). GHRIH infusion significantly suppressed GH levels in all the patients and blunted the hpGRF-44 stimulated GH increase. The different patterns of GH response to hpGRF-44 in acromegalic patients suggest a different sensitivity of the adenomatous somatotrophs and a possible contribution by normal GH-secreting cells to hpGRF-44 induced GH response.

Acromegaly↗
PubMed1985

Serum gonadotrophin pulsatile secretion in men with Prl-secreting and non-secreting pituitary tumours.

In order to investigate the possible influence of prolactin (Prl) at the hypothalamic level, serum LH and FSH pulsatility was studied in 16 male patients with prolactinomas, normally LH responders to GnRH (group A): 8 of them were untreated (group A1) and 8 had undergone previous unsuccessful pituitary treatments (group A2). In 7 patients the study was repeated when serum Prl was normalized by bromocriptine treatment (group B). For comparison the secretory pattern of LH and FSH was studied in 6 male patients with non-secreting pituitary tumours (group C). All parameters of LH pulsatile secretion (i.e. arithmetic mean of the single concentration, coefficient of variation from the mean value, frequency of peaks, amplitude of pulses expressed as either absolute or per cent value) were significantly lower in patients of groups A1, A2 and C than in normal subjects and no difference was found between the three groups. Furthermore the 7 patients with prolactinomas studied both before and after bromocriptine-induced Prl normalization showed no difference in all the parameters of LH pulsatility in both conditions. No significant abnormalities of FSH secretory pattern were found in the patients of groups A1, A2, B and C in comparison to normal subjects. In all groups of patients mean serum testosterone basal levels were significantly lower than in normals, while the mean oestradiol-17 beta basal concentration was normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1985

The responses of adrenocorticotrophic hormone and cortisol to insulin-induced hypoglycaemic stress in man are unimpaired during chronic converting enzyme inhibition.

In vitro and animal studies indicate that circulating angiotensin II (ANG II) can stimulate adrenocorticotrophic hormone (ACTH) and cortisol secretion, but it is far from established that ANG II has a physiologically relevant influence on steroidogenesis. We studied the effects of hypoglycaemia induced with insulin injection (0.15 IU/kg) in patients with essential hypertension to answer this question. Hypoglycaemia was induced before and after a short term course of treatment with the converting enzyme inhibitor captopril to obtain a sustained blockade of ANG II formation. Alterations in serum glucose, plasma potassium, plasma ACTH, cortisol, renin activity and aldosterone were examined. In control studies there was a profound fall in serum glucose and plasma potassium after insulin, associated with increments in plasma renin activity, which correlated with those of aldosterone but not with those of ACTH and cortisol. Chronic captopril increased baseline plasma renin activity and lowered baseline aldosterone while leaving ACTH and cortisol unchanged. During converting enzyme inhibition the insulin-induced decrements in glucose and potassium, as well as the increments in ACTH, cortisol and aldosterone, were similar to those observed in control studies, whereas the increments in plasma renin activity were much greater. From these results it does not appear that ANG II has a relevant influence on ACTH and cortisol production, or on their responses to hypoglycaemic stress. Rather, these findings indicate that even under the present experimental conditions ANG II is the primary regulator of aldosterone secretion. However, this function can be taken over by ACTH when the generation of ANG II is blocked.

Adrenocorticotropic Hormone↗
PubMed1983

Effects of sodium-valproate administration on plasma ACTH levels in patients with ACTH hypersecretion.

The effects of the acute administration of sodium-valproate (400 mg po) on plasma ACTH levels were studied in 4 patients with Cushing's disease, 1 with Nelson's syndrome and in 3 with Addison's disease. No significant reduction of corticotropin concentration was observed, as compared to saline infusion. These data do not favor the hypothesis of an inhibitory role of sodium-valproate on ACTH secretion in such patients.

Addison Disease↗
PubMed1983

Clinical use of pre- and postsurgical evaluation of abnormal GH responses in acromegaly.

The criteria by which acromegalic patients are considered "cured" after surgical therapy are still controversial. Since the abnormal growth hormone (GH) increase after the administration of some agents has been demonstrated to be characteristic of the tumoral somatotrophs, its disappearance after surgery may be taken as an index of the complete removal of the tumor. Serum GH increases after thyrotropin-releasing hormone (TRH, 200 micrograms intravenously), gonadotropin-releasing hormone (Gn-RH, 100 micrograms intravenously), and sulpiride (100 mg intramuscularly) injected during dopamine infusion (DA-Slp test), were evaluated in 68 acromegalic patients before and after transnasosphenoidal adenomectomy, and every 12 to 18 months during a follow-up period of 6 months to 11 years (average 42 months). Forty-two patients had abnormal responses to at least one test before surgery: 32 out of 68 (47%) to TRH, six out of 40 (15%) to Gn-RH, and 20 out of 28 (71%) to the DA-Slp test. Of 18 patients who underwent all three tests, 78% had abnormal responses to at least one of them. Twenty-three patients became unresponsive after surgery, and none of them had a recurrence or became abnormally responsive again during the follow-up period. Three out of six patients with postoperative serum GH levels between 5.1 and 10 ng/ml and three out of six patients with postoperative serum GH levels between 2.1 and 5 ng/ml remained abnormally responsive: one of them relapsed 1 year after the operation. The abnormal responses were lost in all 11 patients whose postoperative serum GH levels were below 2 ng/ml, and abnormal responses were maintained in all the patients in whom surgery was considered unsuccessful because postoperative serum GH levels were higher than 10 ng/ml. The TRH, Gn-RH, and DA-Slp tests should thus be considered useful tools in verifying the total removal of an adenoma. The reappearance of active acromegaly in the patient with low postoperative GH levels, who was still responsive to TRH, should be regarded as a reactivation and not a true recurrence of the disease.

Acromegaly↗
PubMed1982

Pituitary function before and after transsphenoidal adenomectomy in patients with Cushing's disease.

Over the past 4 years 11 patients with Cushing's disease have been operated on by a transsphenoidal microsurgical technique. All patients had small intrahypophyseal adenomas found at operation. Eight of the 11 patients had a remission of the disease on the basis of clinical evaluation and hormonal studies. The endocrinological results revealed a transient state of hypocorticism in all successfully treated patients. Within 6-8 months after operation recovery of hypothalamic-pituitary-adrenal function and other tropin function took place. These findings, together with the absence of recurrence up to now, further confirm the efficacy of transsphenoidal surgery in the management of patients with Cushing's disease.

Adolescent↗