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PubMed1976

Suppression of plasma growth hormone levels with glucose infusion in patients with acromegaly.

Intravenous glucose infusion which increased blood glucose levels over 27-8 mmo1/1 suppressed plasma GH levels by 41-74% in five acromegalic patients with basal concentrations of less than 20 mu/1, but not in six patients with basal levels over 80 mu/1. Oral 100 g glucose loading had little suppressing effect in both groups. These results appear to indicate that the suppressibility with hyperglycaemia is partially retained or restored in some, if not all, patients of acromegaly with lower GH secreting activity.

Acromegaly↗
PubMed1978

Bromoergocryptin treatment of acromegaly persisting following conventional therapy.

Bromoergocryptine has been used to lower growth hormone concentrations in ten patients with acromegaly in whom previous attempts at pituitary ablation had failed to cure the disorder. Plasma immunoreactive and plasma receptor-reactive growth hormone concentrations together with plasma somatomedin concentrations and urinary excretion of immunoreactive growth hormone were used to assess the response to treatment. Casual immunoreactive hormone concentrations in plasma were lowered to less than 8 mu/l and to less than 5 mu/l during glucose infusion in seven patients, and urinary growth hormone excretion was also brought into the normal range (less than 40 micromicron/12 h) in this group. There was at least a 40% reduction in these measurements in the remaining three patients who had the highest basal hormone concentrations of the group. Plasma somatomedin fell with treatment in eight patients, and intravenous glucose tolerance improved in seven of eight patients tested. Used in modest dosage (up to 15 mg/day) bromoergocryptine can lower plasma and urinary growth hormone and plasma somatomedin concentrations in acromegalic patients in whom previous treatments had decreased but not cured hormone overproduction.

Acromegaly↗
PubMed1979

Acromegaly due to production of a growth hormone releasing factor by a bronchial carcinoid tumor.

We have studied growth hormone production in a patient with a bronchial carcinoid and acromegaly. The absence of growth hormone from the carcinoid tumour was demonstrated by extraction, cell culture and immunoperosidase techniques. Using a linked perfusion culture system, effluent from the bronchial carcinoid tumour culture stimulated a rapid release of growth hormone from a rat pituitary monolayer. This is the first time evidence of growth hormone releasing activity by a bronchial carcinoid has been demonstrated in a production.

Acromegaly↗
PubMed1979

The influence of bromocriptine on serum levels of growth hormone and other pituitary hormones and its metabolic effects in active acromegaly.

The effect of treatment with bromocriptine for 12--18 months on serum GH and metabolic responses was studied in sixteen patients with active acromegaly. Of this group ten patients showing a sustained GH reduction of more than 50% during an 8 h bromocriptine test, proved to be responsive to long-term therapy. In the responding patients GH levels decreased to 38% of the pretreatment level after 12 months of therapy. A dose higher than 10 mg did not produce a significantly greater effect. Prolactin and LH levels decreased in all patients, FSH levels showed a significant rise. Testosterone levels in the male patients increased significantly, indicating that the state of hypogonadism can at least be partially reversed. The GH levels became normal in only one patient. We conclude that the role of bromocriptine in acromagaly is limited and selective pituitary operation and/or irradiation is preferred as definitive treatment in most patients.

Acromegaly↗
PubMed1982

Treatment of acromegaly by trans-sphenoidal operation, 90-yttrium implantation and bromocriptine: results in 230 patients.

Two hundred and thirty patients with acromegaly were diagnosed and treated in a prospective cooperative study in twelve university clinics. Primary treatment was: trans-sphenoidal surgery (152 patients), trans-sphenoidal surgery with additional cryotherapy (eighteen patients), Yttrium-90-implantation (thirty patients), bromocriptine (thirty patients). The results of endocrine assessment before treatment and 6 months after operation, 90-Y implantation or commencement of bromocriptine therapy are reported. The best results (low GH, no or little deterioration of pituitary function, low complication rate) were achieved by trans-sphenoidal surgery, especially in patients with intrasellar tumours (basal GH less than 5 ng/ml in 59.7%). Results were less good with increasing tumour size. Additional cryosurgery was accompanied by a high rate of anterior pituitary insufficiency and is no longer employed. Yttrium-90-implantation resulted in less improvement in GH levels (basal GH less than 5 ng/ml in 51.7% of patients with intrasellar tumours), a high rate of pituitary insufficiency and more complications. Bromocriptine treatment was least effective in lowering GH concentrations (basal GH less than 5 ng/ml in 33% of patients with intrasellar tumours). Different criteria for treatment success were compared. In the entire group, basal GH concentrations below 5 ng/ml were attained in 51.7% of all patients whose values were higher than this prior to treatment. Suppressibility of GH below 2 ng/ml during glucose loading occurred in only 34.9%. An abnormal GH response to TRH/LHRH was present in 47.2% before and in 43.4% after/during treatment. The prognostic significance of this latter finding must be evaluated by further study.

Acromegaly↗
PubMed1983

Lack of rise in serum prolactin following yttrium-90 interstitial irradiation for acromegaly.

We have investigated the possibility that the increase in serum PRL levels observed in patients with acromegaly treated with external irradiation could be due to damage to the hypothalamus or portal vessels, by comparing the effects of yttrium-90 interstitial irradiation, which is highly localised and does not normally extend to the hypothalamus, in a similar series of patients. Sixteen acromegalic patients treated by interstitial irradiation with yttrium-90 are described; GH fell from a mean of 131 mU/l (median 113 mU/l) to 17 mU/l (median 8 mU/l) after one year (P less than 0.001). PRL fell in the five initially hyperprolactinaemic patients (mean fall +/- SD: 39 +/- 17 micrograms/l at one year), but remained unchanged in the normoprolactinaemic group; PRL responsiveness to TRH was retained. Five, out of the seven normoprolactinaemic patients examined, were shown by in vitro studies of their pituitary biopsies, to have tumours that also synthesised or secreted PRL. These results are consistent with the hypothesis that the rise in PRL following external irradiation is the result of damage to the hypothalamus or portal vessels. A less likely explanation is that an overgrowth of radio-resistant PRL-secreting tumour cells is occurring after external irradiation, but not after yttrium-90 implantation.

Acromegaly↗
PubMed1984

Differential TSH and PRL responses to dopamine receptor blockade in acromegaly.

The serum TSH and prolactin responses to dopamine receptor blockade (domperidone 10 mg i.v.) were measured in eight acromegalic subjects and seven normal controls. The serum TSH response was exaggerated in acromegalics when compared to controls (sum of the increments 12.2 +/- 2.8 mU/l and 4.0 +/- 1.2 mU/l respectively P less than 0.05), whereas the serum prolactin response was blunted (sum of the increments 5029 +/- 1377 mU/l and 14 673 +/- 2889 mU/l respectively P less than 0.01). Dopamine receptor blockade did not significantly alter basal growth hormone levels in either group. To ascertain whether this response was merely a reflection of high circulating growth hormone levels six normal controls were pretreated for 24 h with either intramuscular growth hormone (three injections of 4 IU) or an equivalent volume of saline before the administration of domperidone (10 mg i.v.). The serum TSH and prolactin responses were not affected by prior growth hormone treatment. The opposite TSH and prolactin responses to dopamine blockade do not allow any firm conclusions to be made about the level of hypothalamic dopamine activity in acromegaly.

Acromegaly↗
PubMed1985

Are there genetic determinants for the glucose intolerance of acromegaly?

A genetic marker identifying the two parental insulin genes has been studied in 51 Caucasian acromegalics by Southern blot hybridization techniques using a cloned insulin gene probe. Two main DNA insertion classes were detected corresponding to the class 1 and class 3 alleles and thus the following genotypes were found: 1/1, 1/3 and 3/3. The acromegalics were subdivided depending on whether they had a normal (n = 30) or abnormal (n = 21) response to a 50 gm oral glucose tolerance test before treatment. The phenotype frequencies in the former group were 1/1, 43%; 1/3, 53%; and 3/3, 4%; and in the latter group the corresponding figures were 76%, 24% and 0%. The relative incidence of concordance of the phenotype 1/1 with abnormal glucose tolerance in acromegaly was 4.2. This phenotype is also associated with insulin dependent (Type 1) diabetes mellitus.

Acromegaly↗
PubMed1986

The sensitivity of growth hormone and prolactin secretion to the somatostatin analogue SMS 201-995 in patients with prolactinomas and acromegaly.

The somatostatin analogue SMS 201-995 has recently been shown to be effective in suppressing GH secretion in most acromegalic patients. In the present study it was investigated whether PRL release in prolactinoma and acromegalic patients might also be sensitive to SMS 201-995 and whether co-secretion of PRL in acromegaly plays a role in determining the sensitivity of GH secretion to SMS 201-995. The s.c. administration of 50 micrograms SMS 201-995 did not affect high plasma PRL levels in four microprolactinoma patients. Therapy of one of these patients for 3 d with 50 micrograms three times a day also did not affect PRL levels. The single administration of 50 micrograms SMS 201-995 in 22 acromegalic patients lowered plasma GH levels for 2-6 h to less than 5 micrograms/l in 14 patients and to less than 50% of control values in 16 patients. In 18 of these 22 patients the immunohistochemical picture of the pituitary tumour was known. Eleven patients had pure GH-containing tumours and in seven patients there were mixed GH/PRL-containing tumours. In two of these latter patients there was evidence for GH and PRL being secreted by the same tumour cells. The sensitivity of GH secretion to SMS 201-995 did not differ between the patients with pure GH or mixed GH/PRL-containing adenomas. Plasma PRL levels were not affected by SMS 201-995 in the patients with pure GH-secreting tumours, but were significantly suppressed in four of the seven patients with mixed GH/PRL containing tumours. Chronic treatment for 16 weeks of one patient with a mixed GH/PRL-containing tumour with SMS 201-995 (100 micrograms three times a day) resulted in normalization of both the increased GH and PRL levels. It is concluded that SMS 201-995 does not affect tumorous PRL secretion in patients with pure prolactinomas. In acromegalic patients with mixed GH/PRL-containing tumours PRL secretion in some patients is sensitive to SMS 201-995, making these patients good candidates for chronic treatment with the analogue. The simultaneous presence of PRL in the GH-secreting pituitary tumour or the presence of hyperprolactinaemia in acromegalics does not play a role in the sensitivity of GH secretion to the somatostatin analogue.

Acromegaly↗
PubMed1987

The higher the growth hormone response to growth hormone releasing hormone the lower the response to bromocriptine and thyrotrophin releasing hormone in acromegaly.

In acromegaly a direct relationship has been demonstrated between GH responsiveness to TRH and to the dopaminergic agent bromocriptine (Br). Recent data show an inverse relationship between GH responsiveness to Br and to GH releasing hormone (GHRH), but not between the GH responses to GHRH and TRH. Thirty-one acromegalic patients, 18 women and 13 men (age 46.2 +/- (SD) 13 years) were studied. Four patients had been treated, but all still had active disease. The GH responses to GHRH (hpGHRH1-44, Bachem 100 micrograms i.v. bolus), TRH (Thyroliberin, Hoechst 200 micrograms i.v. bolus) and Br (Parlodel 5 mg orally) were assessed in most of the patients. The GH responses to GHRH showed a wide interindividual variation (delta GH 1-995 ng/ml), which correlated significantly with the basal GH levels (r = +0.85, P less than 0.0001, n = 31). GH increments in response to GHRH were inversely related to the responses to Br, i.e. the lower the GH increase after GHRH the greater the GH decrease after Br (r = -0.49, P less than 0.01, n = 30). This decrease correlated with the basal PRL level (r = +0.45, P less than 0.02, n = 29) and also the GH response to TRH (r = +0.66, P less than 0.0001, n = 30). An inverse correlation was also found between the GH responses to TRH and to GHRH (r = -0.43, P less than 0.02, n = 29). The data are consistent with the existence of GH-secreting adenomas which are more sensitive to GHRH and less to Br and TRH (pure somatotroph adenomas) and of mixed (lactotroph-like adenomas) responsive to TRH and Br but less responsive to GHRH.

Acromegaly↗
PubMed1987

Sleep apnoea and daytime sleepiness in acromegaly: relationship to endocrinological factors.

Sleep history and pituitary function were studied and sleep polygraphy performed in 11 acromegalic patients before and after pituitary surgery. Excessive daytime sleepiness or habitual snoring or both together, as well as an elevated fasting level of serum GH occurred in all the patients. In five men but in none of the women an abnormal number of episodes of sleep apnoea were observed. Pituitary adenomectomy improved the apnoea frequency in one patient, whereas in the others the abnormality was still present 1 year later. After operation the fasting level of serum GH became normal in eight patients, two of them with persisting sleep apnoea. The sleep apnoea syndrome is common and clinically important in acromegaly. Its early diagnosis using polygraphic monitoring is emphasized, as it is a treatable disorder.

Acromegaly↗
PubMed1987

Effective long-term treatment of acromegaly with a long-acting somatostatin analogue (SMS 201-995).

Nine acromegalic patients, six previously untreated, were studied before and after 3-15 months of treatment with a long-acting somatostatin analogue (SMS 201-995; 100 micrograms injected s.c. three times daily). During treatment, the mean (+/- SEM) 24-h GH concentration fell from 82 +/- 22 mIU/l to 33 +/- 7 mIU/l (P less than 0.001), and eight of the 9 patients showed a reduction of at least 50% in GH levels in the fasting state and/or during a glucose tolerance test. There was a significant 30% fall in serum concentrations of insulin-like growth factor (IGF-1) with SMS. All patients showed rapid clinical improvement, with diminished sweating and headaches, and reduction in skinfold thickness, hand volumes and finger size. Computer tomographic scanning of the pituitary in eight patients showed no change in the size of the pituitary tumour during treatment. The only side-effects of SMS noted were transient abdominal discomfort and loose stools in two patients on initiating therapy. Although fasting plasma glucose concentration did not change during treatment (5.4 +/- 0.3 vs 5.5 +/- 0.3 mmol/l), mean 24-h plasma glucose concentration was higher with SMS (6.6 +/- 0.5 mmol/l vs 6.0 +/- 0.4 mmol/l; P less than 0.02). Mean 24-h plasma insulin concentration fell from 87 +/- 11 mIU/l before treatment to 39 +/- 6 mIU/l during treatment (P less than 0.005). No change in other anterior pituitary hormones was observed. SMS appears to be a safe, rapidly effective, long-term treatment for certain patients with acromegaly.

Acromegaly↗
PubMed1988

Therapy of acromegaly with sandostatin: the predictive value of an acute test, the value of serum somatomedin-C measurements in dose adjustment and the definition of a biochemical 'cure'.

Fifteen acromegalic patient were treated for a mean of 96 weeks with 200-300 micrograms Sandostatin per day. The mean 24 h GH concentration decreased by 86% from 34.3 +/- 6.6 to 4.8 +/- 0.7 micrograms/l (1 microgram/l = 46 pmol/l). There was a close correlation between the mean GH levels from 2 to 6 h after the acute administration of 50 micrograms Sandostatin and the mean 24 h GH levels after chronic therapy (P less than 0.01). Serum Sm-C levels decreased from 6.9 +/- 0.7 to 2.7 +/- 0.5 U/ml (-61%) and normalized in eight of these 15 patients. There was a close correlation between the Sm-C and mean 24 h GH levels after therapy (P less than 0.001). It is suggested that adjustment of the dose and the number of Sandostatin injections can be made in acromegaly on the basis of the measurement of Sm-C levels during the follow-up. This precludes the need of multiple GH determinations throughout the day and/or night. Biochemical 'cure' (as defined by normalized Sm-C levels) was reached in eight patients in whom mean 24 h GH levels were suppressed to 3.3 micrograms/l or less. The normalization of Sm-C levels was even observed in the presence of two or three GH secretory peaks (never exceeding 7.5-10 micrograms/l) during the 24 h period occurring towards the next Sandostatin injection.

Acromegaly↗
PubMed1989

Failure of long-term cyproheptadine therapy in lowering growth hormone levels in acromegaly.

Basal and post-glucose growth hormone (GH) responses were evaluated in 10 acromegalics receiving cyproheptadine (cypro) 4 mg 6 hourly at 2 and 21 days after initiating therapy. Of the 10 patients, six had macroadenomas with varying degree of suprasellar extensions, one a microadenoma and three had persistent hypersomatotropism despite pituitary adenomectomy due to residual tumour. The basal and post-glucose GH showed no significant change in all, except one with a pituitary microadenoma. His GH was reduced from 680 to 108 mU/L on the second and 82 mU/l on the 21st day of cypro therapy. These data do not suggest any therapeutic role of cypro in the management of acromegaly.

Acromegaly↗
PubMed1990

The influence of octreotide treatment on pulsatile growth hormone release in acromegaly.

The pulsatile release of GH was investigated in eight active acromegalic patients before and during a subcutaneous infusion of 300 micrograms octreotide/24 h for 4 weeks. The number of GH pulses increased from a basal value of 14.4/24h to 16.3/24h during octreotide therapy. At the same time the mean GH concentration, valley concentration, peak height and amplitude decreased significantly. The inhibitory effect of octreotide on pulse characteristics did not depend on the time of day. IGF-I levels also decreased significantly; in five patients normal levels were reached. IGF-I levels correlated significantly with the mean GH level (r = 0.714, P less than 0.001), mean valley concentration (r = 0.697, P less than 0.001) and, to a lesser extent, area under the curve (r = 0.436, P = 0.033), but not the number of pulses. Plasma octreotide levels did not correlate with pulse parameters. In all but one patient a circadian rhythm was present during both the basal study and octreotide therapy. Compared with surgically treated acromegalics, the number of GH pulses was higher in untreated and octreotide-treated patients. This study demonstrates the pulsatile release of GH in active acromegaly both before and during octreotide therapy. This result suggests that endogenous GHRH is important for the generation of GH pulses in this disease.

Acromegaly↗
PubMed1990

Pharmacokinetics of the long-acting somatostatin analogue octreotide (SMS 201-995) in acromegaly.

A single-dose study was performed to examine the pharmacokinetics of subcutaneous octreotide in acromegalic patients and to investigate the relationship between growth hormone and the elimination half-life of the drug. Fourteen acromegalic patients (six men and eight women; age range 35-59 years) who had previously received conventional treatment were studied. Two subjects were on long-term octreotide which had been discontinued 72 h before the study. Octreotide 100 micrograms was administered subcutaneously and plasma samples taken every 10 min for 1 h and then hourly for up to 8 h. Growth hormone was measured at 0, 2 and 8 h. Octreotide was rapidly absorbed with a mean (+/- SEM) t1/2abs of 5.4 min (+/- 0.8) peaking at a mean plasma concentration of 3.4 nmol/l (+/- 0.2) in 27.4 min (+/- 3.7). The monoexponential elimination phase had a mean half-life of 110 min (+/- 9.6). The apparent volume of distribution was 29.4 1 (+/- 1.9) and total clearance was 172 ml/min (+/- 10.4). These results were similar to those obtained in normal volunteers. There was no simple relationship between the level of growth hormone and the half-life of octreotide. Growth hormone levels ranged from 2.5 to 34.0 mIU/l but were only greater than 10 mIU/l in three subjects. Further studies of octreotide pharmacokinetics are needed in untreated patients with acromegaly with raised growth hormone levels.

Acromegaly↗
PubMed1990

Effect of octapeptide somatostatin analogue (SMS 201-995) on plasma 7B2 (a neuroendocrine polypeptide) levels in patients with acromegaly.

We studied the sequential changes of plasma levels of immunoreactive '7B2' (IR-7B2), a neuroendocrine polypeptide, after a subcutaneous injection of 50 micrograms of synthetic octapeptide somatostatin analogue (SMS 201-995) in seven patients with acromegaly due to GH-producing pituitary adenoma. Compared to the basal levels, mean plasma IR-7B2 and GH levels significantly decreased, until 5 and 10 h respectively after the administration of SMS 201-995. The mean (+/- SEM) nadir levels of plasma IR-7B2 and GH were 68.1 +/- 10.1 and 13.1 +/- 6.9%, respectively, compared to mean plasma levels before treatment (100%). Plasma IR-7B2 as well as GH levels did not change significantly when saline was administered subcutaneously to three acromegalic patients. In addition, plasma IR-7B2 levels did not change significantly after the administration of SMS 201-995 in normal subjects or in patients with primary hypothyroidism in whom SMS 201-995 induced a decrease of plasma TSH levels. These results strongly suggest that SMS 201-995 has an unequivocal suppressive effect on the synthesis and/or the secretion of 7B2 in human somatotroph adenoma cells.

Acromegaly↗
PubMed1991

Effects of antibodies against octreotide in two patients with acromegaly.

Two patients developed specific IgG antibodies against octreotide after 2-3 years' treatment for acromegaly with this long acting somatostatin analogue. The presence of these antibodies reduced the plasma disappearance rate of total extractable octreotide by 60 and 80% respectively. When compared to that of non-immune acromegalic patients, the plasma half-life of octreotide in these two patients was 300 and 450 vs 110 min in those with no detectable octreotide antibodies. The sole observed consequence of the immunization was a marked prolongation of the interval of maximum GH inhibition from a mean of 5 to 8 and 10 h in the two patients described after octreotide injection.

Acromegaly↗