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PubMed1978

Growth hormone modulation of arginine-induced glucagon release: studies of isolated growth hormone deficiency and acromegaly.

Plasma glucagon and insulin responses to L-arginine were compared in normal controls and patients with isolated growth hormone deficiency and acromegaly. Patients with isolated growth hormone deficiency were characterized by high plasma glucagon response and low plasma insulin response, whereas acromegalic patients showed exaggerated plasma glucagon response and almost normal insulin response. These results suggest that growth hormone is probably required for optimum function of the islets, and since hyperglucagonaemia was observed in both growth hormone deficiency and acromegaly, metabolic disturbances stemming from the respective primary diseases may affect glucagon secretion.

Acromegaly↗
PubMed1978

Acromegaly: insensitivity of the pancreatic alpha cell to hyperglycaemia.

Plasma glucagon levels were determined after 50 g of oral glucose loading in eleven acromegalics and fourteen normal subjects. Basal plasma glucagon levels were significantly elevated in patients with acromegaly, as compared with those in normal subjects. Oral glucose loading caused a decrease in plasma glucagon in normal subjects but not in acromegalics. Since this non-suppressibility of plasma glucagon by orally administered glucose was observed even in acromegalics without diabetes, it is concluded that insensitivity of the pancreatic alpha cell to hyperglycaemia exists in patients with acromegaly as well as in diabetics.

Acromegaly↗
PubMed1978

Evaluation of the results of trans-sphenoidal surgery in acromegaly by assessment of the growth hormone response to thyrotrophin-releasing hormone.

Eighteen acromegalic patients GH-responsive to TRH were reinvestigated following trans-sphenoidal surgery and radiotherapy. Basal serum GH decreased below 10 microgram/1 in thirteen cases; nine of them became GH-unresponsive to TRH 1 month after operation, and another one following conventional pituitary irradiation. Four of these ten patients also showed a normal GH response to L-Dopa after treatment, and five responded normally to insulin-induced hypoglycaemia; two patients had a normal GH secretory pattern after both these stimuli. No recurrences were observed over a follow-up period of 15-80 months among the ten patients who became GH-unresponsive to TRH following operation, while one of the three subjects still responsive to TRH in spite of normalized basal serum GH concentration relapsed 10 months after surgery. Three patients with normalized TRH test following operation were repeatedly reinvestigated over a 3-6 years period and always found unresponsive. The present study shows that the 'paradoxical' GH responses to TRH and L-Dopa frequently disappear after surgery, that complete normalization of GH secretory pattern may rarely be attained, and that the disappearance of GH response to TRH probably indicates satisfactory treatment of acromegaly. These data suggest that the 'paradoxical' GH responses frequently found in acromegaly are dependent on the adenoma per se and not on hypothalamic dysfunction.

Acromegaly↗
PubMed1980

CSF and plasma somatostatin levels in acromegaly.

Cerebrospinal fluid (CSF) and plasma levels of somatostatin have been measured in patients with active acromegaly and the results compared to those obtained in patients with non-endocrine diseases. Plasma levels have also been studied in acromegalics given oral glucose. The mean CSF somatostatin level in twenty patients without endocrine disease was 76 pg/ml (range 46-112) which did not differ significantly from that found in eight acromegalics (mean 87 pg/ml, range 48-160). Plasma somatostatin in twenty-two acromegalic patients on no medical treatment was 43 pg/ml (range 9-113), not significantly different from values in a normal control population. There were no differences in the somatostatin levels of non-diabetic acromegalics. After oral glucose, there was a rise in circulating somatostatin in eleven out of twelve acromegalic patients, and this rise did not differ from that seen in normal subjects. It is probable that altered somatostatin secretion is neither the cause nor the result of acromegaly; however it is possible that local changes in somatostatin concentration which are not reflected in peripheral plasma or CSF levels may occur near the site of its production.

Acromegaly↗
PubMed1980

Bomocriptine treatment of patients with acromegaly resistant to conventional therapy.

Eleven patients with active acromegaly resistant to conventional therapy were treated with bromocriptine for 15 (12--22) months by increasing the daily dose stepwise from 5 to 10--60 mg. A satisfactory response was achieved in all but one of the eight patients, in whom the mean diurnal level of serum GH was less than 50 ng/ml, whereas patients with grossly elevated serum GH levels responded poorly. In the longterm, no overall effects on glucose tolerance or plasma insulin (IRI) levels were observed but the chemical diabetes of three patients ameliorated in two. On the other hand, a dose-dependent acute suppressive effect of bromocriptine on plasma IRI response to oral glucose was observed, suggesting a direct effect of bromocriptine on the release of insulin from beta cells. Bromocriptine seems to be a good alternative in the treatment of patients with acromegaly who have not responded to conventional therapy.

Acromegaly↗
PubMed1981

The effect of bromocriptine on insulin secretion and glucose tolerance in patients with acromegaly.

The oral administration of bromocriptine 5 mg 6-hourly to twelve patients with acromegaly for a mean period of 12 (range 3-27) months significantly reduced whole blood glucose, plasma insulin and plasma growth hormone (GH) concentrations during a 50 g oral glucose tolerance test (OGTT). After this period of treatment, bromocriptine was withdrawn for 48 h resulting in a significant rise in whole blood glucose, plasma insulin and plasma GH concentrations during a repeat OGTT. It is concluded that bromocriptine therapy improves glucose tolerance in acromegaly by suppressing GH secretion and consequently GH-mediated antagonism of insulin.

Acromegaly↗
PubMed1981

Acromegaly and pituitary adenoma with phaeochromocytoma: a variant of multiple endocrine neoplasia.

Two women ahd acromegaly due to a pituitary adenoma associated with phaeochromocytoma. Eight additional patients with this combination of tumours have been described by others. Our first patient had sustained hypertension, mild hypercalcaemia, and elevated basal levels of parathyroid hormone and calcitonin associated with malignant phaeochromocytoma and parathyroid hyperplasia. The second patient had episodic hypertension and normal basal serum calcium, parathyroid hormone, and calcitonin levels with a benign cystic phaeochromocytoma. Four of the ten patients died from causes related to the phaeochromocytoma. Three patients had parathyroid hyperplasia. A separate group of four patients with phaeochromocytoma and pituitary adenoma without acromegaly has also been reported. These fourteen patients probably represent a non-familial variant of the multiple endocrine neoplasia syndrome. Our findings suggest that acromegalic patients with hypertension should be screened for phaeochromocytoma.

Acromegaly↗
PubMed1983

Longterm pergolide treatment of acromegaly.

The effect of pergolide mesylate, a new potent longacting dopamine agonist, was investigated in eight patients with active acromegaly, none of whom had received pituitary irradiation. Patients were assessed at different dose levels for clinical response and biochemical response by measuring mean fasting growth hormone (GH), mean ambulant GH and glucose-induced GH response. Six patients had definite clinical improvement. No major side effects were noted. All patients showed a statistically significant reduction in GH, although in two reduction was not below 75% of pretreatment levels. On 500 micrograms pergolide daily the overall response for the group of eight patients was a reduction of fasting serum GH, mean ambulant GH and of GH response to glucose to 55% of pretreatment values. When the daily dose was increased to 1000 micrograms there was a further significant reduction in GH in some patients; on this dose the response for the group was a decrease in fasting serum GH and mean ambulant GH to 40% of pretreatment values. In three patients GH concentrations of 5 mU/l or less were achieved. In two patients the daily dose was increased to 1500 micrograms but no extra benefit was obtained. We conclude that pergolide given once daily has a beneficial effect in acromegaly, with significant reduction in serum GH; it promises to be a useful therapeutic agent.

Acromegaly↗
PubMed1984

Growth hormone responsiveness to human pancreatic growth hormone releasing factor in acromegaly: modulatory effects of basal hormone levels and of concomitant somatostatin administration.

Human pancreatic growth hormone releasing factor 1-44 (hpGRF), 100 micrograms was administered as an i.v. bolus injection to eleven patients with acromegaly. The mean serum growth hormone (GH) levels rose (P less than 0.001) from 54 +/- 20 ng/ml to 215 +/- 126 ng/ml (+/- SEM) 20 min after the injection. Although the maximum response of GH levels was highly variable it correlated positively with the individual GH levels (P less than 0.01, Rs = +0.80). Thus the higher the GH levels, the greater the responsiveness to hpGRF. Administration of somatostatin (SRIF), 300 micrograms/h, lowered basal GH levels from 76 +/- 38 ng/ml to 13 +/- 5 ng/ml (P less than 0.01) after 1 h. hpGRF administration during concomitant SRIF infusion also led to highly variable growth hormone responses. The maximum GH responses again correlated positively with the GH level before hpGRF after 1 h of SRIF administration (P less than 0.05, Rs = +0.79). GH responses to hpGRF were completely blocked by SRIF in three out of four patients whose GH levels decreased to normal levels during SRIF infusion. Our data illustrate that the pituitary in acromegaly is normally responsive to both SRIF and hpGRF but at a higher setting of basal GH levels.

Acromegaly↗
PubMed1985

Bromocriptine therapy in acromegaly: effects on plasma GH levels, somatomedin-C levels and clinical activity.

Thirty-one patients with active acromegaly were treated with 10-20 mg bromocriptine daily for a period of 6-9 months. The clinical response was evaluated both by a subjective 'score of symptoms', and by a combined subjective and objective 'clinical and metabolic improvement score' (c-m score). The biochemical response was evaluated both by measurement of the mean of four plasma growth hormone (GH) determinations during the day and by measurement of plasma somatomedin-C (Sm-C) concentration. The clinical response as assessed by both methods showed a better correlation with changes in plasma GH levels (respectively r = 0.33; r = 0.50) than with changes in Sm-C levels (r = 0.20; r = 0.36). The study confirms that in some patients clinical improvement is not accompanied by a decrease of plasma GH concentration. However, it is not possible to identify a subgroup of patients who showed clinical improvement with a decrease of Sm-C levels, but whose plasma GH levels remained constant. It is concluded that measurement of plasma GH levels still appears to be the most useful biochemical assessment of disease activity in bromocriptine-treated acromegaly.

Acromegaly↗
PubMed1986

Depot-bromocriptine treatment for prolactinomas and acromegaly.

Fifteen patients with hyperprolactinaemia and pituitary macroadenomas (5 patients), microadenomas (6 patients), or acromegaly (4 patients) were given a single intramuscular injection of 50 mg bromocriptine bound to polylactic acid microspheres, depot-bromocriptine. None of the patients had any short-term or long-term discomfort from the injection. In the 11 patients with prolactinomas, serum prolactin fell to minimum levels 12-72 h post-injection; nine patients were highly responsive to depot-bromocriptine, with a mean serum prolactin of 12.9% of basal levels 24 h post-injection, rising to 19% at 28 days. Two patients with prolactinomas were resistant to both depot-bromocriptine, and large doses of oral dopamine agonists. Initiating side-effects (nausea, vomiting, symptomatic postural hypotension) were seen in five patients in the first 24 h post-injection, but were minimal or absent thereafter. Five of six patients previously intolerant of oral dopamine agonists were able to be transferred successfully to bromocriptine 5 mg daily at 4 weeks. Of the four patients with acromegaly, raised prolactin levels were successfully lowered to normal for 4 weeks after injection; serum GH was also partially lowered, but returned to baseline levels at 2-4 weeks. In one patient serum GH was resistant to suppression by both depot bromocriptine and high doses of oral bromocriptine. One patient with a large tumour and visual field defects showed a rapid and maintained improvement in visual fields and acuity after depot-bromocriptine, and was successfully transferred to high-dose oral bromocriptine at 4 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1989

Basal and saline-stimulated levels of plasma atrial natriuretic factor in acromegaly.

We have studied plasma ANF before and after a 4-h intravenous infusion of normal saline in eight subjects with active acromegaly and in eight age and sex-matched control subjects. Plasma ANF, serum aldosterone and blood pressure were measured basally and after 2 and 4 h and plasma renin activity basally and after 4 h. Basal plasma ANF was similar in each group (4.4 +/- 1.5 pmol/l (mean +/- SEM) in acromegalic subjects and 5.3 +/- 0.7 pmol/l in controls NS). Plasma ANF did not rise significantly after saline in the acromegalic group (2-h value, 5.9 +/- 0.9; 4-h value, 5.1 +/- 0.9 pmol/l) but did rise significantly in the control group (2-h value, 8.9 +/- 1.9; 4-h value 9.5 +/- 1.3 pmol/l, both values P less than 0.05 vs basal level). The 4-h ANF value was significantly higher in the control group than in the acromegalic group (P less than 0.05). Basal and stimulated serum aldosterone values were similar in the two groups. Plasma renin activity suppressed to a lesser extent in the acromegalic group after 4 h. The facts that basal plasma ANF was not raised in acromegalic subjects and did not respond to saline stimulation demonstrate that an abnormality of ANF control may be an important factor in the aetiology of the expanded sodium status of patients with acromegaly and hence may contribute to the hypertension seen in patients with growth hormone excess.

Acromegaly↗
PubMed1989

Treatment of acromegaly by external irradiation.

Despite the place of hypophysectomy as the primary treatment in acromegaly, external radiotherapy maintains a role as a relatively slow but effective therapy for inadequately treated patients or those unsuitable for operation. Over the last 25 years our radiotherapy regimen has differed from the published series in that we give a larger dose per fraction, with fewer treatments. We have analysed the efficacy and side-effects of this regimen in 27 subjects with acromegaly. Growth hormone levels have fallen by, on average, 27% per year in the first five years, 83% of subjects achieving a basal growth hormone of less than 10 mU/l. The acute and chronic side-effects of irradiation are discussed, including the relevance of estimates of biological potency, for example the Time Dose Fraction (TDF). One patient suffered visual loss that was most likely to be secondary to the radiotherapy. We also report the histological appearances of the pituitary fossa in five subjects previously treated with radiotherapy.

Acromegaly↗
PubMed1990

Low-dose pituitary irradiation for acromegaly.

External radiotherapy has been used as primary treatment for acromegaly in 29 patients and in combination with surgery in 41 patients in whom growth hormone levels remained elevated postoperatively. Fourteen further patients who did not receive radiotherapy have also been studied, four of whom had undergone surgical treatment. Radiotherapy schedules consisted of 20 Gy in eight fractions over 11 days (n = 23) or 35-40 Gy in 15 fractions over 21 days (n = 47). Growth hormone hypersecretion was either unchanged or increased with time in non-irradiated patients. In those patients who underwent radiotherapy, the likelihood of the mean GH level during GTT falling to less than 5 mU/l was unaffected by the total dose of radiation administered. However, patients with a pre-radiotherapy GH level of less than 30 mU/l showed a significantly increased probability of achieving a post- radiotherapy GH level less than 5 mU/l (P = 0.002). Previous surgery, initial serum prolactin and the age or sex of the patient did not predict the successful outcome of radiotherapy. In view of the known dose dependency of radiation-induced hypopituitarism, lower radiation dose schedules (20 Gy; eight fractions in 11 days) can be used in acromegaly with some benefit, especially in younger patients. However, all patients should undergo operative removal of as much GH-secreting tissue as possible, in order to lower GH levels and increase the probability of achieving a cure following radiotherapy.

Acromegaly↗
PubMed1990

Successful treatment by chemotherapy for acromegaly associated with ectopic growth hormone releasing hormone secretion from a carcinoid tumour.

Acromegaly secondary to the secretion of ectopic growth hormone releasing hormone (GHRH) is rare. We have documented the presentation and unusual clinical course of a patient with a disseminated GHRH-secreting bronchial carcinoid tumour associated with acromegaly over a 17-year period. Recurrent widespread metastatic lesions have been treated over a 10-year period by repeated cycles of the nitrosourea CCNU and 5-fluorouracil with evidence of tumour regression and reduction of circulating growth hormone (GH) and urinary 5HIAA excretion. This cytotoxic regimen, which has been well tolerated, may prove valuable in the management of disseminated carcinoid tumours.

Acromegaly↗
PubMed1990

Colon cancer and polyps in acromegaly: increased risk associated with family history of colon cancer.

A cohort of 52 subjects diagnosed with acromegaly in southeastern Michigan and northern Ohio between 1935 and 1985 were followed to determine the incidence of colon cancer and polyps. Medical records were reviewed, subjects or their next-of-kin were interviewed, and screening examinations of the colon were offered to the living patients who were located. Data on demographics, personal histories of cancer and colon polyps, family history of colon cancer, and cure from acromegaly were obtained for both living and deceased subjects. The risk for colon cancer compared to the general population was estimated using standardized incidence ratios (SIRs). The expected number of cases was determined utilizing age, sex and race-specific rates provided by the cancer registry in southeastern Michigan. Among the 52 subjects, one could not be located and nine were deceased, none from colon cancer, with one known to have a history of colon polyps. Of 13 (31%) who declined the screening physical, one had a history of polyps and none reported a history of colon cancer. Two of 29 screened patients were found to have right-sided adenocarcinoma of the colon. Of the entire cohort, eight people (including one deceased) had a current or previous diagnosis of polyps, with five known to be histologically adenomatous. The SIR for colon cancer was 4.7 (95% confidence interval 0.6-17.1). Seven subjects, including the two with detected adenocarcinoma and four of the six living subjects with polyps only, reported a family history of colon cancer. The SIR for the subset of subjects with a family history of colon cancer was 29.1 (95% confidence interval of 3.5-104.6).(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1992

Impact of octreotide, a long-acting somatostatin analogue, on glucose tolerance and insulin sensitivity in acromegaly.

OBJECTIVE: We aimed to investigate the impact of a long-acting somatostatin analogue, octreotide, on glucose tolerance and on insulin sensitivity in acromegaly. DESIGN: We performed a non-randomized controlled trial. PATIENTS: Seven patients with active acromegaly were assessed before and during octreotide therapy given in a dose of 500 micrograms three times daily subcutaneously. MEASUREMENTS: The effects of octreotide on carbohydrate metabolism were assessed by performing a glucose tolerance test and a euglycaemic hyperinsulinaemic clamp. These latter tests were undertaken 8 hours after the last dose, allowing GH and glucagon to return to pretreatment levels during the study. RESULTS: Octreotide significantly reduced (P less than 0.05) mean +/- SEM 12-h GH (from 42 +/- 13 to 10 +/- 3 mIU/I) and IGF-I (from 4.2 +/- 0.5 to 2.1 +/- 0.5 U/ml) concentrations. Glucose tolerance was normalized in four of five patients with impaired glucose tolerance without a significant change in mean insulin concentrations. The improvement in fasting and mean blood glucose during glucose tolerance testing was dependent on the pretherapy blood glucose concentrations (r = -0.95, P = 0.002). The glucose infusion rate during the hyperinsulinaemic (5 U/h) clamp was significantly increased (P less than 0.05, 15.3 +/- 1.8 vs 24.2 +/- 5.4 mumol/kg min) following octreotide treatment. Insulin infusion during the glucose clamp completely suppressed hepatic glucose production during but not before octreotide treatment (7.9 +/- 2.4 vs 0.7 +/- 2.2 mumol/kg min, P = 0.02). Insulin-mediated stimulation of peripheral glucose uptake was unaffected by treatment. Mean GH and glucagon levels during both clamp studies were not significantly different. CONCLUSIONS: Octreotide improves whole body insulin sensitivity by an increased ability of insulin to suppress hepatic glucose production without affecting the substantial impairment of peripheral insulin action. Octreotide has beneficial effects on carbohydrate metabolism in acromegalic patients with glucose intolerance.

Acromegaly↗
PubMed1992

Acromegaly and its treatment in the McCune-Albright syndrome.

The McCune-Albright syndrome, comprising polyostotic fibrous dysplasia, cutaneous pigmentation and endocrine hyperfunction, is occasionally complicated by acromegaly due to a pituitary adenoma. We report a patient with the McCune-Albright syndrome and acromegaly, who developed secondary hypothyroidism and hypoadrenalism, in whom surgical removal of the pituitary tumour was technically difficult. A combination of a long-acting somatostatin analogue ('Sandostatin') and external irradiation were therefore used as treatment.

Acromegaly↗