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PubMed1976

Epidermal architecture, growth, and metabolism in acromegaly.

Epidermal architecture, replication, and anabolic activity were studied in six patients with acromegaly. Patients with acromegaly had significant larger viable epidermal cells than controls. The rates of incorporation of tritiated thymidine, proline, and histidine into skin slices in vitro was also significantly increased in acromegalic patients. The mean autoradiographic labelling indices after intracutaneous injection of triated thymidine were 8.4% in the acromegalic patients and 5.1% in the control group. None of the changes observed could be closely correlated with levels of serum growth hormone.

Acromegaly↗
PubMed1980

Sleep apnoea in acromegaly.

Day time somnolence or excessive snoring, or both, occurred in five out of 11 patients with acromegaly. All five had episodes of sleep apnoea, and three had the sleep apnoea syndrome. Growth hormone concentrations were higher (p less than 0.025) in these patients than in the six patients without these symptoms. One patient with daytime somnolence and one asymptomatic patient had flow loop evidence of upper airways obstruction. Two of the patients with the sleep apnoea syndrome had cardiomegaly. Sleep apnoea appears to be common and clinically important in acromegaly, and it may be central, obstructive, or mixed. Polygraphic nocturnal monitoring is indicated to assess these patients properly.

Acromegaly↗
PubMed1984

Circulating growth hormone releasing factor concentrations in normal subjects and patients with acromegaly.

A highly specific and sensitive radioimmunoassay was developed for measuring circulating growth hormone releasing factor (GRF) in human plasma. Before measuring immunoreactive GRF plasma samples were extracted on to Vycor glass. Immunoreactive GRF concentrations in plasma samples from 37 fasting normal subjects ranged from less than 10 to 60 ng/l (mean 21 ng/l). Fasting concentrations in 76 out of 80 acromegalic subjects were within the normal range, but the remaining four patients had values of 92 to 25 000 ng/l. Of these, only the patient with the highest concentration had evidence of ectopic GRF secretion from a disseminated carcinoid tumour. Two of the others had longstanding pituitary tumours, and the fourth patient had a pituitary growth hormone (GH) secreting tumour proved by its removal and subsequent remission of acromegaly. There was no correlation between serum GH and plasma immunoreactive GRF concentrations, irrespective of whether the patients were untreated or had been given radiotherapy or dopamine agonists. The assay should help elucidate the physiological role(s) of GRF and may also prove useful in differentiating between pituitary and hypothalamic defects in patients with acromegaly.

Acromegaly↗
PubMed1974

Long-term infusion of growth hormone release inhibiting hormone in acromegaly: effects on pituitary and pancreatic hormones.

Growth hormone release inhibiting hormone (GH-RIH) was infused at a rate of 1.3 mug/min for 28 hours into four patients with acromegaly, two of whom also had clinical diabetes mellitus. Growth hormone and glucagon were suppressed throughout the infusion though delayed secretion of insulin occurred in association with both meals and an oral glucose load. Glucose tolerance was improved in one diabetic patient who was taking chlorpropamide while the other required much less insulin than usual. Secretion of endogenous thyroid-stimulating hormone was lowered in one euthyroid patient on carbimazole. Luteinizing hormone, follicle-stimulating hormone, ACTH, and prolactin were not affected. Serum somatomedin levels were reduced in one patient. There was a rapid rebound of all the suppressed hormones when the infusions stopped. Longer-acting analogues of GH-RIH will be needed before long-term therapy of acromegaly or diabetes mellitus becomes possible, but such preparations should be available soon for clinical trial.

Acromegaly↗
PubMed1993

Postprandial gall bladder motility and hormone release during intermittent and continuous subcutaneous octreotide treatment in acromegaly.

Repeated daily injections of the somatostatin analogue, octreotide (SMS201-995, Sandostatin) are an effective treatment for acromegaly, but lead to gall stone formation in about 50% of cases during longterm treatment. This is probably because of impaired gall bladder contraction. This study examined whether the timing of intermittent injections in relation to meals, or alternatively, continuous 24 hour subcutaneous octreotide infusion (CSOI) might avert adverse effects on gall bladder contraction. In six patients with active acromegaly, gall bladder volume, plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured in the fasting state and after consumption of a fatty meal. Measurements were made on five separate days: (a) without treatment, (b) 45 minutes after 100 micrograms octreotide given subcutaneously, (c) four hours after 100 micrograms octreotide given subcutaneously, (d) eight hours after 100 micrograms octreotide given subcutaneously, and (e) during CSOI of 300 micrograms/24 h for two weeks. Without treatment, postprandial gall bladder contraction was 86.2 (2.1%). Fasting gall bladder volume increased after octreotide injection and was almost doubled during CSOI. Octreotide injections impaired postprandial gall bladder contraction as well as CCK and PP release for at least four hours. Eight hours after injection and during CSOI, postprandial gall bladder contraction was partly restored (43.4% and 50.8% respectively). Postprandial CCK release was normal at eight hours after injection but very low during CSOI. PP release was suppressed by each mode of octreotide treatment. This study indicates that octreotide injections impair postprandial gall bladder contraction for at least four hours. Eight hours after injection and during CSOI, gall bladder contraction is partly restored.

Acromegaly↗
PubMed1995

Effect of octreotide on fasting gall bladder emptying, antroduodenal motility, and motilin release in acromegaly.

Subcutaneous octreotide (Sandostatin) injections lead to gall stone formation in 13-50% of acromegaly patients during one year of therapy. This study explored the effects of octreotide on interdigestive gall bladder emptying, antroduodenal motility, and motilin release. Ambulatory antroduodenal manometry was performed in six acromegaly patients before and after two months of octreotide therapy (100 micrograms thrice daily, subcutaneously). Ultrasonographic gall bladder volume measurements and plasma motilin concentrations were obtained during two migrating motor complex (MMC) cycles. Before octreotide treatment, nine of 26 phase III activities started in the antrum and 17 of 26 in the duodenum whereas during treatment 47 of 48 of phase III activity started in the duodenum (p < 0.05). Before treatment, interdigestive gall bladder emptying (mean (SEM) 39.9 (4.0)% of maximal fasting volume) and plasma motilin peaks preceded antral phase III but not duodenal phase III. During octreotide therapy no significant motilin fluctuation or gall bladder emptying was seen. Fasting gall bladder volume increased from 40.9 (9.1) ml before to 68.0 (14.8) ml (p < 0.05) during octreotide treatment. In conclusion, two months' treatment with octreotide increases the number of duodenal phase III like activity and virtually abolishes antral phase III, plasma motilin peaks, and interdigestive gall bladder emptying. These effects might contribute to the high risk of gall stone formation during longterm octreotide treatment.

Acromegaly↗
PubMed2003

Octreotide represses secretory-burst mass and nonpulsatile secretion but does not restore event frequency or orderly GH secretion in acromegaly.

Octreotide is a potent somatostatin analog that inhibits growth hormone (GH) release and restricts somatotrope cell growth. The long-acting octreotide formulation Sandostatin LAR is effective clinically in approximately 60% of patients with acromegaly. Tumoral GH secretion in this disorder is characterized by increases in pulse amplitude and frequency, nonpulsatile (basal) release, and irregularity. Whether sustained blockade by octreotide can restore physiological secretion patterns in this setting is unknown. To address this question, we studied seven patients with GH-secreting tumors during chronic receptor agonism. Responses were monitored by sampling blood at 10-min intervals for 24 h, followed by analyses of secretion and regularity by multiparameter deconvolution and approximate entropy (ApEn). The somatostatin agonist suppressed GH secretory-burst mass, nonpulsatile (basal) GH release, and pulsatile secretion, thereby decreasing total GH secretion by 86% (range 70-96%). ApEn decreased from 1.203 +/- 0.129 to 0.804 +/- 0.141 (P = 0.032), denoting greater regularity. None of GH pulse frequency, basal GH secretion rates, or ApEn normalized. In summary, chronic somatostatin agonism is able to repress amplitude-dependent measures of excessive GH secretion in acromegaly. Presumptive tumoral autonomy is inferred by continued elevations of event frequency, overall pattern disruption (irregularity), and nonsuppressible basal GH secretion.

Acromegaly↗
PubMed1998

Psychological features of acromegaly.

Acromegaly is a serious but often undiagnosed condition that is often unrecognized for many years. The delay from onset of symptoms until the time of diagnosis results in a unique constellation of physical and mental problems for patients and health care professionals. The purpose of this chapter is to identify the psychological consequences experienced by individuals affected with pituitary tumors which alter growth hormone release. As little research has been completed on the subject, very little is known, or has been applied, in the treatment of these patients. To identify the presence of psychological features, the research which exists and an in-depth qualitative analysis of the personal experience of one of the author (K.F.), having suffered a pituitary macroadenoma with accompanying acromegaly, is described. Our findings are compared with those from an earlier series and the few published reports.

Acromegaly↗
PubMed2003

Acromegaly induced by growth hormone replacement therapy.

Recombinant human growth hormone (GH) has been shown to be efficacious and safe in the treatment of various growth disorders and GH deficiency. We here report a 61-year-old man with idiopathic hypopituitarism in whom clinically active acromegaly developed. Complete GH deficiency had been diagnosed earlier by arginine stimulation testing, and therapy with recombinant human GH (maintenance dose 2 IU/day) was implemented at the age of 54 years. At presentation, the patient's insulin-like growth factor 1 (IGF-1; 439 ng/ml) and insulin-like growth factor binding protein 3 (4.3 mg/l) levels were highly elevated. Endogenous GH production and pituitary adenoma were excluded. Retrospectively, IGF-1 levels up to 621 ng/ml had been documented (but not appreciated) in the preceding 7 years. Upon GH dose reduction, the IGF-1 serum levels returned to normal, and the patient's clinical status stabilized. No GH receptor polymorphisms were identified in the patient's genomic DNA. This observation demonstrates that the indiscriminate use of recombinant GH bears the risk of active acromegaly, emphasizing the need for long-term patient monitoring programs as integral part of GH therapy.

Acromegaly↗
PubMed2004

Treatment of acromegaly.

Mortality is increased in individuals with acromegaly unless serum growth hormone (GH) levels are below 2 microg/l and serum insulin-like growth factor (IGF)-I levels are normal following treatment. These combined criteria have been used to define remission of the disorder in this review. Transsphenoidal surgery achieves remission targets in an average of 55% of patients. For those not in remission following surgery, options include repeat surgery or use of adjuvant therapy. Fractionated external beam pituitary radiotherapy achieves 10-year remission rates of 47% but leaves patients exposed to excess GH until remission occurs. Stereotactic radiotherapy and gamma knife radiosurgery achieve remission rates of 40% over 3 years, and dopamine agonists produce remission in about 20% of patients. Somatostatin analogues induce remission in 59% of patients within the first year of treatment. The GH receptor antagonist pegvisomant leads to remission in 90% of patients, using IGF-I levels for assessment. Optimal treatment for a patient with acromegaly thus depends on the likely efficacy of treatment, cost, surgical skill, severity of side effects, tolerability, control of tumour growth, and improvement in complications related to tumour mass. A primary surgical approach, followed by medical therapy for those not in remission, remains the preferred option in most centres.

Acromegaly↗
PubMed2004

Acromegaly and serum insulin-like growth factor I.

Random levels of growth hormone (GH) are usually not helpful in diagnosing either GH deficiency or GH hypersecretion because GH is secreted in a pulsatile fashion. Insulin-like growth factor I (IGF-I), however, is a good indicator of GH secretion and action, particularly at the level of the liver. There is a good correlation between IGF-I and several clinical indices of acromegaly. Measurements of both IGF-I and GH are cornerstones of biochemical diagnosis and follow-up of acromegaly, although in patients treated with pegvisomant, IGF-I levels should be followed rather than GH levels. IGF-I immunoassays differ in assay design, label, intra- and inter-assay precision, and calibrator or standard used, so IGF-I assays may be difficult to compare with one another. Hence, it is essential that the assays used in the laboratory are well validated and adequate normal ranges are available for the levels to be interpreted in a robust manner.

Acromegaly↗
PubMed2004

Acromegaly and cancer.

In recent years, it has become increasingly recognized that acromegaly is associated with an increased prevalence of colorectal cancer and pre-malignant tubular adenomas. The aetiology of these tumours is unknown but is likely to reflect increased levels of both insulin-like growth factor I (IGF-I), which is implicated in the development of sporadic colorectal cancer, and environmental factors, such as the bile acid deoxycholic acid. There is also evidence to suggest that the prevalence of breast and perhaps haematological malignancies might be increased in acromegaly, although these associations have been based on mostly small epidemiological surveys and clarification will come in the future once large-scale epidemiological studies have been completed.

Acromegaly↗
PubMed2005

Urinary steroid excretion rates in acromegaly.

Using gas chromatography/mass spectrometry, urinary excretion rates of cortisol, cortisone and of various steroid metabolites were determined in 35 acromegalic patients (18 men, 17 women) and in 45 age- and weight-matched controls. The ratio of excreted cortisol/cortisone was similar in acromegalics (0.75 +/- 0.20) and in controls (0.75 +/- 0.24). Hence, the preponderance of the main cortisone-derived metabolite, tetrahydrocortisone, over the main metabolites of cortisol (tetrahydrocortisol and allotetrahydrocortisol; p < 0.01), which was seen both in female and in male acromegalics and which was directly correlated with the postglucose concentrations of growth hormone (r = 0.508, p < 0.01), suggests a decreased activity of 11beta-hydroxysteroid dehydrogenase type 1 in acromegaly. Furthermore, the preponderance of etiocholanolone over androsterone (p < 0.01) in men (though not in women) with acromegaly--the ratio androsterone/etiocholanolone being negatively correlated with the serum concentrations of insulin-like growth factor type 1 (r = -0.406, p < 0.05)--suggests a relatively reduced activity of hepatic 5alpha-reductase in male acromegalics.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed1995

Transnasal stereotactic surgery of pituitary adenomas concomitant with acromegaly.

Since 1960 we have performed stereotactic transsphenoidal cryohypophysectomy in 70 patients with pituitary adenomas, 42 women and 28 men, aged 11-59 years. The dominant clinical syndrome was acromegaly in 50 patients, galactorrhea in 9, amenorrhea in 5, adiposogenital dystrophy in 4 and gigantism with mild endocrine symptomatology in 2 patients. In 67 patients the histological structure of the tumor was established by biopsy (50 patients with eosinophil adenoma, 10 with mixed-type adenoma, 4 with chromophobe adenoma and 3 with basophil adenoma). Somatotropic hormone, human growth hormone, prolactin, ACTH and 17-ketosteroid levels indicated active/inactive adenomas. In 42 cases the adenoma was only intrasellar, which was confirmed by contrast X-ray investigations, CT scanning, angiography and ophthalmological investigation. Transnasal stereotactic cryohypophysectomy was performed in all 70 cases using a stereotactic apparatus especially designed for operations on the pituitary. All patients (except 2) tolerated the operation well. No complications occurred. Vision deteriorated after operation in 1 patient. Thrombosis of the left middle cerebral artery developed in another patient. All the other patients noted improvement directly after operation - rapid diminution of signs of acromegaly and rapid restoration of normal values in hormonal tests. Six patients with continuing growth of the tumor underwent a second operation 1.5-6 years after the first operation. We conclude from our own clinical experience and information from the literature that transnasal stereotactic cryodestruction is highly effective and relatively safe in the management of pituitary adenoma.

Acromegaly↗
PubMed1991

Sleep in acromegaly before and after treatment with adenomectomy.

Daytime somnolence and fatigue are frequently ignored symptoms in acromegaly. To examine whether sleep apnea or other abnormalities in the sleep structure is the underlying cause, 9 young patients with active untreated acromegaly for 2-7 years were studied with all night polysomnography. It revealed a decrease in REM sleep time in all the acromegalics compared to age- and sex-matched normal subjects (p less than 0.001) and also a reduction in delta sleep (p less than 0.05). None had obstructive sleep apnea. At reexamination 12-15 months posttreatment the daytime sleepiness had disappeared in all patients. REM sleep time increased in all patients (p less than 0.001) to normal level; delta sleep time increased moderately (p less than 0.05). Thus sleepiness in patients with high fasting level of growth hormone (GH) is not related to sleep apnea but more likely to a reduced amount of REM sleep time. By normalizing the GH concentration, REM sleep time became normal and the daytime sleepiness disappeared in all patients.

Acromegaly↗
PubMed1980

Reappraisal of bromocriptine treatment for acromegaly.

11 acromegalics were treated with bromocriptine for 2--18 months. Their hormonal response was assessed by an acute suppression test with bromocriptine (AST), an oral glucose tolerance test (GTT), and by measuring growth hormone (GH) concentrations during a day of hospital life. The GTTs and the 24-hour profiles were performed before and after bromocriptine. During the AST all patients showed a decrease of GH concentrations ranging from 33 to 86% of the basal. Following bromocriptine, the mean GH concentration was lowered in 7 out of 11 patients during the GTT, and in 8 out of 11 during the profile, but it was within the normal range in 4 patients only during the GTT, and in 1 during the profile. Bromocriptine normalises radioimmunoassayble GH levels in a percentage of patients (12%) which is less than those following conventional treatment of acromegaly, surgery (80%) and pituitary irradiation (70%). Clinically, however, bromocriptine was more effective than judged by the changes of GH levels. Subjective and objective symptoms of acromegaly, such as articular pain, excessive sweating, hypertension, amenorrhoea, urinary hydroxyproline excretion and heel pad thickness decreased in our patients after bromocriptine. A specific action of bromocriptine on the degradation rate of 'little' GH may result in a selective reduction of the bioactive monomeric component of GH and may explain the discrepancy between the clinical and the biochemical response to bromocriptine. This discrepancy might also be explained by a specific action of bromocriptine on the somatomedin levels.

Acromegaly↗
PubMed1984

Effect of bromocriptine on serum hormones in acromegaly.

Clinical and hormonal responses to bromocriptine therapy were assessed in 10 patients with acromegaly. Although substantial falls (greater than or equal to 50%) in serum GH occurred in only 4 of the patients, subjective clinical improvement and improved glucose tolerance were seen in 9, including 2 subjects in whom serum GH rose in response to bromocriptine. Serum somatomedin levels, measured by both radioimmunoassay and radioreceptor assay, fell in only 2 subjects (both of whom had falls in GH) and did not correlate with clinical status. These results suggest that some of the reported beneficial effects of bromocriptine in acromegaly may be independent of GH secretion or somatomedin generation.

Acromegaly↗
PubMed1987

Normal calcitonin secretion in acromegaly.

Calcium and phosphate metabolism has been studied in eight patients with active acromegaly. Plasma calcium, phosphate, alkaline phosphatase, creatinine and parathyroid hormone levels were in the normal range in all patients, while urinary calcium excretion, calcium/creatinine ratio and hydroxyproline were higher than in controls (p less than 0.01, p less than 0.01, p less than 0.02, respectively). Basal plasma calcitonin levels were in the normal range and stimulation with calcium (3 mg/kg body weight in 10 min) showed similar calcitonin responses in acromegalic and normal subjects. Our data show that in normocalcemic acromegaly with high bone turnover calcitonin secretion is not abnormal.

Acromegaly↗