Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACROMEGALY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed2001

Regulation of GH secretion in acromegaly: reproducibility of daily GH profiles and attenuated negative feedback by IGF-I.

GH hypersecretion is a hallmark of acromegaly. It is unknown whether the secretory activity of somatotroph adenoma is autonomous or is still governed by central or peripheral mechanisms. In this study we investigated whether GH secretion in acromegaly 1) has a reproducible circadian pattern and 2) is inhibited by exogenous IGF-I. Eleven patients with newly diagnosed acromegaly were studied in 2 protocols. In protocol 1, peripheral blood was sampled every 10 min for 48 h in 6 patients for the determination of concordance between 24-h GH profiles. There was no significant day to day variability in mean 24-h output. There was, however, a significant time effect, and the 24-h GH secretion pattern was maintained between days. In protocol 2, 5 patients were sampled for GH every 10 min twice, once during infusion of normal saline and once during iv infusion of recombinant human IGF-I (10 microg/kg x h). The recombinant human IGF-I infusion increased plasma IGF-I to approximately 230% of the baseline concentration. This resulted in GH suppression (4220 +/- 1950 vs. 3223 +/- 1472 microg/liter.min; P = 0.001), but did not alter GH secretion pattern. There were highly significant cross-correlations for 10 of the 11 of the subjects in the two protocols when the lag was 0 min. By harmonic analysis, nocturnal augmentation of GH was maintained, and maximum daily GH occurred at approximately 2300 h. These data demonstrate that the pattern of GH secretion in acromegaly is not random, but is highly preserved with 24-h periodicity. In addition, negative feedback regulation by IGF-I is preserved, although the degree of negative feedback is grossly attenuated. Thus, secretory activity of somatotroph adenomas is not autonomous or haphazard, but is still subject to both feedback and feedforward regulatory mechanisms.

Acromegaly↗
PubMed2002

Acromegaly with apparently normal GH secretion: implications for diagnosis and follow-up.

The biochemical diagnosis of acromegaly is conventionally based on elevated plasma GH levels that fail to suppress after an oral glucose load. We studied 16 newly diagnosed patients with acromegaly with normal mean plasma GH but elevated age and gender-adjusted plasma IGF-I concentrations (476 +/- 29 microg/liter, mean +/- SE). Plasma GH was sampled every 10 min for 24 h, and an oral glucose tolerance test was performed. The control group included 46 healthy subjects. All patients had 24-h mean GH values that overlapped with those of the healthy controls. Mean plasma GH was less than 2.5 microg/liter in 12 patients. Patients had higher 24-h nadir GH values than healthy controls (P < 0.001). During the oral glucose tolerance test, nadir plasma GH was less than 1 micro g/liter in eight patients. Plasma IGF-I normalized in 11 of 14 patients after transsphenoidal surgery. Four patients with normal IGF-I after transsphenoidal surgery were restudied. Mean and nadir GH decreased in all of them. In our experience in many patients with acromegaly, the diagnosis could be missed if only the existing GH-based criteria are used. Revised GH criteria in combination with plasma IGF-I should be used for the diagnosis and follow-up of acromegaly.

Acromegaly↗
PubMed1994

Voice changes in acromegaly.

The fundamental frequency of 14 patients undergoing hypophysectomy was studied. Eight patients had acromegaly, 3 had a prolactinoma, and 3 had nonfunctioning adenomas. The fundamental frequency of 22 normal, healthy volunteers was measured for comparison. In addition, the external size of the larynx of all patients and volunteers was measured and a relationship between external laryngeal size and the mean fundamental frequency was identified in the volunteers. The mean fundamental frequency in patients with acromegaly was significantly lower than the other 6 patients undergoing hypophysectomy and, in addition, was also lower than the 22 normal volunteers. Postoperatively the fundamental frequency of the acromegalic patients increased rapidly to within the expected normal range. Patients with acromegaly have a lowered fundamental frequency which is most likely due to altered vocal cord mass and elasticity, which is a reversible change. Patients with acromegaly can expect a rapid and complete return of normal fundamental frequency within 2 weeks of surgery to remove the pituitary adenoma.

Acromegaly↗
PubMed2003

Somatostatin analogs in medical treatment of acromegaly.

Although acromegaly remains a disease primarily addressed by pituitary microsurgery, most patients require secondary treatment for persistent growth hormone (GH) hypersecretion and elevated serum insulin-like growth factor-1 (IGF-1) concentrations following adenomectomy. Persistently abnormal serum GH and IGF-1 can be reduced to normal concentrations in better than half of post-surgery acromegalics using the pharmacologic treatments available at present, the dopamine agonists (DA) and somatostatin (SST) analogs. The long-acting SST analogs octreotide LAR and lanreotide SR have become the mainstay of medical treatment for acromegaly, having largely supplanted DA agents since the introduction of bromocriptine for the suppression of GH secretion in the 1970s. The DA cabergoline may be effective in up to half of patients, however, in particular those patients whose tumors cosecrete prolactin. On the horizon is the GH-receptor antagonist pegvisomant, which is expected to enable the reduction of serum IGF-1 to the normal range in the vast majority of postoperative acromegaly patients, representing a revolutionary development in the medical treatment of this disease. We here review the choices available to the endocrinologist in the pharmacologic treatment of acromegaly, focusing upon the SST analogs.

Acromegaly↗
PubMed1991

[The frequency and mechanisms of urolithiasis in acromegaly].

It is generally accepted that acromegaly is often associated with hypercalciuria, but there are few reports on the frequency and the mechanisms of urolithiasis. Recently we consecutively experienced 2 cases of acromegaly with urolithiasis, and these experiences made us investigate the association between urolithiasis and acromegaly. Among 18 acromegalies from 1977 to March 1990 (10 males, 8 females, 24-64 years old), 13 cases (72%) fulfilled the criteria of hypercalciuria (urinary calcium (u-Ca) greater than or equal to 200 mg/day or u-Ca/urinary creatinine (u-Ca/u-Cr) greater than or equal to 0.15), and 7 cases (39%) suffered from urolithiasis that was diagnosed by KUB (4 cases) or X-ray computed tomography (CT) (3 cases). Especially in the last 2 years, 5 out of 7 cases (71%) were complicated with urolithiasis and all 7 cases were associated with hypercalciuria. These results suggest that hypercalciuria and urolithiasis are both much more frequent than previously reported. In 6 cases who were treated by pituitary adenomectomy from 1988-1989 (4 males, 2 females, 24-59 years old), we examined Ca metabolism before and after operation. Before operation, the levels of serum growth hormone (GH), u-Ca (mg/day), u-Ca/u-Cr (in all cases) and plasma somatomedin-C (Sm-C) (in 4 cases) were increased above the normal range. To determine the etiology of hypercalciuria, we performed the oral Ca load test under restriction of Ca (400 mg/day) and P (650 mg/day) intake. The results suggested that the hypercalciuria might be mainly due to the increased absorption of Ca from the intestine (so-called "Absorptive hypercalciuria"). However, the levels of serum vitamin D (Vit. D) metabolites were all within the normal range before operation. After operation, GH and u-Ca/u-Cr (in 5 cases) and u-Ca (mg/day) (in all cases) decreased significantly compared with before operation, and the levels of Sm-C (in all cases), serum 25-(OH)D3, 1 alpha, 25-(OH)2D3 (in 4 cases) and 24,25-(OH)2D3 (in 3 cases) were also reduced after operation. Surprisingly, u-Ca and u-Ca/u-Cr normalized only in 4 cases who showed a reduction in 1 alpha, 25-(OH)2D3 levels after operation, although there were no correlations between u-Ca (mg/day) or u-Ca/u-Cr and 1 alpha, 25-(OH)2D3. Significant correlations were found between u-Ca (mg/day) or u-Ca/u-Cr and Sm-C. The parathyroid function evaluated by the rapid Ca infusion test or nephrogenous cyclic adenosine monophosphate (NcAMP) was normal before and after operation.(ABSTRACT TRUNCATED AT 400 WORDS)

Acromegaly↗
PubMed1995

Hypertension in acromegaly: hereditary hypertensive factor produces hypertension by enhancing IGF-I production.

Sixty-four patients with acromegaly were retrospectively analyzed to study the incidence and cause of hypertension in acromegaly. WHO criteria indicate that 37.5% patients with acromegaly have hypertension. The blood pressure was positively correlated with age, the insulin-like growth factor I (IGF-I) and serum sodium (Na) concentration. In addition, IGF-I and Na were significantly different in hypertensive and normotensive groups. Seventy-five percent of hypertensive patients had a family history of hypertension. IGF-I, Na and blood pressure were significantly higher in patients with a family history of hypertension than in those without it. In patients with a family history of hypertension, blood pressure was positively correlated with IGF-I and serum Na, but IGF-I was not correlated with serum Na. In patients without such a family history, blood pressure had a good correlation only with age, and IGF-I was not significantly correlated with blood pressure. In addition, the incidence of hypertension in this group was the same as or lower than that in the general population. The above results suggest that the genetic factor produces hypertension in acromegaly by two ways, by increasing Na and enhancing IGF-I production by GH.

Acromegaly↗
PubMed1997

Two cases of acromegaly in a family.

We report two cases of acromegaly due to pituitary adenoma without any other endocrinopathy in a family. The patients had high plasma GH and were improved by transsphenoidal adenomectomy. Acromegaly is usually a clinical syndrome of sporadic nonfamilial occurrence. The familial occurrence of acromegaly not associated with multiple endocrine neoplasia is very rare. Our patients are unlikely to be associated with the multiple endocrine neoplasia type 1 syndrome. Here we describe two patients with acromegaly, a father and his daughter, and review familial cases reported.

Acromegaly↗
PubMed1976

The diurnal rhythm of plasma aldosterone, plasma renin activity, plasma cortisol and serum growth hormone and subnormal responsiveness of aldosterone to angiotensin-II in the patients with normotensive acromegaly.

The diurnal rhythm of plasma aldosterone concentration (PA), plasma renin activity (PRA), plasma cortisol (PC) and serum growth hormone (GH) were examined in 5 cases of normotensive acromegaly and the results were compared with the observations in normal subjects. Moreover, the response of PA to angiotensin-II infusion was studied in 6 cases of normotensive acromegaly. A normal diurnal rhythm with the lowest values in the evening or midnight and the highest values in the morning was observed in 3 of 5 cases in PA and 3 of 4 cases in PC. On the other hand, no apparent rhythm of GH was observed in any cases and that of PRA in 4 of 5 cases. Although there was a significant positive correlation between PA and PC, no significant correlation was demonstrated between PA and PRA. The response of PA to angiotensin-II fusion was significantly suppressed in normotensive acromegaly as compared to the normal subjects in spite of normal levels of PRA except for 1 case. The above observations were interpreted to suggest that the aldosterone regulation system is slightly altered in a certain number of patients with normotensive acromegaly in contrast to the normal subjects in which PRA is the main contributing factor. The low PA and suppressed response of PA toangiotensin-II infusion may suggest the defective action of angiotensin-II infusion on the adrenal gland.

Acromegaly↗
PubMed2004

Pegvisomant: a novel pharmacotherapy for the treatment of acromegaly.

Pegvisomant is a pegylated analogue of growth hormone (GH) that functions as a growth hormone receptor antagonist. Clinical trials of its use in acromegaly commenced in 1997; the drug was approved in the US in March 2003 and in Europe in November 2003. In the same year, it was made available on prescription in several European countries, with further launches due in 2004. Pegvisomant is capable of normalising serum insulin-like growth factor-I concentrations (the chief mediator of disease activity in acromegaly) in 97% of patients with active acromegaly, and therapy is associated with a significant improvement in the symptoms and signs of GH excess. Disease control is achievable with pegvisomant in patients who are wholly or partially resistant or do not tolerate somatostatin analogues; preliminary data suggest that the drug may be particularly suitable for patients with acromegaly and co-existent diabetes mellitus.

Acromegaly↗
PubMed2005

Treatment strategies for acromegaly.

Acromegaly is a chronic debilitating disorder caused by a growth hormone (GH)-producing pituitary adenoma. Active acromegaly is associated with a two- to fourfold increased mortality risk, mainly from cardiovascular disease. Transsphenoidal surgery is considered as the treatment of choice because of the rapidity of cure and normalisation of survival. Secondary treatment modalities are radiotherapy and medical treatment, and are important because surgery in the best hands cures only approximately 60% in long-term studies. Medical treatment with slow-release formulations of somatostatin are now widely used, also as primary treatment, and appear to be safe and effective in 50-60% of the patients. However, no data on mortality risk with these drugs is available. Recently, a GH-receptor blocking agent, pegvisomant, was licensed for use in acromegaly and appears to normalise IGF-1 in almost all patients. This article examines the pathophysiology of acromegaly, currently used medicines and their safety and efficacy, and the new drugs that are in development.

Acromegaly↗
PubMed1976

Thyroid function in acromegaly before and after transsphenoidal hypophysectomy followed by cryoapplication.

Thyroid function was studied in acromegaly before and after transsphenoidal hypophysectomy followed by cryoapplication. The clinical material comprised 36 euthyroid, 1 hypothyroid and 3 hyperthyroid patients. In addition to the usual thyroid parameters a standard thyrotrophin-releasing hormone (TRH) stimulation test using 200 mug of synthetic TRH given iv was used. In untreated acromegaly with euthyroidism the response of serum TSH to TRH was significantly less than in normal controls, the increment being 7.1 mU/1 vs. 12.5 mU/1. In 23% of the patients the response was subnormal (less than 3.0 mU/1). The total thyroxine was significantly higher than in controls. Goitre occurred in 53% of the patients. After operation 3 patients became hypothyroid. In 30% of the patients remaining euthyroid the response to TRH was subnormal and the mean response in this group was close to the lower normal limit of 3.0 mU/1. In 7 patients who showed a subnormal response to TRH before or shortly after the operation there was a gradual increase and normalization of the response during the next few years. A subnormal, and also a low normal response to TRH before or after hypophysectomy does not necessarily indicate an increased risk for the development of hypothyroidism, and indeed the pituitary remnant seems to have a remarkable capacity for regeneration. In the hypothyroid patient there was a low normal response to TRH, the reason being unknown. In one of the hyperthyroid patients the basal TSH level was 6.5 and 8.9 mU/1 on two occasions in the thyrotoxic phase, showing a small response to TRH. The possibility that hyperthyroidism was due to increased secretion of TSH is discussed but not claimed proven. The incidence of hyperthyroidism in a large material of acromegaly from this department equals 9% which is above the prevalence of hyperthyroidism in the general population in Finland, indicating that acromegaly in one way or another seems to increase the incidence of manifest thyrotoxicosis.

Acromegaly↗
PubMed1984

Effects of ovine corticotrophin-releasing factor and hydrocortisone on growth hormone secretion by pituitary adenoma cells of acromegaly in culture.

In an attempt to test the hypothesis that pituitary adenomas of acromegaly may possess altered cellular membrane receptors, the response of growth hormone (GH) secretion to ovine corticotrophin-releasing factor (CRF) in cultured adenoma cells of acromegaly was studied. In three out of seven experiments using different pituitary adenoma cells in culture, nanomolar concentrations of CRF caused a significant increase in GH release. The CRF-induced GH release was reproducible and a dose-response relationship was observed between the CRF concentrations and the amounts of GH released into the incubation media. Hydrocortisone, at a concentration of 1 microM, on the other hand, resulted in a significant decrease in GH secretion in four out of five experiments. When adenoma cells were co-incubated with CRF and 1 microM hydrocortisone, CRF-induced GH release was partially overcome. In one experiment, the inhibitory effect of hydrocortisone was reversed by co-incubation with CRF, although CRF alone was ineffective in the stimulation of GH. These results suggest that CRF may stimulate GH release in some, though not all, patients with acromegaly, and that glucocorticoids may block this effect of CRF acting directly on the pituitary adenoma cells of acromegaly.

Acromegaly↗
PubMed1988

Secretion of growth hormone-releasing hormone in patients with idiopathic pituitary dwarfism and acromegaly.

The plasma levels of immunoreactive-GHRH in patients with idiopathic pituitary dwarfism and acromegaly were studied in the basal state and during various tests by a sensitive and specific RIA. The fasting plasma GHRH level in 22 patients with idiopathic pituitary dwarfism was 6.3 +/- 2.3 ng/l (mean +/- SD), which was significantly lower than that in normal children (9.8 +/- 2.8 ng/l, N = 21), and eight of them had undetectable concentrations (less than 4.0 ng/l). Little or no response of plasma GHRH to oral administration of L-dopa was observed in 7 of 10 pituitary dwarfs, and 3 of the 7 patients showed a response of plasma GH to iv administration of GHRH (1 microgram/kg). These findings suggest that one of the causes of idiopathic pituitary dwarfism is insufficient GHRH release from the hypothalamus. The fasting plasma GHRH level in 14 patients with acromegaly and one patient with gigantism was 8.0 +/- 3.9 ng/l, which was slightly lower than that in normal adults (10.4 +/- 4.1 ng/l, N = 72). One acromegalic patient with multiple endocrine neoplasia type I had a high level of plasma GHRH (270 ng/l) with no change in response to L-dopa and TRH test. In 3 untreated patients with acromegaly L-dopa did not induce any response of plasma GHRH in spite of inconsistent GH release, and in 4 patients with acromegaly, TRH evoked no response of plasma GHRH in spite of a marked GH release, suggesting that the GH responses are not mediated by hypothalamic GHRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1990

Cell metabolic activity in acromegaly: a microcalorimetric study of lymphocyte metabolism.

A discrepancy between the clinical impression of disease activity and basal serum levels of growth hormone is often seen in patients with acromegaly. A slightly better relation has been found to serum levels of IGF-I, but a technique for evaluation of cell metabolic activity in this disease is still missing. For this purpose we used microcalorimetry to determine heat production rate in lymphocytes from 15 patients with acromegaly. The mean heat production rate was 2.90 +/- 0.15 pW/cell, significantly higher than in 13 healthy subjects, 2.31 +/- 0.12 pW/cell (p less than 0.01). Heat production rates did not correlate significantly with basal growth hormone levels, but increased, in a statistically significant manner (p less than 0.001), in parallel with the score index used to evaluate the clinical activity of the disease. Using the technique of microcalorimetry we could thus demonstrate an increased metabolic activity at a cellular level in patients with acromegaly, a finding that is in accordance with the view that an increased cell metabolic activity is a component of the disease process in acromegaly.

Acromegaly↗
PubMed1991

Failure to confirm a growth hormone-releasing activity of corticotropin-releasing hormone in acromegaly: comparison with the effects of other hypothalamic hormones.

We re-examined whether CRH stimulates GH secretion in acromegaly. Human CRH (100 micrograms) was given as an iv bolus to 15 patients with active acromegaly, and plasma GH levels were measured before and at intervals up to 120 min after the injection. For comparison, we assessed in all the patients the effects of TRH (500 micrograms), GnRH (100 micrograms), vasoactive intestinal peptide (100 micrograms) and peptide histidine methionine (100 micrograms), which are known paradoxically to stimulate GH secretion in acromegaly. A paradoxical GH response (greater than 50% above the basal) to TRH, GnRH, vasoactive intestinal peptide and peptide histidine methionine was observed in 12 (80%), 4 (27%), 5 (33%) and 2 (13%) patients, respectively. All the patients were responsive to at least one of these 4 peptides. However, none of the patients showed a positive GH response to hCRH. These results do not support a GH-releasing activity of CRH in acromegaly. Even if CRH has such an effect, it does not appear as potent as TRH, GnRH, vasoactive intestinal peptide and peptide histidine methionine. However, the possibility cannot be excluded that our negative data might have been due to the use of hCRH vs ovine CRH in earlier studies.

Acromegaly↗
PubMed1992

Relationship between plasma growth hormone concentration and cellular sodium transport in acromegaly.

We investigated the relationship between mean plasma growth hormone (GH) concentration and cellular sodium transport in untreated and treated acromegaly. Seventeen patients (age 55 +/- 3 years) with active acromegaly were studied with respect to plasma GH (mean of 24 h GH profile) and erythrocyte electrolyte content as well as transmembrane sodium transport. The patients were reinvestigated two weeks after successful surgery (N = 14) and again after one year (N = 13). Erythrocyte electrolytes were analyzed by flame photometry and sodium influx and efflux rate constant determined by in vitro incubation using a modified Keyne's formula. In patients with active acromegaly there was a significant positive correlation between IGF-1 and cellular sodium transport, while GH tended to show a negative relationship to the same parameter. After successful treatment, both IGF-1 and GH disclosed a positive relationship to cellular sodium transport. After one year, a significant increase in erythrocyte sodium content was seen in the patients compared to the preoperative situation. In conclusion, if this is a generalized phenomenon the results are compatible with a sodium-retaining effect of GH via stimulation of transmembrane sodium transport. In active acromegaly this may be counteracted by a sodium transport inhibitor giving the reverse relationship between GH and cellular sodium transport.

Acromegaly↗
PubMed1994

Decreased chemotaxis of neutrophils in acromegaly and hyperprolactinemia.

Both growth hormone (GH) and prolactin (PRL) modulate immune responses in vitro. We studied chemotaxis under agarose of polymorphonuclear cells from patients with acromegaly or hyperprolactinemia. Polymorphonuclear cells were purified by dextran sedimentation and subjected to stimulation with N-formylmethionyl-phenylalanine. The results showed a decrease in both directed migration (acromegaly: 971 +/- 155 microns; hyperprolactinemia: 1123 +/- 137 microns, expressed as mean +/- SEM) and spontaneous migration (acromegaly: 270 +/- 77 microns; hyperprolactinemia: 298 +/- 77 microns) when compared to similar features from normal controls (directed migration: 2019 +/- 99 microns; spontaneous migration: 590 +/- 49 microns) and from patients with non-GH/PRL-secreting pituitary tumours (directed migration: 1633 +/- 282 microns; spontaneous migration: 562 +/- 116 microns), suggesting that this defect is selective for acromegaly and hyperprolactinemia. Our results point to a putative direct or indirect effect of GH and PRL on polymorphonuclear cell chemotaxis.

Acromegaly↗
PubMed2000

Slow-release lanreotide in the treatment of acromegaly: a study in 66 patients.

OBJECTIVE: Slow-release (SR) lanreotide is a long-acting somatostatin analog that has been developed in order to overcome the inconvenience of multiple daily subcutaneous injections of octreotide, required for metabolic control in acromegaly. Lanreotide SR has been found to be well tolerated and effective in reducing GH and IGF-I levels but clinical data are still limited compared with those with subcutaneous octreotide treatment. DESIGN: Sixty-six unselected patients with active acromegaly were therefore evaluated in a multi-center, prospective, open label study. Lanreotide SR was given at a dose of 30mg intramuscular every 7-14 days. METHODS: At baseline and after 2, 4, 8, 12, 24, 36 and 48 weeks patients underwent a clinical examination with assessment of acromegaly related symptoms, and blood was sampled for serum GH, IGF-I, prolactin, glycosylated hemoglobin, fasting glucose, hematology, kidney function and liver function tests. Biliary ultrasonography and pituitary magnetic resonance imaging were performed at baseline and after one year. RESULTS: Treatment resulted in a significant improvement in the symptom score from 2.69+/-0.27 to 1.06+/-0.17 (P<0.0001). Serum IGF-I levels fell from 699+/-38microg/l at baseline to 399+/-26microg/l (P<0.0001, n=60) after one month, after which levels remained stable: 480+/-37microg/l after 6 months (n=54) and 363+/-32microg/l after one year (n=46). GH levels dropped from 13.8+/-3.2microg/l to 4.3+/-0.7microg/l after one month (P<0.0001, n=60) and remained stable thereafter: 3.9+/-0.4microg/l (n=54) after 6 months and 3.5+/-1.1microg/l after one year (n=46). Twenty-nine out of 66 patients (44%) attained a normal age-corrected IGF-I level and 30 patients (45%) attained a GH level below 2.5microg/l. Pituitary adenoma shrinkage of at least 25% was found in 5 of 14 patients (36%) after one year. Side effects were mainly transient gastrointestinal symptoms and pain at the injection site, resulting in drug discontinuation in only 6 patients (9%). Two patients developed new gall stones. No difference was found between subcutaneous octreotide and lanreotide SR in efficacy and almost all patients preferred the easier dose administration of lanreotide SR. CONCLUSIONS: Long-term treatment of acromegaly with SR-lanreotide is effective in controlling GH and IGF-I levels and symptoms and is well tolerated in the majority of patients. Compared with subcutaneous octreotide, lanreotide SR considerably improves patient's acceptance of therapy while having the same overall efficacy.

Acromegaly↗