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PubMed2002

Hemangiopericytoma in the setting of acromegaly.

Acromegaly is associated with an increased incidence of neoplasia thought to be related in part to tonic increases in circulating levels of insulin-like growth factor-1 (IGF-1). Hemangiopericytomas, particularly those occurring in soft tissues, are known to possess IGF receptors. These tumors often behave aggressively and can be recalcitrant to surgery and radiation therapy. A 49-yr-old man presented with an erosive, midline scalp mass and cutis gyrata. Further diagnostic imaging and endocrinologic analysis confirmed two diagnoses: a hemangiopericytoma and acromegaly associated with an intrasellar pituitary tumor. Both the hemangiopericytoma and the pituitary adenoma were surgically resected; Western blot analysis confirmed the presence of IGF-1 receptors in the hemangiopericytoma. Two years later, the patient underwent resection of a right frontal hemangiopericytoma with an identical histologic phenotype and receptor positivity for IGF-1. The occurrence of a central nervous system hemangiopericytoma in patient with acromegaly is rare. Growth and recurrence of hemangiopericytoma may have been fostered by the presence of IGF-1 receptors. Paracrine mechanisms related to IGF-1 may have contributed to its pathogenesis and growth. The presence of IGF-1 receptors in hemangiopericytomas may have treatment implications for additional adjuvant therapies.

Acromegaly↗
PubMedDate not supplied

Growth hormone binding protein and acid labile subunit levels in the assessment of acromegaly treatment.

OBJECTIVE: Post-treatment monitoring of acromegalic patients is a matter of controversy, as discrepancies between GH and IGF-I levels have been reported. The aim of our study was to evaluate the role of acid-labile subunit (ALS), a component of the 150 kD IGF-I/IGFBP-3/ALS complex, and the growth hormone binding protein (GHBP) in the follow-up of patients with acromegaly after therapeutic intervention. DESIGN: Forty-one patients with acromegaly, 10 at the time of diagnosis and 31 post therapeutic intervention, were studied. Patients were evaluated by the determination of baseline (fasting) IGF-I, ALS and GHBP and of glucose and GH during OGTT. RESULTS: Significantly lower ALS and higher GHBP levels were detected in successfully treated acromegalics compared to patients before treatment (34.1+/-1.6 vs. 52.8+/-2 mg/L and 0.9+/-0.08 vs 0.4+/-0.1 ìg/L, respectively P<0.05). Furthermore, no difference was noted in ALS and GHBP values between patients successfully treated with either somatostatin analogues or another type of treatment. CONCLUSIONS: a) Successfully treated acromegalic patients demonstrate lower ALS and higher GHBP levels than patients before treatment, and b) somatostatin analogue treatment does not have a direct effect on GHBP and ALS concentration in acromegaly. Studies in larger groups of patients are needed to disclose whether these alterations will be useful in the post-treatment assessment of acromegalic patients.

Acromegaly↗
PubMed1975

[Comparison with growth hormone responses to various drugs or substances in patients with active acromegaly (author's transl)].

Growth hormone (GH) responses to L-dopa, 2-Br-alpha-ergocryptine (CB-154), thyrotropine-releasing hormone (TRH), luteinizing hormone-releasing hormone (LH-RH), glucagon and glucose were investigated in six patients with active acromegaly. The following results were obtained. 1) Subcutaneous injection of 1 mg glucagon caused a clear-cut decrease in plasma GH levels in 5 out of 6 active acromegalic patients at 30 minutes after the injection. In 2 out of 6 patients a rebound of plasma GH was observed. 2) In three out of six patients with active acromegaly, oral administration of 0.5 g L-dopa caused a significant suppression of plasma GH levels. 3) CB-154 (2.5mg) administered orally elicited a marked decrease in plasma GH levels in the same three patients who showed a significant suppressive GH reponse to L-dopa, and the inhibitory effect of CB-154 on GH secretion lasted for 6 hours. These patients who had a GH response to L-dopa or CB-154 were named "responders". 4) Intravenous administration of TRH resulted in a significant increase in plasma GH in 4 patients 3 of whom were responders and the other a non-responder. 5) Pretreatment with CB-154 did not modify the TRH-induced GH increase in all patients who had a positive response to TRH. 6) A significant increase in plasma GH was elicited by the intravenous injection of 100 mug LH-RH in 3 out of 6 patients with acromegaly. 7) When oral administration of CB-154 had been given 2 hours before LH-RH, the GH response to LH-RH was blunted in two of three patients who had a LH-RH-induced increase in plasma GH levels.

Acromegaly↗
PubMed1987

[Suppression by dopamine of GH release induced by GRF in a case of acromegaly].

Inhibition of plasma GH by dopaminergic agonists is one of the characteristics of the GH secretion in acromegaly. GRF is known to stimulate GH secretion in most patients with acromegaly. In order to elucidate the relationship between GRF and dopamine in regulating the secretion of GH in this disease, we examined plasma GH responses to dopamine (DA) infusion (4 micrograms/kg/min), GRF injection (100 micrograms i.v.), sulpiride (SP) injection (200 mg i.v.), a DA blocker, DA plus GRF and SP plus GRF in a 51-year-old male patient with acromegaly. Plasma GH was reduced to 14% of the initial level by iv infusion of DA, and was elevated to 158% by iv injection of GRF. No considerable change was observed in plasma GH by iv infusion of SP (114% of the initial level). GH release induced by GRF was remarkably reduced by simultaneous administration of DA (28% of the initial level), whereas SP administration did not affect GRF-induced GH release (154%). The marked reduction of GH release after DA plus GRF seems to suggest that the effect of DA on the GH regulation is stronger than that of GRF in this acromegalic patient. It is suggested also that endogenous DA may not play an inhibitory role in GH secretion in this case since DA blockade by SP did not raise basal GH levels and the GH response to GRF.

Acromegaly↗
PubMed1993

Acromegaly with hyperprolactinemia developed after bilateral adrenalectomy in a patient with Cushing's syndrome due to adrenocortical nodular hyperplasia.

A 27-yr-old woman was referred for evaluation of acromegaly and hyperprolactinemia. She had undergone left adrenalectomy at 12 and right adrenalectomy at 17 for Cushing's syndrome due to adrenocortical nodular hyperplasia. At this time a pituitary tumor was found by brain computerized tomography, but plasma levels of growth hormone (GH), prolactin (PRL) and adrenocorticotropin (ACTH) were normal. When she was 23, symptoms and signs of acromegaly and subsequently galactorrhea-amenorrhea had developed. Plasma GH and PRL were increased and she was followed up by the administration of bromocriptine (2.5 mg-12.5 mg/day, p.o.). However the plasma GH level had been increasing gradually. On admission, plasma GH and PRL were high (19.5 micrograms/L, 61.0 micrograms/L, respectively) and increased in response to thyrotropin releasing hormone (TRH, 500 micrograms i.v.). An intrasella mass, which had been detected when she was 17, had become enlarged and was removed by Hardy's operation. Microscopically, the resected tumor was an eosinophilic adenoma. Immunohistochemical studies showed GH, PRL and ACTH positive cells localized in the tumor. Immunoultrastructural analysis of the tumor confirmed that GH, PRL and ACTH were present in secretory granules and Golgi apparatus in the tumor cells. The patient was a rare case of acromegaly with hyperprolactinemia developed after bilateral adrenalectomy of Cushing's syndrome due to adrenocortical nodular hyperplasia, all of which manifestations may be caused by a GH, PRL and ACTH secreting pituitary adenoma.

Acromegaly↗
PubMed1994

Body composition assessed by bioelectrical impedance analysis (BIA) and the correlation with plasma insulin-like growth factor I (IGF-I) in normal Japanese subjects and patients with acromegaly and GH deficiency.

Body composition was assessed by bioelectrical impedance analysis (BIA) in 100 Japanese normal adults, 9 patients with acromegaly and 11 patients with growth hormone (GH) deficiency. Body weight (BW) was greater in normal males than in normal females. Percent body fat (BF/BW) was greater in females than in males and was increased with age in both sexes. Percent total body water (TBW/BW) was less in females than in males. Although percent extracellular water (ECW/BW) was not different between both sexes, the ECW/TBW ratio was greater in females than in males. Percent body cell mass (BCM/BW) was lower in females than in males. The patients with acromegaly had a lower percent BF but a higher percent TBW, percent ECW and ECW/TBW ratio than normal subjects, while the patients with GH deficiency had a higher percent BF and ECW/TBW ratio, but lower percent TBW. Percent body cell mass (BCM/BW) was higher in acromegaly and lower in GH deficiency than in normals. There was a negative correlation (r = -0.62) between plasma IGF-I levels and percent BF, whereas a positive correlation (r = 0.51) was found between the plasma IGF-I level and percent BCM. It is suggested, therefore, that body composition is affected by sex and age in normals, and by GH secretion in patients with pituitary dysfunction. Plasma IGF-I levels may be one of the factors responsible for alterations in body composition.

Acromegaly↗
PubMed1996

Acute promyelocytic leukemia in the course of acromegaly: a case report.

Acromegaly is an uncommon disease due to excessive amounts of growth hormone. Benign and malignant tumors have been reported in acromegalic patients. A 41-year-old female patient who had been followed up because of acromegaly by the endocrinology department for two years, was admitted to the hematology department for the evaluation of pancytopenia and the related signs and symptoms. Dopamine agonists were being used till a diagnosis of 'acute promyelocytic leukemia' was made. Occurrence of 'acute promyelocytic leukemia' in the course of acromegaly may have been caused by excessive endogenous GH or may be a coincidental situation.

Acromegaly↗
PubMed1998

Effects of successful adenomectomy on body composition in acromegaly.

The purpose of the present study was to investigate postsurgical change in body composition in patients who have undergone surgery for acromegaly. Eight patients with acromegaly had determination of serum GH, insulin-like growth factor-I (IGF-I), height, body weight, and bioelectric impedance before surgery and at 2 weeks, 1 month, 3 months, and 6 months after surgery. Body composition was analyzed by bioelectric impedance analysis (BIA). We analyzed body fat (BF), body lean mass (BLM), body cell mass (BCM), total body water (TBW), intracellular water (ICW) and extracellular water (ECW). The serum GH concentration and IGF-I had decreased significantly 2 weeks after surgery. Body weight had decreased significantly 1 month after surgery and recovered 3 months after surgery. BIA showed that TBW and BCM had decreased significantly 2 weeks after surgery. BF gradually increased up to 1 month after surgery and was increased significantly at 3 months after surgery. The percent ratio of TBW/body weight decreased and the percent ratio of BF/body weight increased during the 6 months after surgery. The percent ratio of ECW/TBW did not change during the 6 months following surgery. In conclusion, the rapid body weight loss which occurred within 2 weeks after surgery was caused by decreases in TBW and BCM. The recovery of body weight, which was seen later than 1 month after surgery, was caused by an increase in BF. The postoperative change in body composition in acromegaly ceased 3 months after surgery.

Acromegaly↗
PubMed1999

A case of acromegaly accompanied by adrenal preclinical Cushing's syndrome.

We encountered a 58-year-old woman with acromegaly accompanied by a cortisol-secreting adrenal tumor without clinical features of hypercortisolism. The simultaneous occurrence of these two endocrinopathies in one individual is extremely rare. She was diagnosed as having diabetes mellitus 8 years ago. Afterwards, in spite of insulin therapy, her hyperglycemia could not be well controlled. Her acromegaly and preclinical Cushing's syndrome were histopathologically proven to be due to a pituitary adenoma and an adrenocortical adenoma, respectively. Successful treatment for these endocrinopathies resulted in greatly improved blood sugar control because of a reduction in insulin resistance. In this case of preclinical Cushing's syndrome, replacement therapy with glucocorticoid was able to be discontinued at only 8 weeks after adrenalectomy, so that the period of necessary replacement was much shorter than that for overt Cushing's syndrome. This is the first report describing insulin resistance before and after treatment in a case of acromegaly accompanied by adrenal preclinical Cushing's syndrome.

Acromegaly↗
PubMed2002

A kindred of familial acromegaly without evidence for linkage to MEN-1 locus.

Familial acromegaly (FA) is a rare inherited disease characterized by clustering of somatotrophic adenomas and acromegaly within a family without other manifestations of multiple endocrine neoplasia-type 1 (MEN-1). The genetic basis of this pituitary-specific phenotype is largely unknown, and its relationship to the MEN-1 locus on chromosome 11q13 also remains unclear. To test the hypothesis that FA results from a germline mutation of the MEN-1 locus, we performed a linkage analysis in a Japanese family with 2 members showing manifestations of acromegaly due to somatotroph adenomas. We also examined the adenoma of one patient for loss of heterozygosity (LOH) at 11q13 locus and for the presence of mutations of codon 201 and 227 in the gene for Gsalpha. Our results provided no evidence that either germline alterations of the MEN-1 locus, LOH at 11q13, or somatic mutation of Gsalpha plays a causative role in the development of somatotroph adenomas in our FA family. Together with the previous reports, these results suggest that there are at least two distinct subgroups of FA: one that results from a mutation in MEN-1 locus and the other whose causative gene is located outside the 11q13 locus.

Acromegaly↗
PubMed2006

Acromegaly associated with monoclonal gammopathy of undetermined significance (MGUS).

Here we report the case of a 65-year-old woman with acromegaly complicated with monoclonal gammopathy of undetermined significance (MGUS). The patient visited Shimane University Hospital for treatment of spinal canal stenosis, and was diagnosed as acromegaly with GH 43.1 ng/ml, insulin-like growth factor (IGF)-I 510 ng/ml and the detection of a pituitary adenoma by MRI. She was also diagnosed as MGUS with IgG 2208 mg/dl, the existence of IgG-kappa type monoclonal protein, and 5.6% plasma cells in bone marrow. After a pituitary adenoma was operatively removed by transsphenoidal approach, IgG levels, as well as GH and IGF-I levels, decreased spontaneously and simultaneously. We suspect a pathogenetic link between acromegaly and MGUS in this case, because both GH and IGF-I are known to directly promote immunoglobulin production from plasma cells, thus inducing the proliferation of the cells in vitro.

Acromegaly↗
PubMed1988

Provocation of a paradoxical growth hormone response to corticotropin-releasing hormone by pretreatment with metoclopramide in patients with acromegaly and normal subjects.

Two of 7 patients with acromegaly and one of 7 normal subjects exhibited a paradoxical rise in growth hormone (GH) to human corticotropin-releasing hormone (CRH) when pretreated with metoclopramide, although CRH alone did not induce an increase in GH. In one of these two patients with acromegaly, the GH increase to metoclopramide alone also reached the criteria of a paradoxical response. These two acromegalic patients showed a GH increase to metoclopramide pretreatment before and up to two months after surgery. In another acromegalic patient, whose GH level remained high 5 months after surgery, metoclopramide induced an increase in GH level, while in a patient who had an above-normal GH level 18 months after surgery, the resumption of physiological GH secretion after surgery was evidenced by a postoperative absence of a GH response to metoclopramide. It is suggested from these results that the GH response to metoclopramide and the metoclopramide-provoked GH response to CRH in patients with acromegaly result from the secretion of GH from nonadenomatous cells of the pituitary.

Acromegaly↗
PubMed2004

The role of growth hormone-receptor antagonism in relation to acromegaly.

Acromegaly is a rare but disabling condition associated with reduced life expectancy. It is caused almost invariably by a growth hormone-secreting pituitary adenoma. Transsphenoidal surgery and/or radiotherapy are still considered to be the treatment of choice, but despite recent advances in both these forms of treatment, the overall surgical cure rate remains approximately 60%, and radiotherapy is characterised by delayed effect and a high incidence of hypopituitarism. Medical therapy in the form of dopamine agonists and somatostatin analogues has traditionally been used as an adjunct to surgery and/or radiotherapy, but is increasingly being used as first line therapy in the treatment of acromegaly. Recently, a third form of medical therapy, the growth hormone receptor antagonist, pegvisomant, has been licensed for use in acromegaly. This article examines the design, properties, clinical efficacy and safety of pegvisomant.

Acromegaly↗
PubMed2005

Current pharmacotherapy for acromegaly: a review.

Acromegaly is associated with considerable morbidity and excess mortality; however, after effective treatment, both morbidity and mortality risks improve. Growth hormone excess in acromegaly can be controlled in many patients by pharmacotherapy alone, and with a combination of transsphenoidal surgery and pharmacotherapy in almost all patients. Since the clinical introduction of pegvisomant, a growth hormone-receptor antagonist, the role of radiotherapy is restricted. This review focuses on the treatment options for acromegaly (e.g., surgery, radiotherapy and pharmacotherapy with the depot preparations of the somatostatin analogues octreotide long-acting release formulation, lanreotide slow-release formulation and lanreotide Autogel, the growth hormone antagonist pegvisomant and the dopamine agonist cabergoline). Pharmacological characteristics of these drugs and the clinical and adverse effects are discussed individually and in relation to the other treatment modalities. The evidence for biochemical goals aimed at during medical treatment and the costs of pharmacotherapy are discussed. A new treatment algorithm is proposed, in which the choice between primary medical treatment and primary surgery is individualised, dependent on adenoma size and extension, patient factors (age, preference for therapy, contraindication for surgery), surgical experience of the centre and octreotide sensitivity of the adenoma. The high cost of lifelong medical treatment, especially of pegvisomant, must be weighed against the cost of a single surgical procedure.

Acromegaly↗
PubMed1984

Somatomedin A increments are diminished in acromegaly with concomitant hyperprolactinaemia.

The influence of prolactin (Prl) on growth hormone (GH) regulated somatomedin A (SMA) levels was studied in 30 patients with acromegaly before and after transsphenoidal pituitary surgery. Pre-operative GH levels were elevated in all patients and SMA levels in all but one patient. Eleven patients (33%) showed hyperprolactinaemia. There was no correlation between GH and SMA levels. Plasma GH did not differ in patients with GH and Prl producing adenomas compared to those with isolated GH hypersecretion. SMA levels, however, were significantly lower in patients with hyperprolactinaemia than in those with normal serum prolactin (P less than 0.001). After surgery GH decreased in all and SMA levels in all but one patient. Despite similar post-operative GH levels SMA decreased to significantly lower levels in patients with combined hypersecretion of GH and Prl compared to patients with normal prolactin levels (P less than 0.05). Nine of the 11 patients with hyperprolactinaemia showed normal Prl after surgery. The SMA levels in patients with acromegaly seem to be suppressed in patients with pre-operatively concomitant hyperprolactinaemia before as well as after adenomectomy regardless of the normalization of Prl. Our findings offer one explanation of the lack of correlation between SMA and GH levels in acromegaly.

Acromegaly↗
PubMed1985

Evidence of a circulating growth hormone stimulating factor other than growth hormone releasing hormone in a patient with pituitary tumour and acromegaly.

This study is a report on the growth hormone (GH) stimulatory effect of serum and plasma from a patient with notably active acromegaly due to a GH producing pituitary adenoma. Pituitary adenomatous tissue from 7 patients with GH producing adenomas, one with a prolactin (Prl) producing adenoma, one with a TSH producing adenoma, and one with a non-secreting adenoma, were cultured in vitro for 8-10 days. Media were changed every 48-72 h and contained Neumann Tytell buffer with the addition of 1) foetal calf serum, 2) patients' own serum or plasma, 3) serum or plasma from the patient with notably active acromegaly. GH release expressed as microgram GH/1/48-72 h between day 6 and 8 in culture did not differ when adenomatous tissue was cultured in buffer, foetal calf serum or the patients' own serum or plasma. In contrast, GH release was increased in 9/10 patients, when media contained serum or plasma from the patient with notably active acromegaly. This GH stimulatory effect was demonstrated in vitro in human pituitary adenomatous tissue from patients with pathological as well as normal GH secretion in vivo. Furthermore, this GH releasing plasma in a concentration of 10% increased GH release in cultures of dispersed rat anterior pituitary cells. In the same system, synthetic growth hormone-releasing hormone (GRF)-44 stimulated the release of GH in a dose-dependent manner. However, at all dose levels including maximally stimulating doses of GRF, an additive effect on GH release was seen with 10% of the GH releasing plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1986

Somatostatin, insulin and glucagon after arginine stimulation in active and treated acromegaly.

Ten acromegalic patients, 28-71 years old, were compared with 10 normal controls, 21-39 years old. In another study, 7 patients with active acromegaly, 19-70 years old, were investigated before and 4-9 months following transsphenoidal adenectomy and radiation. They were all investigated following an arginine infusion (0.5 g/kg/20 min). Although the mean plasma somatostatin (somatotrophin release inhibiting factor (SRIF] was somewhat higher in acromegalic patients compared to normal controls (mean basal values 21 +/- 3.8 and 16.6 +/- 2.1 pmol/l, respectively), the difference was not significant. The patients had higher serum insulin (peak values 118 +/- 23.9 and 63 +/- 11.8 mU/l, respectively) and lower plasma glucagon (peak values 171 +/- 29.0 and 310 +/- 52.7 pmol/l, respectively). Plasma SRIF increased during arginine infusion, but the concentrations were similar before and following the operation (mean basal values 18.2 +/- 2.6 and 15.2 +/- 2.3 pmol/l, respectively). Serum insulin was significantly higher before the operation (peak values 154 +/- 38.8 and 91 +/- 24.9 mU/l, respectively). Plasma glucagon was similar before and after the operation (peak values 143 +/- 23.4 and 127 +/- 22.7 pmol/l, respectively). Plasma SRIF is similar in active acromegaly and normal controls, and in acromegaly before and following treatment, despite differences in serum growth hormone (GH), serum insulin and plasma glucagon. This points towards a modulating role for GH on plasma SRIF, possibly by affecting the other islet cell hormones.

Acromegaly↗
PubMed1991

The interaction of GHRH with TRH in acromegaly: a controlled study.

In a single-blind placebo-controlled study, the effect of an iv bolus injection of 100 micrograms GHRH(1-29)NH2 on the response to 200 micrograms TRH was assessed in 10 untreated patients with acromegaly to determine whether GHRH interacts with TRH in acromegaly, as previously described in healthy subjects. The combination of GHRH(1-29)NH2 with TRH resulted in a larger increment of peak and of integrated plasma TSH and PRL levels than after TRH alone. GHRH alone had no effect on TSH secretion and only a modest effect on PRL secretion. These findings suggest that in acromegaly, like in healthy individuals, GHRH potentiates the TSH response to TRH and that the effects of GHRH and TRH on PRL secretion are additive.

Acromegaly↗