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Consensus statement: benefits versus risks of medical therapy for acromegaly.

A consensus panel defined the risks and benefits of medical management of acromegaly and determined a place for the use of the somatostatin analogue, octreotide, in the overall management strategy of patients with acromegaly. Octreotide was considered effective in managing acromegaly, and its role as an adjuvant to surgery was defined. Octreotide is beneficial to radiotherapy-treated patients in that the drug suppresses growth hormone (GH) secretion until the long-term effects of radiation occur. Complications associated with octreotide are minor relative to the benefits, but requirements for multiple daily injections and drug cost are drawbacks. Approximately 20% to 30% of octreotide-treated acromegalic patients develop gallstones or sludge, which are usually asymptomatic and require no treatment. Surgery continues to be the principal therapeutic approach for GH-secreting pituitary tumors, and improved octreotide delivery methods and second-generation analogues will provide further advantages for pharmacotherapy.

Acromegaly↗

Efficacy of lanreotide Autogel administered every 4-8 weeks in patients with acromegaly previously responsive to lanreotide microparticles 30 mg: a phase III trial.

OBJECTIVE AND DESIGN: Depot somatostatin analogues are well accepted as either adjuvant or primary therapy for acromegaly, and their long dosage intervals facilitate adherence to treatment. Our objective was to evaluate whether lanreotide Autogel 120 mg, every 4-8 weeks, was as effective in controlling acromegaly as lanreotide microparticles 30 mg, every 1-2 weeks. PATIENTS DESIGN AND MEASUREMENTS: Patients who had used lanreotide microparticles 30 mg, >or= 2 months prestudy, and had responded to treatment were recruited to this open, prospective, multicentre phase III trial. Three to five injections of lanreotide Autogel 120 mg were administered. Lanreotide Autogel 120 mg was injected every 4, 6 or 8 weeks in patients previously receiving lanreotide microparticles every 7, 10 or 14 days, respectively. GH and insulin-like growth factor (IGF)-1 levels were assessed one dosing interval after the final injections. RESULTS: Ninety-eight patients were enrolled and 93 completed. Steady-state GH concentrations demonstrated similar efficacy between the formulations (upper 95% confidence interval of the quotient, 77.7%). Mean (SE) GH levels were lower with lanreotide Autogel than with lanreotide microparticles (3.8 (0.5) vs 4.3 (0.5) ng/ml; P < 0.001). GH levels < 2.5 ng/ml were observed in 54% and 46% of patients; 40% and 35% having GH < 2.5 ng/ml and normalized IGF-1 with lanreotide Autogel and microparticles, respectively. Symptoms were controlled better with lanreotide Autogel and treatment was well accepted. CONCLUSIONS: Lanreotide Autogel 120 mg every 4-8 weeks, is at least as effective and as well tolerated in acromegaly as lanreotide microparticles 30 mg injected every 7-14 days.

Acromegaly↗

The relationship between serum GH and serum IGF-I in acromegaly is gender-specific.

In patients with acromegaly, there is a linear association between log10 serum GH and IGF-I. Healthy females secrete three times more GH than males but have broadly similar serum IGF-I levels, and in adult GH deficiency, the dose of exogenous GH required to achieve a given serum IGF-I is significantly greater in females than males. We report the influence of gender on the relationship between serum GH and IGF-I in subjects with active acromegaly. A single, fasted, serum sample was obtained from 153 subjects with active disease (87 males; median age, 47.8 yr; range, 20-82 yr) in whom serum IGF-I was at least 30% above the upper limit of an age-related reference range after washout from medical therapy. A linear correlation between serum IGF-I and log10 serum GH was observed (r = 0.53; P < 0.0001), but this relationship was significantly influenced by gender. For a given serum GH value, females were estimated to have serum IGF-I values 82 ng/ml less than males [P < 0.02; 95% confidence interval (CI), 15.2-149]. In females receiving oral E, mean serum IGF-I for a given GH value was 130 ng/ml lower than in males (P = 0.01; 95% CI, 29.8-230.2) but only 60 ng/ml less than the remaining 45 females (NS; P = 0.2). This study demonstrates a gender difference in the relationship between serum GH and IGF-I in patients with active acromegaly consistent with relative GH resistance observed in normal and GHD females, which may, in part, be mediated by E. This observation has important implications for the use of IGF-I as a measure of disease activity.

Acromegaly↗

Acromegaly from ectopic growth hormone-releasing hormone secretion by a malignant carcinoid tumor. Successful treatment with long-acting somatostatin analogue SMS 201-995.

A 26-year-old man with acromegaly secondary to ectopic growth hormone-releasing hormone (GHRH) secretion by a metastatic carcinoid tumor is the subject of this study. He previously failed to respond to conventional therapeutic modalities (partial hypophysectomy, pituitary irradiation, high-dose bromocriptine and a combination of streptozotocin and 5-fluorouracil) and was treated with long-acting somatostatin analogue SMS 201-995 (Sandoz, East Hanover, NJ). Growth hormone and somatomedin C concentrations became normal, and GHRH-LI (GHRH-like immunoreactivity) was suppressed by more than 60%. The growth hormone response to exogenous GHRH 1-40 was stopped and growth hormone rise to thyrotropin-releasing hormone (TRH) was significantly attenuated. A significant shrinkage of the pituitary gland was observed. Similarly, the size of the metastatic carcinoid lesions decreased dramatically and was accompanied by a normalization of liver function. After almost 2 years of SMS 201-995 therapy, the patient was well and had no clinical signs of acromegaly. Thus, SMS 201-995 appears to be a remarkably effective agent for treatment of acromegaly secondary to ectopic GHRH secretion.

Acromegaly↗

Immunocytochemistry of four mixed pituitary adenomas and intrasellar gangliocytomas associated with different clinical syndromes: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome.

Four tumors consisting of pituitary adenomatous cells (AD) intricated with ganglion cells (GC) were studied. Each case was associated with a different clinical syndrome: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome with no hormonal hypersecretion. (a) In the case with acromegaly, immunoreactive growth hormone (IR-GH) was present in 80% of AD. IR-vasoactive intestinal peptide (VIP) was found in 5%-10% of AD and in few GC. Rare GC and processes showed IR-GH-releasing hormone (GRH), -somatostatin (SRIH), -gonadotropin-releasing hormone and -adrenocorticotropin-releasing hormone. (b) In the case with amenorrhea-galactorrhea, IR-prolactin (PRL) was seen in 90% of AD. IR-PRL and -VIP were present in rare GC. (c) In the case with Cushing's disease, 60% of AD and very few GC contained IR-adrenocorticotropin (ACTH) and beta-lipotropin. Rare GC processes contained IR-SRIH. (d) In the case without pituitary hormone hypersecretion, PRL was localized in rare AD and GC. Pituitary hormone and neuropeptides were never colocalized in the same cells. No case displayed IR-neurophysins or -thyroliberin. Pituitary hormones were localized by ultrastructural immunogold labeling. These findings show that: (i) in three cases, pituitary hormones (PRL and ACTH), and, in one case, VIP could be localized in both adenomatous and ganglion cells; (ii) the pituitary hormone-containing cells in the tumors could be related to the hypersecretory syndromes; (iii) intratumoral IR-VIP and -GRH might be involved in GH and PRL hypersecretion in the cases with acromegaly and amenorrhea-galactorrhea.

Acromegaly↗

Morphology of a GHRH producing pancreatic islet cell tumour causing acromegaly.

A 54 year old woman suffered from acromegaly due to a pancreatic islet cell tumour producing GHRH. The tumour was demonstrated on CT scan. The diagnosis was established from elevated plasma levels of GHRH, GH and prolactin, and by the lack of signs of a pituitary adenoma in trans-sphenoidal surgery. Acromegaly was cured by tumour removal. Light microscopically, the tumour showed a medullary and microlobular pattern. The cells were large and often cuspidal. Small granules were found in semi-thin sections. Small aggregations of amyloid fibres were seen, mostly around capillaries. Immunocytochemistry revealed GHRH, NSE, neurotensin, serotonin, VIP and PP. S 100 was positive only in nerve fibres. Staining for GH, ACTH, calcitonin, alpha-HCG, beta-HCG, insulin, glucagon, gastrin, substance P, bombesin and somatostatin was negative. Ultrastructure showed oval partly lobulated nuclei with small nucleoli, moderate amounts of rough endoplasmic reticulum, many free ribosomes, some large Golgi fields and small numbers of secretory granules measuring 150 nm or, in a few cells, 650 nm. Only 4 other cases of pancreatic endocrine tumours causing acromegaly by ectopic GHRH secretion are described in the literature and these were similar to our case in many respects.

Acromegaly↗

Treatment results of acromegaly as analyzed by different criteria.

Results of treatment of acromegaly are often incomparable due to the different criteria which have been used for defining cure or control of disease. At the present time it is widely accepted, that the main criteria of cure must be normalization of IGF-1 and a GH in the OGTT < 2 ng/ml. In this retrospective study we investigated the endocrinological results of 56 patients, who were surgically treated because of a GH-producing pituitary adenoma, by different criteria. Twelve of our patients had had additional medical treatment after surgery, two received radiotherapy. At a mean follow-up of 34 months after surgery 66% of patients had a basal GH < 5 ng/ml, 64% had a GH in the OGTT < 2 ng/ml and 73% had normalization of IGF-1. The combined criteria of OGTT < 2 ng/ml and IGF-1 normalization have been fulfilled in 59% of patients. None of these latter patients developed a clinical recurrence during the follow-up period. An optimal result (endocrinological cure, no permanent surgical complications and intact pituitary function) was achieved in 43% of patients. Although surgery was responsible for 19 new pituitary axis deficiencies (7 corticotropic axis, 8 thyrotropic axis and gonadotropic axis), 22 partial deficiencies improved to normalization after surgery (respectively 6, 3, and 13). Pre-operatively 55% of patients had no pituitary deficiency, after surgery this was 61%, leaving a net positive result of 6% less pituitary deficiencies. The authors conclude that normalization of IGF-1 combined with an OGTT < 2 ng/ml are adequate criteria for the definition of cure of acromegaly. However, the authors propose to include post-treatment hypopituitarism as an additional criterion by which treatment of acromegaly should be evaluated.

Acromegaly↗

Carpal tunnel syndrome and acromegaly.

50 patients with acromegaly and carpal tunnel syndrome have been examined electrophysiologically before and after transnasal operation of the pituitary adenoma. 32 of the 50 patients (64%) had symptoms of carpal tunnel syndrome. 13 of them had neurological deficits. 28 of the examined patients had pathological neurographical findings only. About 1 week post-operatively DL was decreased in 43%; in 10 out of 13 patients with neurological deficits DL decreased. GH was normalized in 80% and reduced to 5-10 micrograms/l in a further 10%. The investigation did not show whether the carpal tunnel syndrome only depended on a GH increase or on other factors also such as e.g., on the duration of symptoms or tissue changes. None of the patients had the transversal carpal ligament operated on. The coincidence between acromegaly and carpal tunnel syndrome was 64%. In 3 cases the carpal tunnel syndrome was the leading sign to the diagnosis of acromegaly.

Acromegaly↗

[Comparative studies of growth hormone secretion in acromegaly after isolated and combined application of insulin hypoglycemia, LH-RH- and TRH tests (author's transl)].

Growth hormone (GH) release was measured in 17 patients with active acromegaly following the administration of insulin, LH-RH and TRH given intravenously either combined or each separately. The simultaneous application of insulin and the hypothalamic releasing hormones resulted in a striking increase of plasma GH in 15 out of 17 patients. Inappropriate stimulation of GH release was found in 9 out of the 17 patients with acromegaly, when TRH was given as the only hormone; conversely this phenomenon due to LH-RH application was observed in 4 cases. In insulin-induced hypoglycemia GH release could be stimulated in 5 patients. After selective, transsphenoidal hypophysectomy, 4 of 13 patients still showed a definite stimulation of GH release after the combined use of test substances. Two of these also exhibited a comparable stimulation of GH after TRH, indicating adenoma cells remaining active after operation. The combined insulin-induced hypoglycemia/LH-RH/TRH-test is therefore advisable for patients with acromegaly, since GH release as well as other hypophyseal partial functions can be tested. The performance of individual tests is essential for evaluating selective stimulation of GH release.

Acromegaly↗

Osteopenia occurs in a minority of patients with acromegaly and is predominant in the spine.

Acromegaly may induce abnormalities in bone metabolism; however, there are limited data related to bone mineral density (BMD) in this condition. To evaluate the effects of an excess of growth hormone/ insulin-like growth fractor I (GH/IGF-I) in the skeleton, we measured the BMD in spine and femoral region, total body calcium and body composition in 45 patients (24 females and 21 males) aged 21-77 years (median 43 years) with acromegaly for 11.4 +/- 7.5 years (range 0.5-26 years) using a dual-energy X-ray absorptiometer (Lunar DPX). Thirty-four patients had had hypogonadism for 8.6 +/- 6.5 years (1-24 years). Mean serum GH and IGF-I levels were respectively 159 +/- 183 micrograms/l and 843 +/- 497 micrograms/l. Total body calcium was increased in the acromegalics (males: 1272 +/- 217 g, range 916-1816 g; females: 1041 +/- 223 g, range 739-1609 g) when compared with normal individuals (males: 1115 +/- 144 g, range 856-1398 g; females: 909 +/- 144 g, range 511-1311 g; p = 0.01). The lean body mass was significantly higher in acromegalic patients (p < 0.001) compared with normal individuals. There was a tendency for a lower fat percentage in the acromegalics; however, this difference was not significant. Osteopenia (1 Z-score below the mean) was found in the spine in 20% (n = 9) of the patients, while BMD was decreased in the femoral region in only 8.8% (n = 4). The group with osteopenia had a greater duration of hypogonadism than the normal BMD group (14 +/- 11 years vs 4.4 +/- 4.0 years; p = 0.01). A negative correlation was also found between the duration of hypogonadism and BMD in spine (r = -0.4; p = 0.003) and femoral region (r = -0.37; p = 0.013). The hypogonadal patients had a lower BMD in spine (p < 0.005), but not in other regions analyzed. No correlation was found between duration of hypersomatotropism, GH/IGF-I levels and BMD. We conclude that the majority of patients with acromegaly have preserved BMD despite the presence of hypogonadism.

Absorptiometry, Photon↗

Acromegaly and hypertension: prevalence and relationship to the renin-angiotensin-aldosterone system.

The prevalence of arterial hypertension was evaluated in a retrospective study of 158 patients with acromegaly, and results were compared to control populations, namely, the Munich Blood Pressure Study (MBPS) and the Framingham Study. The prevalence of hypertension (defined according to WHO criteria) was significantly increased in female patients but not in men; hypertensive acromegalics were older and tended to have higher body weight compared to normotensive patients. Hypertension was not related to serum concentrations of growth hormone. After successful treatment of acromegaly, growth hormone levels and systolic and diastolic blood pressure fell only in female hypertensive acromegalics; this did not occur in normotensives. The rise in plasma renin activity in response to upright posture was diminished in 57.9% of acromegalic patients. The prevalence of low-renin hypertension in our group of patients was 31.6%, which is similar to figures reported for unselected non-acromegalic subjects with essential hypertension. Orthostatic renin activity was weakly and inversely related (r = -0.3) to blood pressure. No relationship between plasma aldosterone concentration and blood pressure could be detected; however, in acromegalic women, aldosterone rose higher after ambulation than in men. In conclusion, hypertension is a common problem in acromegaly and at least in part related to similar risk factors in control populations. The association with abnormalities of the renin-angiotensin-aldosterone system is difficult to interpret and does not offer an explanation for the slight increase in the prevalence of hypertension.

Acromegaly↗

Effects of octreotide on biliary lipid composition and occurrence of cholesterol crystals in patients with acromegaly. A prospective study.

Treatment with the somatostatin analog octreotide is associated with increased gallstone formation. The mechanism of formation of these stones is unclear. The purpose of this study was to examine the effect of a three-month treatment with octreotide on biliary lipid composition and the occurrence of cholesterol crystals in patients with acromegaly. Thirteen patients with active acromegaly, aged 24-76 years, received octreotide (100 micrograms three times daily) for three months. Fasting gallbladder bile was obtained during upper gastrointestinal endoscopy after ceruletide stimulation. Bile was studied before and at the end of the treatment period (N = 7), only before (N = 4), or only at the end of treatment (N = 2). Before treatment, all bile samples but one were supersaturated with cholesterol. However, none contained cholesterol crystals on microscopic examination. At the end of the treatment period, all but two samples were supersaturated with cholesterol. Three of nine samples contained cholesterol crystals, a proportion significantly higher than before treatment. The relative proportions of bile acids, cholesterol, and phospholipids, and the mean cholesterol saturation index were not different before and during treatment. Follow-up ultrasonography showed the occurrence of gallstones in four patients, including the three patients who had cholesterol crystals. We conclude that: (1) fasting gallbladder bile of patients with acromegaly is frequently supersaturated with cholesterol; (2) treatment with octreotide does not increase cholesterol saturation index, but may induce the occurrence of cholesterol crystals. The data are consistent with the view that gallstones induced by octreotide are cholesterol stones and suggest that the drug may impair gallbladder motility and/or decrease cholesterol nucleation time.

Acromegaly↗

Atrial natriuretic factor in patients with acromegaly.

In acromegaly the plasma volume is chronically elevated and it returns to normal when the disease is successfully treated. To define the role of ANF in such a chronic disorder of extracellular fluid volume homeostasis the plasma level was assayed in 37 acromegalic patients with active or inactive (successfully treated) disease. Five patients were studied before and after therapy. The effects of acute change in sodium-fluid status on plasma ANF levels was examined in 7 active and 4 inactive acromegalic patients and in 7 healthy subjects. As compared to 14 patients with inactive acromegaly, 23 patients with active acromegaly had an expanded plasma volume (n = 12; 50.1 vs 37.6 ml.kg-1 BW) and an increased blood concentration of growth hormone (n = 23; 22.5 vs 2.1 ng.ml-1). Plasma ANF concentrations in active and inactive acromegalic patients (33.2 and 26.6 pg.ml-1, respectively) did not differ significantly from one another or from the level in the controls (26.9 pg.ml-1). In those patients there was no correlation between plasma volume and ANF level. Infusion of 21 isotonic saline in 2 h led to a similar, significant increase in ANF levels in active (from 26.2 to 72.4 pg.ml-1) and in inactive acromegalic patients (from 33.6 to 96.7 pg.ml-1) as well as in healthy subjects (from 21 to 70.6 pg.ml-1). Successful treatment reduced the plasma volume (from 49.2 to 35.8 ml.kg-1 BW) and growth hormone level (from 10.1 to 2.6 pg.ml-1), while the ANF level remained unchanged (from 33.8 to 35.5 pg.ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

Acromegaly secondary to growth hormone releasing hormone secretion.

BACKGROUND: Acromegaly secondary to growth hormone releasing hormone (GHRH) secretion is exceptionally rare. AIM: To report a case of acromegaly diagnosed in 1984 and assumed to be pituitary in origin. Sixteen years later, the cause was found to be a GHRH secreting neuroendocrine pancreatic tumour. METHOD: A case report. CONCLUSION: Although ectopic GHRH production is very rare, endocrinologists should be aware of this possibility in acromegaly patients if a pituitary tumour was not detected using pituitary imaging.

Acromegaly↗

Lymphocyte subset pattern in acromegaly.

Immune function in acromegalic patients has been poorly investigated. The aim of this study was to evaluate the main surface antigen clusters of circulating lymphocytes in acromegaly. One hundred patients with active acromegaly (55 women and 45 men, aged 20-70 yr) and 200 healthy subjects sex- and age-matched with the patients (110 women and 90 men, aged 20-70 yr) were enrolled in this study. All patients and controls were born and live in Southern Italy. No patient had received octreotide, bromocriptine or corticosteroids for at least 3 months before entering the study. The analysis of lymphocyte subset pattern was performed by flow cytometry and fluorescein isothiocyanate or phycoerythrin directly conjugated monoclonal antibodies specific for the cell surface antigen clusters (CD) representing T-cell population as a whole (CD3), T helpers (CD4), T suppressors (CD8), natural killer cells (CD16) and B-cell population as a whole (CD19). Acromegalics had significantly increased levels of CD3 (67.1+/-7.2 vs 64.3+/-8.8%; p=0.03) and CD4 (37.8+/-3.5 vs 36.4+/-4.3%; p=0.004) and decreased levels of CD8 (31.4+/-3.3 vs 33.7+/-8.2%; p<0.01) and CD19 (12.1+/-3.1 vs 15.2+/-5.1; p=0.01) without age-difference. The results of the current study demonstrate an increase in T-cell activity together with a decrease in B-cell activity in a very large series of patients with active acromegaly. These data further support the existence of abnormalities of the immune system in patients with chronic GH/IGF-1 excess.

Acromegaly↗

Acromegaly: an epidemiological study.

Although morbility and mortality in acromegaly are higher than in the general population, there have been very few previous epidemiological studies. This study tries to answer "why". Seventy-four patients affected by acromegaly in Vizcaya (Spain) between 1970 and 1989 were considered for an epidemiological study. The prevalence of known cases at the end of 1989 was 60 per million inhabitants. The average incidence of newly diagnosed cases was 3.1 per million people per year. Unexpectedly, acromegaly was more frequent in women (n = 48) than in men (n = 26), with a ratio of 1.8:1. Mean age at diagnosis was significantly higher in women (46.1 +/- 2.2 yr) than in men (39.5 +/- 2.2 yr) (p < 0.05) There was a positive correlation between age at diagnosis and the estimated duration of the disease (r = 0.56, p < 0.05) and a negative one between age and basal GH serum levels (r = -0.52 p < 0.002). The age at diagnosis was significantly higher in patients with invasive tumors (grade III and IV) than in those with enclosed tumors (grade I and II) (47.7 +/- 1.8 vs 40.1 +/- 3.3 p < 0.05). In general, mortality was higher than the expected for the control population (standardized mortality ratio, SMR = 3.2, 95% confidence interval. Cl = 1.55-5.93). However, mortality was higher in men (SMR = 7, 95% Cl = 2.81-14.4) but not in women (SMR = 1.4 95% Cl = 0.29-4.17).(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

Elevated circulating somatostatin levels in acromegaly.

GH increases hypothalamic somatostatin (SS) synthesis and secretion but it is unknown if chronic GH excess, as found in acromegaly, may influence circulating SS levels, that are mainly of enteropancreatic source and affect several gastrointestinal functions, including motility. Circulating SS occurs in several post-translational forms including somatostatin-14 (SS-14), somatostatin-28 (SS-28) and other small peptides. The aim of the present study was to characterize the fasting and postprandial pattern of plasma circulating somatostatin in normal subjects and patients with acromegaly. Fasting total SS and SS-28 levels were measured in 32 subjects, 16 acromegalic patients with a new diagnosis (A) (8 F, 8 M, median age 48) and 16 matched healthy volunteers (C) (8 F, 8 M, median age 45). SS was also determined after a standard solid-liquid meal (550 kCal) in 24 of the subjects (12 C and 12 A). Fasting SS and SS-28 were significantly higher in acromegalic patients as compared to healthy subjects. In the former, a positive correlation was found between IGF-I and SS levels (r = 0.525 p < 0.05). Furthermore, the ratio between SS (as pmol equivalent SS-14/I) and SS-28 was higher in the acromegalic patients than in the controls (3.4 +/- 2.1 vs 2.0 +/- 1.6, p < 0.05). The postprandial SS peak, as well as the incremental area above baseline values, was similar in the patients and controls. In conclusion, fasting but not postprandial hypersomatostatinemia, mainly due to an increase in SS-14, characterizes acromegaly. Excess GH/IGF-I could be a causal factor in somatostatin hypersecretion. Conceivably this abnormality might play a role in some alterations of gastrointestinal function of acromegalic patients such as prolonged bowel transit.

Acromegaly↗

The GH-releasing hormone (GHRH) test in acromegaly before and after adenomectomy.

The GHRH test may represent a new tool in the study of GH dynamics in acromegaly. GH responsiveness to GHRH 1-40 (50 micrograms iv) has been studied in 21 acromegalic patients. Nineteen out of 21 had active disease. Five patients were also studied 1-12 months after neurosurgery. Two apparently cured acromegalics were studied 1-2 yr after surgery. GH secretion has been evaluated in all patients by means of TRH, bromocriptine and insulin hypoglycemia tests, too. GH response to GHRH has also been performed in 14 normal subjects. In acromegaly, GH responses after GHRH (p less than 0.01 vs placebo) were variable. The GH peak ranged from 8 to 445 ng/ml in patients with active disease. Maximum GH increase after GHRH (calculated as peak/basal value ratio) was significantly reduced in acromegaly (2.9 +/- 0.5 ng/ml; mean +/- SE) in comparison to controls (34.1 +/- 10.9 ng/ml; p less than 0.01). No significant differences in GH pattern after GHRH were found between untreated and previously treated patients with active disease. A significant correlation was found between GH basal levels and GH incremental area (p less than 0.05) and between GH basal and peak levels (p less than 0.01) after GHRH. A significant increase in PRL secretion was observed in acromegalic patients after GHRH (p less than 0.01 vs placebo). No discernable variation was found in the other pituitary hormones pattern after the peptide administration. A positive correlation was observed between GH increase after GHRH and insulin hypoglycemia (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗