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PubMed2005

Gross total resection or debulking of pituitary adenomas improves hormonal control of acromegaly by somatostatin analogs.

INTRODUCTION: Invasive GH-secreting pituitary adenomas are rarely cured by surgery and although long-term therapy with somatostatin analogs (SSAs) may be employed, hormonal control is achieved in only 60% of cases. The impact of tumor debulking on subsequent control of acromegaly with SSAs has not been studied previously. METHODS: We studied retrospectively the response to SSA therapy in acromegalic patients before and after incomplete surgical tumor excision. A case review identified 24 acromegalic patients who had received SSA therapy for > or = 1 month before and after gross total resection or debulking of adenomas. No patient received radiotherapy or combination treatment with SSAs and dopamine agonists during the study. GH and IGV-I responses to SSAs were recorded pre- and postoperatively. Postoperative SSA therapy was begun after a washout period of 1-3 months to assess the hormonal effects of the surgery alone. RESULTS: Before preoperative SSA treatment, 24/24 (100%) patients had elevated GH levels and IGF-I levels were elevated in 19/21 (90.5%) patients with recorded values. During preoperative SSA treatment, GH and IGF-I levels were normalized in 7/24 (29.2%) and 11/24 (45.8%) patients respectively. Following postoperative washout, GH was controlled in only 3/24 (12.5%) patients, while IGF-I was controlled in 8/19 (42.1%) patients with available data. During the second SSA treatment period, normal GH levels were seen in 13/24 (54.2%) patients, while IGF-I control was noted in 18/23 (78.3%). CONCLUSION: Gross total tumor resection or debulking increases the likelihood of achieving biochemical disease control with SSAs in acromegalic patients with adenomas that were not amenable to complete surgical resection and in whom primary SSA therapy was unable to achieve good biochemical control.

Acromegaly↗
PubMed2005

The outcome of surgery in 668 patients with acromegaly using current criteria of biochemical 'cure'.

BACKGROUND AND AIM: The aim of this study was to illustrate the present role of transsphenoidal surgery as primary therapy in GH-secreting adenomas, and to compare the results concerning control of disease with previous series using older criteria of cure. METHOD: We report on a consecutive series of 688 acromegalic patients treated over a time period of 19 years. Biochemical cure was defined as normalisation of basal GH level, suppression of GH levels to below 1 ng/ml during an oral glucose load and normalisation of IGF-I levels. Of the 506 patients undergoing primary transsphenoidal surgery, a total of 57.3% postoperatively fulfilled the criteria used. RESULTS: The rate of biochemical 'cure' correlated with the magnitude of the initial GH levels, the tumour size and invasion. The overall complication rate was below 2%. Mortality in this series was 0.1% (1 of 688). During a follow-up period of 10.7 years only two recurrences (0.4%) occurred. However, in the patients treated by transcranial surgery and by repeat surgery the cure rate was found to be relatively low (5.2 and 21.3% respectively). CONCLUSIONS: These data suggest that surgery remains with very few exceptions the primary treatment of acromegaly for (i) a high cure rate, (ii) low morbidity, (iii) low recurrence rate and (iv) immediate decline of GH. Based on current criteria of cure, recurrences are uncommon. However, cure by surgery alone is improbable in patients harbouring extended, invasive tumours with high secretory activity, in whom further adjuvant treatment is mandatory.

Acromegaly↗
PubMed2005

Transsphenoidal surgery in acromegaly investigated by intraoperative high-field magnetic resonance imaging.

OBJECTIVE: The aim of the study was to evaluate the effect of intraoperative high-field (1.5 Tesla) magnetic resonance imaging (MRI) on the results of transsphenoidal surgery of GH-secreting pituitary macroadenomas. METHODS: Twenty-three acromegalic patients (mean tumor size, 25 +/- 12 mm; untreated preoperative GH, 4.2-159 microg/l; IGF-I, 349-1111 microg/l) were investigated by intraoperative high-field MRI. If intraoperative imaging depicted an accessible tumor remnant, resection was continued. RESULTS: In five patients intraoperative MRI led to further tumor removal, two of these met the consensus criteria for endocrine remission after 3 months. In two patients basal GH and oral glucose tolerance test (OGTT) were <2 microg/l, only IGF-I was slightly elevated, and in one patient GH was <5 microg/l and OGTT was 2 microg/l, with elevated IGF-I. Final intraoperative MRI showed no tumor remnants in 14 patients; eight of them met the consensus criteria for remission of acromegaly. In the patients with MRI showing incomplete removal (four suspect findings and five patients with intended partial removal) none was normalized. CONCLUSION: With regard to the patients with a tumor configuration in whom complete tumor removal was considered (n = 18), intraoperative MRI increased the rate of endocrine normalization from 33 to 44% applying the consensus criteria, and improved endocrine outcome to 'nearly normalization' in another 17%. With regard to preoperative GH levels and tumor size, intraoperative MRI can help to achieve endocrine remission in patients who are normally considered not to be curable. However, taking GH as the tumor marker, even intraoperative high-field MRI was not able to detect tumor remnants in every case.

Acromegaly↗
PubMed2006

The octreotide test dose is not a reliable predictor of the subsequent response to somatostatin analogue therapy in patients with acromegaly.

In many centres, a test dose (TD) of octreotide is administered before commencing somatostatin analogue therapy (SAT), although the merits of this procedure are uncertain. We have analysed the value of the GH response to a TD in predicting the efficacy of subsequent SAT in 47 patients with acromegaly (25 male, median age 51 years, range 20-82). The primary goal of SAT was a mean GH of < 5 mU/l. Median baseline GH was 19.3 mU/l (2.2-233 mU/l) and with the TD fell by 78% (35-98%) to a nadir of 4.2 mU/l (< 0.3-85 mU/l). Optimal predictive power was observed when GH fell to < 5 mU/l after the TD. With this criterion, the TD had a positive predictive value (PPV) of achieving the primary goal on SAT of 82% and a negative predictive value (NPV) of 50%. However, baseline GH was also highly predictive of the likelihood of successful SAT (GH < 5 mU/l). The GH response to the TD had PPV of 83% and NPV of 61% of normalising IGF-I on SAT. In summary, baseline GH and nadir after a TD are highly predictive of a good response to SAT; however, a poor response to a TD does not exclude an optimal response to SAT. Furthermore, failure to achieve biochemical control does not equate to no benefit, as biochemical improvement was seen in every patient; therefore, no patient should be deprived of octreotide therapy because of the result of a TD. In conclusion, our data indicate that the octreotide TD has no place in selecting patients for SAT.

Acromegaly↗
PubMed1991

Ruptured chordae tendineae in acromegaly. An autopsy case.

A 57-year-old woman with acromegaly associated with mitral chordal rupture is reported. She was noted to have abnormal development in the size of her hands and feet in childhood. She occasionally suffered from shortness of breath on exertion and nocturnal dyspnea for several years, and was diagnosed and treated as having congestive heart failure due to valvular heart disease. On admission to our hospital, chordal rupture was suspected on the basis of M-mode and two-dimensional echocardiography. Seven years after discharge, she died of congestive heart failure. On autopsy, the heart weight and ventricular wall thickness were increased. Rupture of the posterior chordae was confirmed, but evidence of an old myocardial infarction was not found. There was severe interstitial fibrosis in the left ventricular wall. A possible etiology of the chordal rupture in this case was thought to be the excessive stretching caused by the disproportional visceromegaly of the heart.

Acromegaly↗
PubMed2006

[Acromegaly and thyroid disease: prevalence of thyroid cancer].

The relationship between cancer and acromegaly has been subject of study for many years. From a case of differentiated thyroid carcinoma in one of our acromegalic patients, we reviewed a series of 100 acromegalics and found two others cases of thyroid cancer, which are described in this work. From that point, we have got data from the literature about this last association and its possible pathogenesis. The prevalence of thyroid disease is increased among acromegalic patients, mainly due to nodular goiter. This association will be discussed, as well as the relation between insulin-like growth factor-I and cancer, in an effort to have a better understanding of its meaning for our cases. We concluded that it would be prudent to do periodic ultrasonographic evaluation of acromegalic patients, follow by fine needle aspiration biopsies of suspect nodules.

Acromegaly↗
PubMed2006

[Cardiac morphology and performance alterations and analysis of determinant factors of left ventricular hypertrophy in 40 patients with acromegaly].

Acromegaly has a high mortality rate due mainly to cardiovascular complications. The aim was to evaluate the determinant factors of left ventricular hypertrophy (LVH) and cardiac alterations in 40 acromegalic patients submitted to clinical-laboratorial studies and echocardiogram. The variables analyzed were age, sex, disease duration, arterial hypertension (AH), impaired glucose tolerance/DM, previous treatment with octreotide, GH and %IGF-I. Univaried analysis showed that patients with LVH were older (p= 0.031), had higher prevalence of AH (p= 0.009) and higher %IGF-I (p= 0.002), than those without LVH. Multivaried analysis showed AH and %IGF-I as determinants of LVH (p= 0.035 and p= 0.016). After dichotomizing of %IGF-I, a score was created and the frequency of LVH was 9%, 65%, 92% x 0, 1, 2; p< 0.0001. Prevalence of aortic ectasia was higher and valvar disease was smaller than reported in the literature. We conclude that AH and %IGF-I were determinants of LVH.

Acromegaly↗
PubMed1997

[Acromegaly. Diagnostic and therapeutic aspects. Analysis of 18 cases].

The authors present a retrospective study of a series of eighteen patients with acromegaly diagnosed, treated and followed by the Endocrinology and Neurosurgery Services of the Hospital Universitário Clementino Fraga Filho of the Federal University of Rio de Janeiro. The average age of the patients was 43.2% years (varying between 15 and 63). Initial complaints were mainly due to somatic alterations in 83.33%; half the cases had manifestations secondary to tumor compression and 53.33% had neuro-ophtalmological alterations. Hypersecretion of growth hormone was demonstrated by basal hormone determinations and dynamic tests. Neuroradiological assessment showed supraselar expansion in 61.11% of cases. Surgical approach was transsphenoidal in all cases. The main objective of this study was to establish diagnostic criteria, discuss the therapeutic conduct and evaluate the results obtained, comparing them with other series of literature.

Acromegaly↗
PubMed1976

Differences in autonomity of growth hormone secretion in patients with acromegaly.

Thirteen patients with acromegaly were subjected to the examination of autonomity in growth hormone (GH) secretion. TRH (500 mug iv), arginine (0.5 g/kg of body weight iv infusion), LH-RH (100 mug iv) and L-dopa (500 mg orally) were administered, and plasma GH was measured. Among them, 11 patients showed some response in plasma GH to at least one agent, but the other 2 cases showed no response to any of the above 4 agents. In the former 11 cases, the patients were regarded as belonging to the less autonomous type and in the latter 2, to the more autonomous type in GH secretion. Six cases (4 cases of the less autonomous and 2 cases of the more autonomous type) received an administration of 500 mug of synthetic somatostatin parenterally. Following administration of somatostatin, the patients of both types showed significant GH decrease, although GH decrease in the more autonomous type was smaller than that of the less autonomous type. These results would suggest that there might be no acromegalics secreting GH FROM THE PITUITARY WITH COMPLETE AUTONOMITY, AND THE DIFFERENCE OF AUTONOMITY IN ACROMEGALIC PATIENTS MIGHT DEPEND EITHER ON THE DIFFERENCE IN SENSITIVITY AND/OR THE NUMBER OF RECEPTORS IN THE PITUITARY RATHER THAN THOSE IN HYPOTHALAMUS TO EXOGENOUS STIMULI.

Acromegaly↗
PubMed1977

Abnormal growth hormone responses to L-dopa and thyrotropin-releasing hormone in patients with acromegaly.

Changes in growth hormone (gh) release in response to L-dopa, TRH, arginine and LH-RH were studied in 15 patients with acromegaly to investigate the mechanism of so-called 'paradoxical decrease' of GH secretion often observed in acromegalics after the administration of L-dopa. Among 15 patients, 11 showed GH increase with TRH, 8 with arginine, and 4 with LH-RH. On the other hand, six out of these 15 patients showed a distinct paradoxical GH decrease after L-dopa administration. Two cases showed an increase in GH on L-dopa as seen in normal subjects. The responses of GH release, either an increase or a decrease, was proved fairly constant when several patients had been examined repeatedly. Changes of GH induced by L-dopa were compared wwith those by TRH, arginine, and LH-RH. There were no correlation between the changes by L-dopa and those by TRH, arginine, and LH-RH when compared simply. But a significant negative correlation (r=-0.861) was found between percent changes by L-dopa and logarithm of increase ratio (peak value of GH after the stimulation/basal value) induced by TRH. More close correlation (r=-0.881) was obtained when the percent changes by L-dopa was (formula: see text). This result would imply that paradoxical GH decrease by L-dopa in acromegalic patients is more remarkable when their GH secretion is more responsive to TRH and less responsive to arginine. When this correlation is considered in connection with the reported effects of L-dopa on GH and thyroid stimulating hormne (TSH) in man, the following hypothesis might be proposed: L-dopa has two opposing actions on the hypothalamo-pituitary system; 1) inhibition of TRH release or suppression of GH release from TRH sensitive GH producing cells, and 2) arginine-like facilitation of GH release presumably via stimulation of GH-RF. The paradoxical GH decrease in acromegalics on L-dopa is explained by the dominance of the former action.

Acromegaly↗
PubMed1985

Comparative study on the responses of plasma GH to synthetic GH-releasing factor and other stimulatory and inhibitory agents in patients with acromegaly.

Ten patients with active acromegaly received synthetic human pancreatic GH releasing factor (hpGHRF-44), and the GH responses to GHRF were compared with the basal GH levels and with the GH responses to arginine, TRH, LH-RH, somatostatin, and L-dopa. There were no significant relationships between the plasma GH responses to GHRF and the results of the stimulatory and inhibitory tests mentioned above, except that the responses to GHRF showed weak positive or negative correlations with the responses to LH-RH (r = +0.56) or with the basal GH levels (r = -0.57). These results indicate that acromegalic somatotrophs would have GHRF receptors as well as several other receptors to hypothalamic hormones and to dopamine, and that there might be no distinct relationship between the somatotroph sensitivities to GHRF and to other stimulatory or inhibitory stimuli. Further studies are required regarding the weak correlations between the response to GHRF and that to LH-RH or basal GH value.

Acromegaly↗
PubMed1995

Prolactin receptor expression in lymphocytes from patients with hyperprolactinemia or acromegaly.

Previous reports demonstrated that prolactin receptors (PRL-R) are widely expressed on cells of the immune system. We analyzed a possible regulation of PRL-R expression on human mononucleated blood cells by prolactin (PRL) itself. PRL-R expression was analyzed by immunofluorescence on T and B lymphocytes and monocytes from peripheral blood mononucleated cells (PBMC) of patients with hyperprolactinemia or acromegaly compared with sex- and age-matched control subjects. The frequency of PRL-R positive cells and the intensity of PRL-R expression was only modified among the CD8+ T cell population of hyperprolactinemic patients with macroadenoma. No correlation was reported between PRL-R expression and circulating PRL levels. The percentage of PRL-R+ cells on B or T lymphocytes and monocytes as well as the capacity of PBMC to proliferate in response to T cell mitogens were not significantly different in bromocriptine-treated compared with untreated patients. These findings suggest that factors other than pituitary PRL play the major role in regulating PRL-R expression on cells of the immune system.

Acromegaly↗
PubMed1994

Acromegaly. Recognition and treatment.

Acromegaly is a chronic debilitating disease caused by growth hormone (GH) hypersecretion, usually from a pituitary adenoma. It is frequently diagnosed after many years of active GH hypersecretion, and causes significant morbidity and mortality due to cardiac, pulmonary and musculoskeletal changes. Local complications resulting from the pituitary tumour can also occur. The most important feature that will enable a physician to diagnosis the disease is clinical vigilance. Measurement of elevated plasma mecasermin (insulin-like growth factor I, IGF-I) is the single best test to make the diagnosis. Once the diagnosis is confirmed, a GH-secreting tumour should be sought, by performing a careful magnetic resonance imaging or computed tomography scan of the pituitary gland and hypothalamus. Therapy is directed at both preventing local complications of the tumour mass as well as normalising GH secretion. Surgical resection of the tumour is almost always the first step in treatment. If GH secretion is not normalised, which is best assessed by determining whether plasma IGF-I returns to the normal range, further treatment with radiation and/or medical therapy is required. Bromocriptine normalises GH in approximately 10% of patients and causes pituitary shrinkage in a similar fraction of patients. Octreotide is considerably more expensive than bromocriptine and is given subcutaneously, but is more effective in both normalising GH secretion and in shrinking tumours. Octreotide treatment of the pituitary tumours prior to surgical resection may be of value, but requires further investigation.

Acromegaly↗
PubMed2005

Hypercalcemia in a patient with primary hyperparathyroidism and acromegaly: distinct roles of growth hormone and parathyroid hormone in the development of hypercalcemia.

We herein report a case of primary hyperparathyroidism associated with acromegaly. Although serum parathyroid hormone (PTH) levels increased after the resection of a pituitary adenoma, levels of serum 1a, 25-dihydroxyvitamin D [1, 25(OH)2D] decreased but remained above the normal upper limit. After resection of a parathyroid adenoma, serum PTH, 1, 25(OH)2D, calcium (Ca), and phosphate were all normalized. Since serum 1, 25(OH)2D levels decreased in spite of the increase in serum PTH levels after normalization of levels of growth hormone (GH), GH may have contributed to the elevation of serum 1, 25(OH)2D. It is therefore suggested that the mechanism by which elevation of serum 1, 25(OH)2D occurred in the present case may involve an increase in serum GH distinct from the PTH-mediated pathway.

Acromegaly↗
PubMedDate not supplied

Thyrotropin releasing hormone (TRH)-induced release of 7B2 (neuroendocrine polypeptide) in vivo and in vitro using adenoma cells of a patient with acromegaly.

We demonstrated TRH-induced release of 7B2 (a neuroendocrine polypeptide) in vivo and in vitro (somatotroph adenoma cells) in a patient with acromegaly. The mean basal plasma 7B2 and growth hormone (GH) levels before operation were 142.8 +/- 3.2 ng/l and 52.4 +/- 1.6 micrograms/l (mean +/- SEM), respectively and these levels significantly rose after an i.v. administration of 500 micrograms of thyrotropin releasing hormone (TRH). After the transsphenoidal adenomectomy, the basal level of plasma GH was restored to the normal level and that of plasma 7B2 was slightly decreased. In addition, TRH-induced response of plasma 7B2 and GH disappeared post-operatively. In a primary culture of somatotroph adenoma cells obtained at surgery, TRH significantly induced secretions of both 7B2 and GH. Immunohistochemical studies showed the positive 7B2 and GH immunoreactivities in somatotroph adenoma cells. These findings strongly suggest that the somatotroph adenoma cells in this case produced and released 7B2 concomitant with GH.

Acromegaly↗
PubMed1993

Subclinical carpal tunnel syndrome in acromegaly.

Median nerve conduction was studied in 16 acromegalic patients with asymptomatic carpal tunnel syndrome (CTS) to examine the incidence of subclinical CTS. Thirteen patients (81%) and 23 hands (72%) demonstrated subclinical CTS, 10 bilaterally and three unilaterally in the dominant hand. The incidence reflects the greater sensitivity of the inching method for detecting focal conduction abnormalities. Two of three patients without subclinical CTS showed normal plasma somatomedin-C concentration despite growth hormone hypersecretion. Following adenomectomy, nerve conduction normalized in only six hands (26%). The postoperative persistence of the conduction delay implies that irreversible narrowing of the carpal tunnel rather than reversible soft tissue edema is the principal cause of CTS associated with acromegaly.

Acromegaly↗
PubMed1976

Osteosarcoma associated with acromegaly: a case report.

A case of acromegaly who developed an osteosarcoma is recorded, with persistently raised levels of growth hormone. It is possible that there was some aetiological relationship between the increased rate of bone formation and the development of the osteosarcoma.

Acromegaly↗
PubMed1986

Acute and long-term effects of SMS 201-995 in acromegaly.

The subcutaneous administration of 50 micrograms SMS 201-995 at 0815 h in 18 acromegalic patients reduced plasma growth hormone (GH) levels from 2 to 6 h after injection from 36 +/- 2 to 7 +/- 1 microgram/l (-80 +/- 5%). Circulating GH concentrations had normalized to less than 5 micrograms/l during this period in 11 of 18 patients. Postprandial blood glucose levels after breakfast were significantly (p less than 0.01) higher after SMS administration but significantly lower (p less than 0.01) after supper. Chronic treatment of five acromegalic patients with 200-300 micrograms SMS 201-995 daily for 8-24 weeks resulted in a rapid clinical improvement in all patients and complete disappearance of the complaints in four of five patients. This was accompanied by tumour shrinkage as estimated by computerized tomography scanning in three of four patients. In parallel, mean plasma GH levels and serum somatomedin-C and phosphorus levels fell to or within the normal values. SMS 201-995 represents a new tool in the medical management of acromegaly and may become the treatment of choice, especially in patients who do not benefit sufficiently from surgery and/or radiotherapy.

Acromegaly↗