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PubMed2005

Review of Cortina criteria for the diagnosis of acromegaly.

Diagnostic protocols for acromegaly have evolved over time reflecting the refinement of assays for the biochemical assessment of the GH-IGF-I axis and greater understanding of disease process. In February 1999, an International Consensus Conference was held in Cortina, Italy, to define the criteria for cure of acromegaly. This review paper summarizes the diagnostic guidelines proposed in the consensus statement by Giustina et al. In recent years, however, the criteria for both biochemical assessment and long-term monitoring in patients with acromegaly have changed with the development of increasingly sensitive and specific GH assays coupled with the widespread availability of reliable IGF-I assays. For this reason, constant updating of the assessment criteria proposed in the workshop held in Cortina, in 1999, would be advisable.

Acromegaly↗
PubMed2005

IGF-I and mortality in patients with acromegaly.

There are several studies in the literature relating mortality in patients with acromegaly to GH levels either as random samples or as a mean of several spontaneous samples or GH nadir after oral glucose load. Fewer articles have been published until now on the relationship between IGF-I and mortality, with several of these studies reporting a clear association, while two databases did not find an association between mortality and IGF and have instead shown an interrelationship between mortality and GH levels. These latter studies report databases in which fewer individuals have been sampled for IGF-I than for GH. Moreover, reliable immunoassays for GH measurement have existed for almost 20 yr more than immunoassays for IGF-I. Since between-method results diverge for both GH and IGF-I, it appears desirable to have levels of both biochemical markers measured in the follow-up of acromegaly, preferably in a central laboratory setting. Only by this prospective effort, it will be possible in the future to evaluate the relative ability of IGF-I and GH in predicting the residual risk of patients with acromegaly in relation to mortality, but also to co-morbidities.

Acromegaly↗
PubMed1991

Preoperative diagnosis of acromegaly by growth hormone-releasing factor radioimmunoassay.

Acromegaly was diagnosed in a 37-year-old woman with classical physical and biochemical findings; an enlarged sella on computed tomography suggested the presence of a pituitary macroadenoma. Radiologic evidence of a lung mass prompted radioimmunoassay of plasma growth hormone-releasing factor (7,500 pg/ml; normal less than 100 pg/ml). After resection of a bronchial carcinoid, which stained positive for growth hormone-releasing factor, circulating growth hormone-releasing factor levels normalized. Subsequently, her clinical, biochemical, and radiologic evidence for acromegaly resolved. This case represents the first reported use of the human pancreatic growth hormone-releasing factor 1-40 radioimmunoassay to preoperatively diagnose this rare etiology of acromegaly.

Acromegaly↗
PubMed1977

Hypothalamic hypopituitarism after pituitary apoplexy in acromegaly.

Pituitary apoplexy in acromegaly is an uncommon event having been recorded approximately 30 times in the English literature. This report records two additional cases that included growth hormone measurements and an assessment of pituitary function. The apoplectic event developed spontaneously in one, and in the other it developed within two weeks of completing a course of radiotherapy to the pituitary gland. Autocure of the acromegaly was apparent. Basal levels of growth hormone were in the normal range but failed to change with provocative stimuli. Luteinizing hormone and follicle-stimulating hormone titers, although detectable, were inappropriately low for the degree of hypogonadism. Pituitary insufficiency was associated with a significant thyroid-stimulating hormone response to protirelin in one patient tested. It is suggested that these experiments of nature lend credence to the proposal that the hypothalamus may play a critical role in the perpetuation of growth hormone hypersecretion in some patients with acromegaly.

Acromegaly↗
PubMedDate not supplied

[Medical treatment of acromegaly with dopaminergic agents].

The medical treatment of acromegaly with dopaminergic drugs has its physiopathological premise in the observation that agents capable of stimulating dopaminergic receptors directly are capable of determining GH secretion inhibition in a large percentage of acromegalic patients. Chronic administration of 5-20 mg/die of bromocryptin, long acting dopaminergic agonist, leads to a stable reduction in the levels of GH and somatomedin C (SmC) in about 50% of patients. However, these are only normalised in 20%. Treatment induces marked improvement in the clinical and metabolic changes typical of acromegalic disease. The therapeutic effect of dopaminergics may be maintained for periods of treatment lasting years but upon suspension of treatment pH levels return quickly to pretreatment levels. The antitumoral effect of the dopaminergic frequently encountered in prolactinomas is a rarer event in acromegaly and occurs more readily in patients with mixed secreting GH and PRL tumours than in pure GH. Currently octractide, a long lasting somatostatin analogue, is the most effective drug in the medical treatment of acromegaly; however the dopaminergic agonists remain a valid alternative.

Acromegaly↗
PubMed1990

Studies on the pathogenesis of hypertension in Cushing's disease and acromegaly.

The pathogenesis of the hypertension associated with Cushing's syndrome and with acromegaly is poorly understood. We have investigated the possible roles of sodium retention, activation of the renin-angiotensin system and increased sympathetic nervous system activity in untreated patients. In 11 patients with Cushing's disease, seven of whom were hypertensive, total exchangeable sodium was normal despite increased levels of the mineralocorticoid hormones, 11-deoxy-corticosterone and corticosterone. The renin-angiotensin system was also normal. Cardiac sensitivity to the beta-receptor agonist isoprenaline was increased, but this was not due to an increase in beta-adrenoceptor density. Hypertension in Cushing's disease is neither sodium-dependent nor angiotensin II-mediated, but increased cardiac sensitivity to catecholamines, by increasing cardiac output, may contribute to the pathogenesis of hypertension. In nine patients with acromegaly (three of whom were hypertensive) total exchangeable sodium was elevated. Although no correlation between blood pressure and exchangeable sodium was found, hypertension in acromegaly is probably sodium dependent. No evidence was found for a pathogenetic role for either the renin-angiotensin-aldosterone or the sympathetic nervous system.

Acromegaly↗
PubMed1989

Inhibitory effects of atropine on growth hormone release in normal subjects and acromegaly.

Growth hormone (GH) secretion is mediated by hypothalamic factors, mainly growth hormone releasing factor (GRF) and somatostatin (SS). The hypothalamic hormones, under direct neurotransmitter control, stimulate GH secretion through different central mechanisms. Atropine, an anticholinergic agent, can cross the blood-brain barrier and inhibit GH secretion stimulated by exercise and sleep in normal persons. In order to study the inhibiting effect of atropine on GH release and whether glucose can be replaced by atropine, normal persons and acromegaly patients were observed during exercise, after atropine, and 100 g glucose loading. The results confirmed that GH secretion increases after exercise and that this GH elevation can be inhibited by atropine in normal subjects. But in acromegaly patients high basal GH levels can not be inhibited by 100 g glucose loading or 0.6 mg atropine during the active phase of the disease. Blood sugar levels remained unchanged during the atropine test. It is suggested that the atropine test can be used as a GH inhibitory test in acromegaly patients with overt diabetes.

Acromegaly↗
PubMedDate not supplied

[Endocrine function in the late period after radiation therapy of acromegaly].

The results of treatment of pituitary adenomas manifested by the acromegaly syndrome with catamnestic follow-up of up to 10 years are discussed. The dynamics of changes in acromegaly and various endocrine functions with the use of distance gamma therapy and proton beam irradiation were studied in the comparative aspect, on the basis of which the indications for these methods of radiotherapy in acromegaly were specified.

Acromegaly↗
PubMedDate not supplied

[The soft tissues of the foot in acromegaly].

X-ray investigation of foot soft tissues and measurement of foot soft tissue thickness (FSTT), clinical examination and determination of the level of plasma STH were performed in 43 previously untreated patients with acromegaly and in 9 patients in clinical remission. The results obtained suggest that elevated FSTT over 22 mm and changes in foot soft tissues are characteristic for acromegaly. A conclusion is that determination of the state of foot soft tissues and a FSTT value can serve as an auxiliary sign for the diagnosis of early stages of disease as well as for the assessment of a degree of activity and efficacy of long-term results of therapy of acromegaly.

Acromegaly↗
PubMed1988

Neurological features of acromegaly: a review and report of two cases.

The neurological features of acromegaly are reviewed and two cases are reported. The most common neurological complications of active hypersomatotropism are headache, acroparesthesia and visual disturbance. Primary peripheral neuropathy, myopathy, entrapment myelopathy and/or cauda equina syndrome are uncommon, especially in young acromegalics. It is postulated that peripheral neuropathy in acromegaly is due to the entrapment of a nerve secondary to a soft tissue edematous mechanism by traumatic compression, angulation and/or stretching of the nerve in acquired extraspinal intermuscular, fibrous or osseofibrous tunnel stenosis; and/or in acquired spinal lateral recess stenosis, rather than true primary neuropathic or secondary endocrinological complications of hypersomatotropism. Proximal weakness is more likely arthropathic rather than myopathic, neuropathic or endocrinologic. Differential diagnosis of backache is briefly discussed. Further investigations of the mechanisms and the conservative treatment for neurological involvements in acromegaly are needed.

Acromegaly↗
PubMed1986

[Acromegaly due to a pancreatic tumor producing growth hormone releasing hormone: clinical picture and morphology].

Acromegaly due to ectopic production of growth hormone releasing hormone (GH-RH) by a tumor is rare, but several cases have been described after isolation and identification of GH-RH from a pancreatic tumor. The authors observed a patient with acromegaly caused by a pancreatic tumor in whom GH-RH production was demonstrated by measurements of GH-RH in peripheral plasma, tumor veins, tumor extracts and immunohistochemical identification. Endocrinological, histological and ultrastructural results are discussed. The problem of potential malignancy is investigated in the light of DNA measurements. This observation shows that GH-RH measurements can be a useful diagnostic procedure before surgery for acromegaly.

Acromegaly↗
PubMed1988

The nature of cardiac hypertrophy in acromegaly: an echocardiographic study.

M-mode echocardiography was used to study cardiac involvement in 78 patients with acromegaly. Proportionate concentric or eccentric left ventricular hypertrophy (LVH) was a common finding. Calculated left ventricular mass (LVM) was increased significantly in a hormonally active disease group compared to an inactive disease group or a control group (153 +/- 7 vs. 96 +/- 8 and 89 +/- 3 g/m2 resp.; p less than 0.001 for both). The increase of LVM in hormonally active disease is due to predominantly LV dilatation, whereas associated hypertension, if present, aggravates the LVH exclusively due to thickening of the LV wall. Hypocorticalism, if present, does not influence the degree of LVH. Asymmetric septal hypertrophy was not found to be specific for acromegaly and was seen in only 7.7% of patients. There was no correlation between LVM and both the plasma levels of growth hormone and duration of disease. On the basis of a retrospective analysis of LVM in successfully treated patients the authors conclude that specific heart muscle disease in acromegaly, manifesting itself as LVH, is slowly reversible after cessation of the growth hormone hyperproduction.

Acromegaly↗
PubMedDate not supplied

[Mechanisms of disturbance of the secretion of prolactin in patients with acromegaly].

Metoclopramide (DA-antagonist, M) tests were performed in 21 patients with acromegaly and in controls; the levels of adrenohypophyseal hormones were determined before and after drug administration. Irrespective of the basal level of prolactin (P) all the patients demonstrated a decrease in stimulated P secretion which was more noticeable in patients with hyperprolactinemia. The hyperergic response of TSH to M administration was observed in some of the patients with acromegaly. Such a response indicated an elevated tone of the dopaminergic (DA) system. The results obtained were suggestive of dysfunction of DA regulation of P secretion in all the patients with acromegaly.

Acromegaly↗
PubMed1988

Growth hormone, body composition and somatomedin C after treatment of acromegaly.

Acromegaly is associated with abnormal indices of body composition (as determined by exchangeable sodium, exchangeable potassium and total body water estimations) which may be corrected by treatment. We related these indices of body composition to the attained growth hormone levels (mean of five daytime values) in 42 treated acromegalics. Somatomedin C was measured in 30 subjects. The mean duration of treatment was 7.7 years (range 1-26). Exchangeable sodium, potassium and total body water were significantly lowered by treatment. After treatment of acromegaly subjects whose growth hormone level was below 5 mU/l achieved normal body composition more often than those with higher levels. Growth hormone concentration of below 5 mU/l after treatment should be regarded as more appropriate index of control of acromegaly than the higher levels previously recommended.

Acromegaly↗
PubMed1988

Abnormal orbicularis oculi reflex response in sleep apnea secondary to acromegaly. Evidence of pontomedullary dysfunction in sleep apnea syndrome.

Severe sleep apnea was present in a patient with upper airway obstruction due to acromegaly. The study of orbicularis oculi reflex responses (OORR) disclosed a marked prolongation of the late response prior to tracheostomy. Following the surgical relief of upper airway obstruction, sleep apnea disappeared, and the latency of the late response of the OORR was dramatically reduced but failed to normalize. The OORR and especially its late response were normal in a patient with acromegaly who did not experience sleep apnea. In two patients with sleep apnea, but without acromegaly, the late responses of the OORR were abnormal. It is suggested that the presence of abnormal OORR in sleep apnea may reflect a basic defect in pontomedullary control of respiration during sleep.

Acromegaly↗
PubMed1987

[Cardiological findings in acromegaly].

Acromegaly involves cardiovascular complications mostly due to the presence of hypertension, diabetes and atherosclerosis. However the appearance of cardiac decompensation and arrhythmias in the absence of predisposing factors tends to support the hypothesis of a specific myocardiopathy caused by excess GH. In order to assess the existence and course of subclinical cardiac alterations, 8 acromegaly patients were examined: 4 males and 4 females aged 31-56 with GH levels of 24-70 ng/ml (M + CD X 47 +/- 16) and no cardiovascular symptoms. One of the patients had moderate hypertension and 2 reduced glucose tolerance. The basal ECG showed sporadic ventricular extrasystoles in 2 cases and alterations compatible with left ventricular hypertrophy in another, while the effort ECG produced an asymptomatic depression of the ST segment in the hypertensive patient. The chest X-ray was normal in all cases. The echocardiography study investigated: the thickness of the interventricular septum (IVS = 13.9 +/- 2.8 mm), the thickness of the posterior wall of the left ventricle (LPW = 10.6 +/- 2.9 mm), the septum/posterior wall ratio (IVS/LPW = 1.3 +/- 0.2 the diastolic diameter (DD = 15.4 +/- 11.4 mm), the fraction of shortening (FS = 39.1 +/- 14.5%), the ejection fraction (EF = 64.1 +/- 18.4%) and revealed asymmetrical septal hypertrophy in 3 cases, concentric hypertrophy in another two. In two cases the DD and EF were distinctly altered. The patients were re-examined 2-4 years after surgical or radiation treatment. GH levels (M +/- SD = 10.3 +/- 10.1 ng/ml) were normal in 4 cases and still high, though lower in another two. The remaining two patients had borderline GH levels with high Sm-C. The ECG and chest X-ray were unchanged while echocardiography revealed a significant deterioration in heart function as far as DD (56.4 +/- 10.8 mm, p less than 0.05) were concerned with frankly pathological results in 4 and 3 cases respectively. These data confirm the view that most acromegalic patients present subclinical abnormalities in cardiac function and that the evolution of these is slightly influenced by the reduction in GH and Sm-C. levels. In fact, while the persistence of high GH and Sm-C. levels may explain the progression of cardiac alterations in some cases, it does not in others. It is also emphasised that echocardiography appears to be the most sensitive non-invasive technique for the diagnosis and follow-up of cardiac involvement in acromegaly.

Acromegaly↗
PubMed1985

[Cardiac insufficiency in acromegaly. Apropos of a case].

The authors report the case of a patient with acromegaly. The clinical history was dominated by left ventricular failure, for which acromegaly was the only evident cause. The cardiac index, pulmonary arterial pressure and the average pulmonary capillary pressure were measured before ablation of the hypophyseal tumour; the measurements were repeated 3 months and 8 years later. The postoperative course followed two phases: transient improvement of the haemodynamic parameters, then relapse of cardiac failure. This case confirms the possibility of a true cardiomyopathy during acromegaly; but the fact that the cardiac failure did not regress despite the decreased growth hormone levels was unusual and raises several physiopathological hypotheses.

Acromegaly↗
PubMedDate not supplied

[Cryohypophysectomy in acromegaly and gigantism by the stereotaxic method].

The authors report results of surgical treatment of 30 patients treated by cryohypophysectomy by the stereotactic method through the nose and sphenoid sinus in the years 1967-1979. The material included 28 cases of acromegaly and 2 cases of gigantism. The pathological manifestations in acromegaly and gigantism were analysed for demonstration which of them can regress after surgical treatment. The results of hormonal determinations, particularly the levels of growth hormone, 17-KS and hydroxysteroids, as well as blood glucose curves, were compared before and after cryohypophysectomy and their normalization was observed after the operation. There was principally no need for substitutive treatment after surgical treatment with the exception of 4 cases in which this treatment was given during several postoperative months. The indications to this method of therapy include cases of acromegaly and gigantism with presence of active intrasellar adenomas. Patients should be referred for treatment early before development of skeletal deformities.

Acromegaly↗