Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACROMEGALY”

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

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

At least 1,297 records · Page 72Linked to original sources
PubMed1974

Growth hormone release inhibiting hormone in acromegaly.

Growth hormone release inhibiting hormone (GHRIH) was administered by constant infusion over 75 minutes to eight acromegalic patients at different doses. 100 to 1,000 mug were equally effective in reducing circulating growth hormone (GH) levels; 25 mug lowered GH levels in only five patients, and at this dose the extent of the fall was smaller than from doses of 100 mug or more. 10 mug was ineffective. Injection of single doses of 500 mug by intravenous, subcutaneous, and intramuscular routes caused only small and transient reductions in GH levels, though the effect was improved by injecting the hormone intramuscularly in 2 ml of 16% gelatin. Injection of a suspension of 4 mg GHRIH in 1 ml of arachis oil lowered growth hormone levels for between three and four hours.In four acromegalic patients an oral 50-g glucose tolerance test was performed during a continuous infusion of either saline or 1,000 mug GHRIH. The "paradoxical" rise in growth hormone seen in these patients during the saline infusion was suppressed by GHRIH. The blood glucose responses were, moreover, modified by GHRIH in that the peak was delayed and occurred at the end of the infusion in each case. A "normal" glucose tolerance curve was converted to a "diabetic" type of response in two patients. This effect could be accounted for by the inhibition of insulin secretion known to occur with large doses of GHRIH.We speculate that acromegaly may be primarily a hypothalmic disease due to deficiency of GHRIH resulting in excessive secretion of growth hormone from the pituitary and adenoma formation due to inappropriate and prolonged stimulation of the pituitary.

Acromegaly↗
PubMed1975

Bromocriptine treatment of acromegaly.

The effects of oral bromocriptine in acromegaly have been studied. A dose of 5 mg six-hourly suppressed circulating growth hormone (GH) levels in nine out of 11 patients treated for seven to 11 weeks. This was associated with considerable clinical improvement in all patients, with abolition of excessive sweating, reduction in soft-tissue thichening, loosening of rings, decrease in shoe size, improvement in facial features, and loosening of dentures. Metabolic changes included improvement in glucose tolerance and reduction in hydroxyproline excretion. Unlike the actions of growth hormone release inhibiting hormone the suppression of GH was not accompanied by a reduction in insulin or glucagon secretion, though prolactin levels were suppressed. Side effects other than mild constipation were not seen when the full dose regimen was reached by slowly increasing the dose from 2-5 mg once daily. Bromocriptine holds promise as a safe and orally effective medical treatment to augment surgical or radiotherapeutic measures directed at the pituitary tumour. Its efficacy during longterm administration remains to be established.

Acromegaly↗
PubMed1977

Long-term treatment of acromegaly with bromocriptine.

Seventy-three patients with active acromegaly were treated for three to 25 months with bromocriptine 10-60 mg/day. Seventy-one patients showed symptomatic and objective clinical improvement. This included reduction in excessive sweating, hand and foot size, and the number of headaches; improved facial appearance; and increased energy and libido. Abnormal visual fields became normal in two patients, one of whom had concomitant radiotherapy. Mean circulating growth hormone levels, obtained by averaging serial samples through the day, fell by more than 7 microng/l or became undetectable in 58 patients (79%) but did not reach normal values: only 15 patients had mean levels on treatment of 5 microng/l or less. Twenty-three patients were diabetic before treatment, and glucose tolerance became normal in 15 and improved in a further five. Provided the drug was started slowly side effects were minor when compared with the considerable clinical benefit obtained.

Acromegaly↗
PubMed1976

Muscle changes in acromegaly.

Muscle biopsy specimens were obtained from 18 patients with acromegaly of varying degrees of severity. Half the specimens showed hypertrophy of type 1 fibres, while atrophy was most often seen in type 2 fibres. A direct correlation between muscle appearances and growth hormone levels was not observed. The needle biopsy technique is particularly suitable for determining the natural history of acrometalic myopathy.

Acromegaly↗
PubMed1968

Calcium metabolism in acromegaly.

A total of 78 acromegalic patients were studied before and after treatment by yttrium-90 needle implantation.Among the untreated patients 16% had a borderline or raised serum calcium. In half of these patients the serum calcium fell to normal after remission of their acromegaly. In the others the hypercalcaemia was due to associated proved or probable hyperparathyroidism. A downward trend of the serum calcium was noted even in the normocalcaemic patients with remission of their disease.Only 20% of untreated patients had a raised serum phosphate, and follow-up showed this measurement to be a poor index of disease activity.Net calcium absorption and calcium balances in five patients in this series and 12 others from the literature were essentially normal for their given level of calcium intake. No patient showed definite radiological evidence of osteoporosis and vertebral fractures.Bone uptake rate of calcium-47 and stable strontium was raised in the untreated state in all nine patients studied. The 24-hour strontium space was raised in 73% of untreated patients and fell to normal after treatment in all the retested patients in whom it was high initially.

Acromegaly↗
PubMed2005

Octreotide induced prolongation of colonic transit increases faecal anaerobic bacteria, bile acid metabolising enzymes, and serum deoxycholic acid in patients with acromegaly.

BACKGROUND: Acromegalic patients have slow colonic transit, increased rates of deoxycholic acid formation, and an increased prevalence of cholesterol gall stones, especially during long term octreotide treatment. However, the effects of this prolonged large bowel transit time on the numbers of faecal anaerobes and the activities of the enzyme systems which biotransform conjugated cholic acid into unconjugated deoxycholic acid (cholylglycine hydrolase and 7alpha-dehydroxylase) are unknown. METHODS: Therefore, in 10 non-acromegalic controls, 11 acromegalic patients not treated with octreotide, and 11 acromegalics on long term (8-48 months) octreotide (100-200 mug three times daily subcutaneously), we measured large bowel transit time and, in freshly voided faeces, the activities of the two bile acid metabolising enzymes, and related the results to the proportion of deoxycholic acid in fasting serum. Moreover, in patients with acromegaly, we measured quantitative bacteriology in faeces. RESULTS: Mean large bowel transit time in acromegalics not treated with octreotide (35 (SEM 6.5) hours) was 66% longer than that in non-acromegalic controls (21 (3.1) hours; NS) and became further prolonged during octreotide treatment (48 (6.6) hours; p<0.001). These octreotide induced changes in transit were associated, in acromegalic patients, with more total (15.0 (2.5) v 6.3 (1.3)x10(9) colony forming units (cfu)/g; p<0.05) and Gram positive (6.3 (2.3) v 3.2 (1.0)x10(9) cfu/g; p<0.05) faecal anaerobes. Mean faecal cholylglycine hydrolase activity in the long term octreotide group (22.0 (6.0)x10(-2) U/mg protein) was 138% greater than that in non-acromegalic controls (12.0 (6.0)x10(-2); p<0.01). Similarly, mean 7alpha-dehydroxylase activity in octreotide treated acromegalics (11.1 (1.18)x10(-4) U/mg protein) was 78% greater than that in patients not receiving long term octreotide (6.3 (0.5)x10(-4); p<0.001). The mean proportion of deoxycholic acid in fasting serum also increased from 18.0 (2.88)% in the untreated group to 29.6 (2.3)% during long term octreotide (p<0.05). There were significant linear relationships between large bowel transit time and: (i) faecal 7alpha-dehydroxylase activity; and (ii) the proportion of deoxycholic acid in fasting serum and between 7alpha-dehydroxylase activity and the proportion of deoxycholic acid in serum.Summary/interpretation: These data suggest that increased deoxycholic acid formation seen in acromegalics during octreotide treatment is due not only to the greater numbers of faecal anaerobes but also to increased activity of the rate limiting enzyme pathway (7alpha-dehydroxylation) converting cholic acid to deoxycholic acid.

Acromegaly↗
PubMed1993

Effect of octreotide on gall stone prevalence and gall bladder motility in acromegaly.

Octreotide therapy in acromegaly is associated with an increased prevalence of gall stones, which may be the result of an inhibition of gall bladder motility. Gall stone prevalence in untreated acromegalic patients relative to the general population is unknown, however, and the presence of gall stones and gall bladder motility in these patients and in acromegalic patients receiving octreotide was therefore examined. Thirty four percent of 39 patients who had taken octreotide for a mean of 20 months had gall stones compared with 16% of 38 patients who had not been treated with octreotide (p < 0.005). In a subgroup of 21 patients studied prospectively over 4 to 18 months, two patients developed stones. No patient had symptoms referrable to their gall stones. In 31 untreated acromegalic patients, the mean fasting gall bladder volume was similar to that in normal subjects. Maximal percentage emptying, however, was impaired (34 v 64%, p < 0.001) and the mean postprandial residual gall bladder volume increased (21.7 v 9.0 ml, p < 0.001). Treatment with octreotide increased the mean postprandial residual volume further to 36.8 ml (p < 0.001). Gall bladder emptying in untreated acromegalic subjects is impaired. Octreotide further increases postprandial residual gall bladder volume and this may be a factor in the increased gall stone prevalence seen in these patients.

Acromegaly↗
PubMed1979

Heart size and function in acromegaly.

Cardiac size and function was studied in 23 acromegalic patients using echocardiography and systolic time interval measurements. Thirteen patients (56%) had increased left ventricular mass, and in the 20 treated patients this correlated well with the mean of the recent basal growth hormone levels. It is suggested that myocardial hypertrophy may regress in proportion to the degree of control of growth hormone levels. The ejection fraction was normal in all patients except one, and increased left ventricular mass was not associated with detectable impairment of left ventricular performance. Thus, most acromegalic hearts function normally even when their mass is considerably increased, though the long-term effects of this are unknown, Echocardiography will be valuable in the serial monitoring of the cardiac effects of acromegaly.

Acromegaly↗
PubMed1984

The neuromuscular features of acromegaly: a clinical and pathological study.

A study of the neuromuscular features of acromegaly was performed in six patients. Clinical assessment was supplemented by quadriceps force measurements, plasma creatine kinase (CK) activities, electromyography (EMG) and nerve conduction studies. Muscle mass was measured by urinary creatinine/height indices (CHI) and cross sectional area (CSA) of thighs and calves on computed tomography. Quadriceps force/unit cross sectional area was derived. Needle biopsies of vastus lateralis were studied by histochemical and ultrastructural methods. Mean fibre area (MFA) and fibre type proportions were measured. Most of the subjects studied had muscle pain and proximal muscle weakness confirmed by quadriceps force measurements. This occurred in the absence of muscle wasting, as shown by cross sectional area measurements and normal or raised creatinine/height indices. "Myopathic" features were demonstrated by needle biopsy in half the patients and occasionally by electromyography and raised plasma creatine kinase activity. Abnormalities on needle biopsy included variation in fibre size, type 2 fibre atrophy and large type 1 MFA relative to type 2 MFA. Electronmicroscopy showed the non-specific findings of increased glycogen accumulation, excess lipofuscin pigment and myofilament loss.

Acromegaly↗
PubMed1987

Generalised peripheral nerve dysfunction in acromegaly: a study by conventional and novel neurophysiological techniques.

Twenty four patients with clinical, radiological and biochemical evidence of acromegaly were investigated by a number of independent neurophysiological tests. Two-thirds of the patients showed evidence of generalised peripheral nerve dysfunction. A significant correlation was found between total exchangeable body sodium, an indicator of disease activity, and the severity of the neuropathy. The generalised peripheral nerve abnormality was found to occur independently of the associated carbohydrate intolerance human growth hormone levels and other endocrinological dysfunction in this disorder.

Acromegaly↗
PubMed1981

Bromocriptine therapy in acromegaly. A long-term review of 35 cases.

Bromocriptine (CB-154, Parlodel, Sandoz) was given to 35 acromegalic patients for a period of 6-36 months. Basal and post-therapy endocrine functions including estimation of serum growth hormone (GH) profile; and GH kinetics during oral glucose tolerance test, augmented insulin tolerance test and thyrotrophin releasing hormone test were determined. The pituitary tumour size was delineated by a pneumoencephalogram. The mean GH levels ranged from 14 micrograms/l to 316 micrograms/l. Bromocriptine suppressed GH values to 5 micrograms/l or less in 16 patients and less than 10 micrograms/l in a further 6 patients. In 33 patients GH values fell to 50% of the basal value or less. There was no significant GH reduction in 2 'nonresponders'. Bromocriptine did not block the stress-induced GH secretion. It did not disturb pituitary functions other than prolactin which was suppressed much earlier and was maintained with smaller doses. GH suppression on the other hand was shortlived and rebounded when the drug was omitted. It had no adverse effect on tumour size in 2 patients having suprasellar extension of the tumour. Bromocriptine improved carbohydrate tolerance and sexual function although it did not affect insulin and gonadotrophin values. It seems reasonable to offer a trial of bromocriptine in all patients with acromegaly where therapy is deemed necessary as it is well tolerated, has insignificant side effects and no adverse drug interactions. Its high cost and prolonged course are obvious disadvantages. Caution should be exercised in cases with suprasellar extension and visual field involvement.

Acromegaly↗
PubMed1987

Growth hormone responses to hp GRF 1-44 amide, bromocriptine and stress in acromegaly are correlated.

The results of testing growth hormone (GH) reserve using human pancreatic growth hormone-releasing factor 1-44 amide (hp GRF 1-44 amide) have been compared with the GH responses in a variety of other dynamic tests in seven acromegalic patients. The GH release following hp GRF 1-44 amide correlated with the GH suppression following bromocriptine, but showed an inverse correlation with the GH release following stress tests (insulin-induced hypoglycaemia/glucagon). There was no correlation between the GH responses in these three tests and any of the other tests: TRH, GnRH and glucose. A hypothesis is proposed to explain these findings on the basis of varying degrees of GH secretion from adenomatous and normal pituitary somatotrophs in acromegaly.

Acromegaly↗
PubMed1988

Sequential growth hormone deficiency and acromegaly.

This is the case of a patient with a pituitary tumour presenting initially with growth hormone deficiency and requiring treatment with human growth hormone. Eight years later he represented with acromegaly. This sequence of events has not to my knowledge been reported previously.

Acromegaly↗
PubMed2003

Modern treatment of acromegaly.

Acromegaly is an endocrine disorder characterised by increased morbidity and mortality. It is usually caused by a growth hormone secreting pituitary adenoma and is manifested by a variety of clinical features. Surgery is usually the treatment of choice, however over the last few years, several new methods of treatment have been developed. A recent consensus on the targets for treatment has led to multiple studies being conducted to assess the efficacy of the currently available options. This review examines the evidence for and against these treatments.

Acromegaly↗
PubMedDate not supplied

[Incidental diagnosis of lymph node tuberculosis in an 111-indium-octreotide scintigraphy during a study of acromegaly].

A patient with clinical suspicion of acromegaly and no radiologic visualization of pituitary adenoma is presented. (111)In-DTPAOC scintigraphy was performed in order to localize an ectopic foci of GH production. Scintigraphy showed uptake in right paratracheal and hiliar lymph nodes that seemed residual in CT. Biopsy through mediastinoscopy showed tuberculous granulomas. After treatment, scintigraphy normalized. This case illustrate that (111)In-DTPAOC can be positive not only in tumoral but in benign pathology and, in specific cases, it can be a marker of inflammatory activity and useful for treatment monitoring.

Acromegaly↗
PubMed2006

Transsphenoidal microsurgery for newly diagnosed acromegaly: a personal view after more than 1,000 operations.

The aim of this short review is to inform about the possibilities and limits of transnasal microsurgery in acromegaly. The current reports on surgical remissions, according to the strict criteria with international consensus using age- and sex-related normal levels for insulin-like growth factor-I and suppression of growth hormone (GH) with oral glucose tolerance below 1 mug/l, are more or less agreeable with values between 34 and 74%. In microadenomas (<10 mm in diameter), 59-95% remissions are published. Some improvement might be achieved in macroadenomas which presently have a chance of 26-68% to be satisfactorily operated on. Special instruments introduced by us to visualize and remove partially invasive adenoma parts are described. Intraoperative magnetic resonance imaging is discussed. With intraoperative measurement of GH, small adenoma rests <3 mm can be diagnosed. When GH did not sufficiently decline, an additional tumor search resulted in a significant improvement in results in resectable macroadenomas. With these techniques, we achieved remission rates which can hardly be further increased (micros 95%, macros 68%). In grossly invasive grade 4 adenomas, which are frequent in our unit, only an 80-95% reduction in tumor mass is feasible. Preoperative treatment with somatostatin analogues as used in most of our patients reduces the comorbidity and facilitates adenoma removal which is still controversially discussed in the literature. The complication rate of microsurgery in experienced hands is low.

Acromegaly↗