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PubMedDate not supplied

Pachydermoperiostosis in a 13 year-old boy presenting as an acromegaly-like syndrome.

A thirteen year-old boy with progressive enlargement of the joints and distal extremities, clubbing, coarse facial features and hyperhidrosis was investigated. His endocrine profile was normal. Radiological studies demonstrated bilateral symmetrical periosteal new bone formation with acroosteolysis. After extensive investigation to exclude systemic and endocrine causes, a diagnosis of pachydermoperiostosis was made. Awareness of this condition helps to differentiate this syndrome from pulmonary osteoarthropathy and acromegaly.

Acromegaly↗
PubMed1975

Dynamic evaluation of growth hormone (GH) and prolactin (hPRL) secretion in active acromegaly with high and low GH output.

Ten patients with active acromegaly were studied. In 9 plasma GH levels failed to suppress after glucose (OGTT), in 8 an increase in serum GH occurred after thyrotropin releasing hormone (TRH). After L-Dopa, 4 patients showed no change in serum GH, 3 exhibited a decrease and in 3 an increase in serum hGH occurred. With a combined insulin (ITT) and arginine (ATT) test, 2 patients exhibited an increase in hGH, and in 6 no change occurred. Fasting serum GH concentration was less than 11 ng/ml in 5 patients. Basal prolactin (hPRL) levels were normal in all patients including two with galactorrhea. L-Dopa suppressed and TRH stimulated hPRL secretion in all, but the responses which were seen were subnormal. Hydrocortisone infusion in two acromegalics did not affect the prolactin induced increase after TRH but blunted the GH increase after TRH.

Acromegaly↗
PubMed1977

Long-term treatment with 2-Br-alpha-ergocryptine in acromegaly.

Thirty acromegalic subjects underwent chronic CB154 therapy (10-20 mg daily) for periods ranging from 3 months up to 2 years. In 18 out of 21 patients, who exhibited consistent HGH reduction following acute administration of the drug, there was also during chronic treatment, a suppression of the plasma HGH levels exceeding 50% of base line values, e.g. from mean daily values between 14-197 ng/ml (mean +/- SEM = 57.8 +/- 12.4 ng/ml pre-treatment) to 2-19 ng/ml (mean 8.3 +/- 1.2 ng/ml post-treatment). In 12 of the subjects who responsed to chronic CB154 treatment, the mean daily values of HGH were below 10 ng/ml. The suppression of plasma HGH was maintained unaltered throughout the whole course of therapy. In the 9 subjects, in whom no consistent HGH decrease was evidenced with acute CB154 administration, there was accordingly a minor or no suppression of HGH values during the chronic treatment. In 13 subjects, irrespective of the degree of their GH responses, the plasma prolactin levels were constantly inhibited by CB154; instead the drug failed to modify significantly the TRH or insulin-induced GH release. These changes in the hormonal parameters were paralleled by marked clinical amelioration and improvement of some of the metabolic alterations frequently encountered in acromegaly, e.g. reduced carbohydrate tolerance, increased insulin resistance, diminished fall of plasma phosphorus after insulin, decreased urinary excretion of phosphate, hyper-hydroxyprolinuria and hyper-calciuria. Collectively, these data demonstrate that CB154 thrapy is effective in reducing HGH hyper-secretion in many acromegalic patients during long-term treatment.

Acromegaly↗
PubMed1978

Long-term treatment of acromegaly with bromocriptine.

Treatment with bromocriptine, 30-55 mg daily, in 13 acromegalics for 1-15 months, resulted in a 60% decrease in growth hormone secretion, as judged from the excretion of growth hormone in 24-h urine. Normal excretion was obtained in 10 patients, while 1 patient showed no response. The plasma growth hormone response to O-GTT was improved, but not normalized, in 4 of 7 patients treated for more than 6 months, and marked glucosuria disappeared in two diabetics. While the secretion of TSH, LH and FSH was unchanged, the prolactin secretion was inhibited. The urine excretion of free cortisol showed a 30% decrease, possibly due to a direct effect of bromocriptine on the ACTH-secretion. Hypercalcaemia was never seen, but the initial hypercalcuria showed a modest decrease without measurable changes in the creatinine clearance. The subjective relief during long-term treatment was marked in 10 of 11 patients and the dominating symptoms disappeared in 40-67%, whereas heal-pad thickness, enlarged sellae, and visual fields remained unchanged. No serious side effects were observed. Treatment with bromocriptine seems effective and should be considered as a remedy amongst others, in suitable cases of acromegaly.

Acromegaly↗
PubMed1978

Urinary hydroxyproline excretion in acromegaly.

The urinary hydroxyproline excretion of 8 acromegalics kept on a collagen free diet has been studied. Urinary hydroxyproline showed a circadian rhythm with maximum excretion rates at night and early morning and minimum excretion rates in the late afternoon and evening. When mean values are compared, there is a significant correlation between fasting GH-levels and 24 h urinary hydroxyproline excretion (Rs = 0.74 and between GH and fasting hydroxyproline:creatinine ratios (Rs = 0.76). No significant correlation could be demonstrated between collagen content of bone biopsies and GH-levels or urinary hydroxyproline excretion. It is suggested that a practical assessment of disease activity in acromegaly can be achieved through a simplified hydroxyproline assay.

Acromegaly↗
PubMed1981

Interstitial pituitary irradiation with 90Y for the treatment of acromegaly. A reappraisal.

The management of 54 acromegalics referred to us between 1974 and 1978 has been analysed. Twenty-two patients were treated with pituitary implants of yttrium-90 (90Y). Eleven are in complete remission (mean growth hormone (GH) less than 11 mIU/l), 8 had improved (mean GH 11-20 mIU/l or 50% less than preoperatively) and 3 were poor responders. Two patients had temporary 6th nerve paresis. Seven patients are on replacement therapy. Thirty-one patients were not implanted for the following reasons with a number of patients having more than one: extension of the tumour into the sphenoid sinus 10, or above the sella 3, partially empty sella 9, internal carotids too close to midline 2, invisible landmarks 1, mild acromegaly 6, poor general health 3, declined investigations or operation 6. It is concluded that pituitary implant of yttrium is an effective and safe form of treatment in carefully selected patients.

Acromegaly↗
PubMed1981

Calcium and vitamin D metabolism in acromegaly.

Acromegalic subjects were found to have elevated serum levels of both 1,25-dihydroxyvitamin D (1,25-(OH)2D), 67 +/- 22 (SD) pg/ml) and 24.25-dihydroxyvitamin D (24.25-(OH)2D), (6.9 +/- 1.5 (SD) ng/ml). The serum concentration of 1,25-(OH)2D correlated positively (P less than 0.02, R = 0.56) to the 24 h urinary excretion of growth hormone, but not to the serum levels of parathyroid hormone, prolactin, thyroid hormones or the urinary excretion of free cortisol. Fourteen patients were treated with bromocriptine at doses from 15-45 mg/day for a period of about 6 months. This was accompanied by a significant decrease in the urinary excretion of growth hormone and calcium and in the serum concentrations of 1,25-(OH)2D and 24.25-(OH)2D. A relationship was demonstrated between the decrease in urinary calcium excretion and the decrease in serum 1,25-(OH)2D (P less than 0.02, R = 0.64). It is concluded that the serum concentration of 1,25-(OH)2D is elevated in acromegaly, perhaps as a consequence of a direct action of growth hormone on the renal 1 alpha-hydroxylase activity.

Acromegaly↗
PubMed1981

Iliac crest bone mass and remodelling in acromegaly.

Iliac crest bone biopsies from 18 patients with active acromegaly, of whom 11 had received tetracycline double-labelling, were evaluated by quantitative histomorphometry and compared with age- and sex-matched normal controls. A significant increase (P less than 0.01) was found in both cortical (175%) and trabecular (130%) bone mass. In trabecular bone, resorption surfaces and active (tetracycline-labelled) and total formation surfaces were increased (P less than 0.05 and P less than 0.01, respectively) causing an enhanced bone turn-over at tissue level (P less than 0.01). The increased trabecular bone mass indicates a positive net balance per remodelling cycle and, therefore, larger than normal bone remodelling units, which in part may explain the increased bone turn-over at tissue level. The activity of the osteoblasts active in mineralization (the appositional rate) was increased (P less than 0.01) and positively related to the fasting serum growth hormone levels (Rs = 0.69, P less than 0.05). The average activity of active and inactive osteoblasts (bone formation rate at basic metabolic unit (BMU) level) was insignificantly increased. The proportion of active (tetracycline labelled) to nonactive formation surfaces was normal. The bone changes were unrelated to serum levels and urinary excretions of calcium and phosphorus or to renal excretion of total and non-dialyzable hydroxyproline or cAMP.

Acromegaly↗
PubMed1981

Pituitary apoplexy in acromegaly during bromocriptine therapy.

Two cases of pituitary apoplexy occurring in the course of long-term bromocriptine therapy for active acromegaly are described. Although bromocriptine was effective in lowering serum growth hormone levels and concomitant clinical improvement was achieved, both patients developed an acute episode suggesting pituitary apoplexy when the therapy was continued for 6 and 24 months, respectively. Surgery verified marked haemorrhage and necrosis of an eosinophilic pituitary adenoma in each case. Bromocriptine may have suppressed the growth of these pituitary adenomas resulting in necrosis of the tumour, followed by haemorrhage into the adenoma. Pituitary apoplexy has not been documented as a complication of bromocriptine therapy. This report points out a possible role of bromocriptine in the development of this catastrophe and that careful follow-up is required when long-term treatment with bromocriptine is attempted.

Acromegaly↗
PubMed1983

Early post-operative growth hormone levels predict the result of transsphenoidal tumour removal in acromegaly.

Serum human growth hormone (hGH) measurements were performed during transsphenoidal microsurgery for acromegaly and in the early period afterwards. There were 14 patients of which 2 were operated on twice. In 11 patients (2 patients at reoperation) the serum hGH concentration was normalized to less than 5 micrograms/l within 3 h after completion of surgery. On five occasions only partial restoration of the hGH values was obtained and additional treatment was given in 2 patients by successful re-operation. The early post-operative hGH concentrations were consistent with the clinical evaluation of the patients and the hGH concentrations during follow-up for an average of 27 months. We conclude that early post-operative serum hGH measurement is of value for evaluation of the efficiency of the tumour removal and the need for further treatment.

Acromegaly↗
PubMed1983

The role of prolactin in the inhibitory action of bromocriptine on growth hormone secretion in acromegaly.

UNLABELLED: Bromocriptine treatment results in clinical improvement and inhibition of plasma GH levels in only part of the acromegalic patients. The possible role of the simultaneous presence of Prl and GH in GH-secreting pituitary adenomas was investigated with regard to the inhibitory action of bromocriptine on GH secretion and the paradoxical increase of GH release in reaction to TRH. Surgically obtained pituitary tumour tissue from 35 consecutive acromegalic patients was studied immunohistochemically. In 21 patients no Prl was present in the tumour tissue. These patients had normal plasma Prl levels. In the other 14 patients Prl was present in the tumour tissue. Hyperprolactinaemia was found in 10 of these 14 patient. Plasma GH levels from 2 till 10 h after the administration of 2.5 mg bromocriptine measured before operation were significantly more suppressed in the patients with mixed GH/Prl-containing than in those with pure GH-containing pituitary adenomas, being 38 +/- 4% and 65 +/- 4% of basal values, respectively (P less than 0.01). The response of GH to TRH, however, did not differ significantly between the two groups. CONCLUSIONS: 1. In about 70% of patients with 'mixed' GH/Prl containing adenomas, hyperprolactinaemia is present. 2. The simultaneous presence of Prl and GH in a GH-secreting pituitary tumour increases the sensitivity of GH secretion to bromocriptine. 3. The plasma Prl level is of value to predict which patients with acromegaly are likely to respond to bromocriptine with an inhibition of GH secretion.

Acromegaly↗
PubMed1983

No acute effect of pimozide on the plasma GH levels in acromegaly.

In 34 acromegalic patients either untreated or inadequately treated by surgery and/or radiotherapy the plasma GH levels and plasma Prl levels were determined during 8 h after the acute administration of the dopamine agonist bromocriptine and during 150 min after the administration of the dopamine antagonist pimozide. A 50% or more suppression of the basal GH levels was arbitrarily defined as a positive response. Seventeen patients displayed a positive response to bromocriptine, 17 patients displayed a negative response to bromocriptine. Plasma Prl levels were elevated in 6 of 17 bromocriptine responders and in 2 of 17 bromocriptine nonresponders. There was no difference in the plasma GH response to pimozide administration in the patients with a positive or a negative GH response to bromocriptine. With one exception there was in no patient a positive GH response to pimozide. In further experiments the plasma GH response to pimozide was measured during 11 h in 6 bromocriptine sensitive and 6 bromocriptine insensitive patients. Again no difference was found between bromocriptine responders and non-responders. There was also no difference in the Prl response to bromocriptine or pimozide between GH responders and GH non-responders. The Prl response to pimozide was blunted in comparison to a control group. The present study does not not lend support to the idea that there is a fundamental difference in the degree of hypothalamic dopaminergic control of GH or Prl secretion between bromocriptine sensitive and bromocriptine insensitive patients with acromegaly.

Acromegaly↗
PubMed1984

Changes in plasma GH levels and clinical activity during bromocriptine therapy in acromegaly. The value of predictive tests.

Twenty-seven patients with active acromegaly despite previous treatment by surgery and/or radiotherapy received bromocriptine in a dose of 10-20 mg daily for a period of 6-9 months. The results of chronic bromocriptine treatment were evaluated by measurement of plasma growth hormone (GH) levels during the day and by subjective and objective criteria of clinical activity. The results of chronic bromocriptine treatment were also compared with four biochemical criteria obtained before treatment e.g. basal plasma prolactin (Prl) levels and the plasma GH response to oral administration of 2.5 mg bromocriptine respectively iv administration of 200 micrograms TRH and 500 micrograms somatostatin. The main observations may be summarized as follows: 1) The mean pre-treatment GH levels during the day ranged from 6-207 mU/1. Hyperprolactinaemia was present in 6 patients. 2) During bromocriptine treatment mean plasma GH levels decreased to less than 50% in 11 patients (GH responders) whereas in 19 patients changes of mean plasma GH and of subjective criteria of clinical activity were concordant. 3) Glucose tolerance improved significantly (P less than 0.01) in 10 GH-responders and the urinary hydroxyproline/creatinine ratio decreased significantly (P less than 0.05) in 8 GH-responders. 4) Five out of 6 patients with hyperprolactinaemia belonged to the group of GH-responders. 5) A single dose of 2.5 mg bromocriptine induced a more than 50% decrease of plasma GH in 8 of 11 GH-responders and in 5 of 16 GH non-responders.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

The influence of bromocriptine and transsphenoidal surgery on urinary androgen metabolite excretion in acromegaly.

The urinary excretion of the androgen metabolites aetiocholanolone (E) and androsterone (A) as well as DHEA, 11-hydroxy-androsterone and the cortisol metabolites 11-oxo-aetiocholanolone and 11-hydroxyaetiocholanolone in normoprolactinaemic and hyperprolactinaemic male and female acromegalics was studied and compared with that of appropriate control groups. In addition several plasma hormones were also measured. The growth hormone level in the patient group varied from 10-550 mU/l. The excretion of both 11-hydroxy-androsterone and DHEA was normal. The excretion of androsterone had decreased, while aetiocholanolone and cortisol metabolite excretion had increased. The ratio between aetiocholanolone and androsterone (E/A) excretion was significantly increased in all patient groups, but no correlation was found between the growth hormone level and the E/A ratio. Treatment with bromocriptine caused a decrease in the E/A ratio in patients with decreased growth hormone levels, but not in patients in whom the growth hormone level remained unchanged. After selective transsphenoidal removal of the pituitary adenoma the E/A ratio decreased significantly. The increased E/A ratio in untreated patients could not be attributed to eventual changes in plasma levels of cortisol, thyroxine, prolactin, testosterone or oestrogens. We therefore suggest that growth hormone is involved in androgen metabolism in acromegaly.

Acromegaly↗
PubMed1985

Changes of molecular forms of growth hormone in bromocriptine treated acromegaly in relation to changes of somatomedin-C and clinical response.

Eleven patients with active acromegaly were treated with 10-20 mg bromocriptine daily for a period of 6-9 months. The clinical response was evaluated by a 'clinical and metabolic improvement score'. The biochemical response was evaluated by measurement of both the mean plasma growth hormone (GH) level during the day and the somatomedin-C (Sm-C) concentration. Before and at the end of the treatment period plasma samples were fractionated by Sephadex G-100 chromatography in order to study the effects of chronic bromocriptine treatment on the concentrations of total GH and its different molecular forms. The main observations may be summarized as follows: Three immunoreactive components were observed on Sephadex chromatography corresponding to molecular weight above 100 000 (big-big GH), 40 000-60 000 (big GH) and 20 000-22 000 (little GH). Bromocriptine treatment induced preferentially a reduction of little GH. There was a very good correlation between the decrease of little GH and total GH, and both were significantly correlated with the clinical response. The correlation between the decrease of Sm-C values and that of little and total GH as well as between the decrease of Sm-C and the clinical response was poor. It is concluded that a) measurement of little GH is not superior to the determination of total GH in the assessment of disease activity of bromocriptine treated acromegalic patients; b) both methods are superior to the measurement of plasma Sm-C levels; c) clinical response out of proportion ot the fall of total GH which can be explained by a preferential reduction of little GH, has not been observed in our investigations.

Acromegaly↗
PubMed1985

Cyproheptadine-mediated inhibition of growth hormone and prolactin release from pituitary adenoma cells of acromegaly and gigantism in culture.

The effect of cyproheptadine on growth hormone (GH) and prolactin (Prl) secretion from cultured pituitary adenoma cells of acromegaly and pituitary gigantism was studied. When varying doses of cyproheptadine ranging from 0.01 to 1 microM were added to the incubation media, GH secretion was consistently inhibited and a dose-response relationship was observed between the cyproheptadine concentrations and the amounts of GH released into the media. In pituitary adenomas which concurrently produced and secreted Prl, cyproheptadine likewise suppressed Prl release in a dose-related manner. This effect of cyproheptadine was not blocked by coincubation with serotonin. Similarly, coincubation with a dopaminergic antagonist, haloperidol, failed to reverse the inhibitory action produced by cyproheptadine. When coincubated with dopamine, cyproheptadine further inhibited GH and Prl secretion. These results suggest that cyproheptadine possesses a direct action on human somatotroph adenoma cells to inhibit GH and Prl secretion by an unknown mechanism that is different from serotonergic and dopaminergic systems.

Acromegaly↗
PubMed1986

Acromegaly and insulin resistance: a case study.

Elevated levels of growth hormone (GH) alter both the glucose tolerance and the sensitivity of peripheral tissue to insulin. We have studied the relationship between impaired glucose metabolism and its variations with different plasma levels of endogenous GH in one patient with acromegaly. To do so, we studied the decline in blood glucose concentration, as induced by iv insulin infusion, from a given hyperglycaemic level. With high levels of GH (GH = 120 micrograms/l), the slope of the straight line representing the decrease in blood glucose after insulin infusion was -0.71, the time required to achieve normoglycaemic levels, 270 min, and the corrected area under the curve representing blood glucose 26 070 units2. After 10 months' bromocriptine treatment, GH plasma concentration fell to 8 micrograms/l, at which point the slope of the straight line was -1.40, the time required to achieve normoglycaemic levels 115 min, and the area under the curve 8956 units2. There was a greater total clearance of glucose when GH levels were lower (1.90 vs 1.00 ml/min/kg), as well as greater elimination of glucose from the extracellular glucose pool (4.02 vs 1.67 mg/min/kg). In conclusion, in this patient the elevated plasma levels of endogenous GH induced insulin resistance. Once GH levels were reduced by the administration of bromocriptine, glucose metabolism improved.

Acromegaly↗
PubMed1988

Which factors predict the results of pituitary surgery in acromegaly?

Thirty-one patients with acromegaly who underwent pituitary surgery were investigated for possible predictive factors of the surgical outcome. The patients were divided into two groups: those whose GH levels normalized (less than 5 micrograms/l) after operation, group A (N = 18), and those whose GH levels remained elevated, group B (N = 13). There were no differences in age, sex distribution and sellar volume between both groups. There was a tendency to a higher incidence of supra-sellar extension of the pituitary tumor in group B (P less than 0.10). The basal GH levels in group A (38 +/- 5 micrograms/l) before operation were significantly lower than in group B (100 +/- 22 micrograms/l, P less than 0.002). Somatomedin C levels after the operation were significantly lower in group A than in group B (P less than 0.05) and were more often in the normal range (P less than 0.05). No differences were found in the occurrence of paradoxical GH responses to TRH and/or to GnRH between the groups and neither were there any differences in GH responses to GHRH and to bromocriptine between the groups. The sensitivity to SRIH tended to be higher in group A. After operation, the paradoxical GH response to TRH disappeared in 7 out of 10 patients and to GnRH in 2 out of 5 patients of group A, whereas in group B this anomaly persisted in all 9 after TRH and all 3 patients after GnRH. Hypopituitarism developed in only 5 out of the 31 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗