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At least 19 recordsLinked to original sources
PubMed1978

Lung function in acromegaly.

Lung function has been assessed by spirometry, body plethysmography, flow volume loops and single breath transfer factor in thirty patients with acromegaly. Having excluded eight patients with kyphosis and/or clinical or radiological evidence of pulmonary venous hypertension we have found a significant correlation between duration of acromegaly and lung size as assessed by total lung capacity. Excluding the same eight patients we have found evidence of small airways narrowing in eight patients, seven of these eight had had acromegaly for nine years or longer, and the duration of acromegaly was significantly longer in the patients with small airways narrowing than in those without. In the absence of other recognized causes it is possible that small airways narrowing in acromegaly is caused either by the increased whole blood volume with pulmonary vascular engorgement, or by increase in size of the soft tissues of the small conducting airways. Six of the eight patients with kyphosis and/or pulmonary venous hypertension also had evidence of small airways narrowing. Thus fourteen of the thirty patients with acromegaly had small airways narrowing. Five men had evidence of extra thoracic airway narrowing and in four the duration of acromegaly was ten years or longer. We conclude that the increase in total lung capacity, the incidence of small airways narrowing and the incidence of upper airway narrowing are all related to the duration of acromegaly. It seems that once duration exceeds eight years patients are very likely to develop abnormalities of lung function either primarily from the effects of acromegaly on the airways and lung or secondarily from the associated cardiovascular and thoracic skeletal abnormalities. It seems probable that the small airways and upper airway narrowing contribute to the morbidity and mortality of this disease. This study provides further evidence that acromegaly should be treated early.

Acromegaly↗
PubMed1992

Basal metabolic rate in adults with growth hormone deficiency and in patients with acromegaly: relationship with lean body mass, plasma insulin level and leucocyte sodium pump activity.

1. The relationship of lean body mass, plasma insulin concentration and leucocyte active sodium transport with basal metabolic rate was investigated in 24 adults with growth hormone deficiency before and after treatment with recombinant human growth hormone and in 10 patients with untreated acromegaly. 2. Based on total-body potassium determined by whole-body 40K counting, patients with acromegaly had increased lean body mass, whereas lack of growth hormone was associated with decreased lean body mass. 3. By indirect calorimetry, patients with acromegaly had increased basal metabolic rates and patients with growth hormone deficiency had decreased values when expressed as percentages of values predicted from the WHO/FAO/UNU equations. Basal metabolic rate expressed in terms of lean body mass was similar in acromegaly and growth hormone deficiency, but was higher than normal in both patient groups. 4. The leucocyte ouabain-sensitive sodium efflux rate constant was decreased in both patients with acromegaly and patients with growth hormone deficiency, and there was no correlation with basal energy expenditure, fasting plasma insulin level or serum growth hormone level. 5. There was no increase in the sodium efflux rate constant in patients with growth hormone deficiency after 1 month on treatment with recombinant human growth hormone. 6. Apparent differences in basal metabolic rate in growth hormone deficiency and acromegaly are due to changes in lean body mass. Both adults with growth hormone deficiency and patients with acromegaly have increased energy expenditure, probably owing to changes in fuel metabolism which are not reflected in the leucocyte sodium pump activity.

Acromegaly↗
PubMed1979

Absent growth hormone response to L-tryptophan in acromegaly.

In acromegaly, regulation of GH secretion by dopamine pathways appears to be qualitatively abnormal. To determine whether regulation of GH secretion by serotonin pathways is also abnormal in acromegaly, we administered L-tryptophan (5 g orally), the initial precursor of serotonin, to 10 patients with active acromegaly (9 treated and 1 untreated), 3 patients with cured acromegaly, and 8 normal subjects. The normal group showed a significant (P less than 0.05) increase in serum GH after L-tryptophan [peak value, 12.3 +/- 4.0 (se) ng/ml], though the magnitude of the response was highly variable. In contrast, subjects with active acromegaly did not show an increase in serum GH after L-tryptophan [mean integrated percentage change in serum GH, -25 +/- 25% (SE); P = NS]. One patient whose acromegaly had been surgically cured did show a GH rise after L-tryptophan. In acromegaly, the GH response to L-tryptophan is absent, suggesting that regulation of GH secretion by serotonin pathways might be qualitatively abnormal.

Acromegaly↗
PubMed1979

Bone isoenzyme of serum alkaline phosphatase in acromegaly.

In 37 patients with active acromegaly and in 15 patients with inactive acromegaly, activity of bone isoenzyme of serum alkaline phosphatase correlated (P less than 0.001) with serum concentration of immunoreactive growth hormone. By using stepwise regression analysis, the predication of serum growth hormone values based on serum levels of bone isoenzyme of serum alkaline phosphatase, gamma-glutamyl transferase and calcium in these patients with acromegaly was within 1 S.D. range in 37 patients and in only 2 patients was it out of 2 S.D. range. By using discriminant analysis, based on bone and liver isoenzymes of serum alaline phosphatase and urinary hydroxyproline excretion, 87%, 60% and 97% of the classification of patients with active and inactive acromegaly and healthy adults, respectively, was correct. The multivariate approach offers a quantitative appraisal of the biochemical parameters of peripheral growth hormone action used as an indicator of growth hormone concentration in patients with acromegaly.

Acromegaly↗
PubMed1975

Empty sella syndrome. Sequela of the spontaneous remission of acromegaly.

Untreated acromegaly is usually a progressive disorder resulting in early death from cardiovascular or pulmonary complications. Although spontaneous remission of the metabolic features of acromegaly is not uncommon, its correlation with return to truly normal serum growth hormone concentrations is not routinely documented. This study reports a patient with the empty sella syndrome occurring as a sequel to the spontaneous remission of acromegaly. This association, as well as the preservation of normal anterior-pituitary function, suggests that selective tumor infarction resulted in the "empty sella" and cessation of active acromegaly.

Acromegaly↗
PubMed1977

Macroglossia in acromegaly and hypothyroidism.

The tongues of two patients with macroglossia were examined at autopsy. One of the patients had acromegaly and the other had hypothyroidism. To evaluate the size of the enlarged tongues, the average weight of the tongue in the human adult was determined first in a series of 20 unselected autopsies, 10 males and 10 females (ages 44 to 85). The weight of the tongue was greater in males than in females and was directly correlated with the height of the subject. Cachexia had relatively little effect on the weight. In acromegaly (case 21) and myxedema (case 22) the tongue was enlarged by at least 50%. Histopathology showed enlargement of muscle fibers especially anteriorly in acromegaly and hypothyroidism, thickening of the epithelium and increased subepithelial and interstitial connective tissue. Incidental findings included venous thrombi and telangiectasia in the subepithelial connective tissue in both hypothyroidism and acromegaly and a corpus amylaceum and two islands of hyaline cartilage in the tongue of hypothyroidism.

Acromegaly↗
PubMed1976

[Stimulation of growth hormone and prolactin secretion with TRH in acromegaly (author's transl)].

Inappropriate stimulation of growth hormone (hGH)-secretion with TRH in acromegalic subjects has been shown previously, whereas prolactin (hPRL) secretion was reported to be blunted in active acromegaly. In this study TRH induced hGH and hPRL secretion was investigated in 23 active (mean hGH level: 68.5 +/- 19.9 ng/ml; +/- SE) and 15 inactive acromegalics (mean hGH level: 2.3 +/- 0.4 ng/ml; +/- SE). Fourteen of the active acromegalics showed a significant increase up to more than double of the basal hGH level after 200 mug TRH while in only one of the inactive acromegalics an inappropriate rise of hGH was induced by TRH. Basal hPRL levels were elevated in 9 and within normal range in 14 of the patients with active acromegaly. Except in 3 patients who had normal basal hPRL levels and in one patient with excessively elevated hPRL and hGH levels due to an hPRL and hGH producing adenoma, all patients had normal hPRL responses to TRH. In those with inactive acromegaly, 9 had hPRL levels below normal and only , out of the 15 patients showed a normal rise of hPRL after TRH. The patients who showed no hPRL response to TRH demonstrated also other signs of pituitary insufficiency due to the operative procedure. In contrast to a previous report these findings demonstrate that normal or enhanced hPRL secretion is found in active acromegaly. The inappropriate rise of hGH after TRH is compatible with a loss of specificity of the receptor for GRH of the adenoma cell and can be found also in patients with normal basal hGH levels after treatment suggesting that remaining adenoma tissue is present in the pituitary fossa.

Acromegaly↗
PubMed1979

Selective total removal of a growth-hormone-secreting adenoma: evidence that acromegaly is a primary pituitary disease.

Acromegaly is caused by hypersecretion of growth hormone by the pituitary. There is some debate as to whether the primary etiology of the disease is abnormal hypothalamic stimulation of the pituitary or a primary pituitary tumor. This paper presents a case of acromegaly in which growth hormone dynamics in response to stimulation and suppression tests were abnormal. After transsphenoidal adenomectomy of a small tumor, growth hormone levels returned to normal and suppression and stimulation test results reverted to normal within 1 wk postoperatively and remained normal for 2 yr. The findings suggest that the acromegaly in this case was due to a primary pituitary dysfunction. Microsurgical removal of growth-hormone-secreting tumors provides a unique opportunity to study the etiology of acromegaly.

Acromegaly↗
PubMed1975

Selected speech and fundamental frequency characteristics of patients with acromegaly.

Selected speech characteristics of patients with acromegaly, a relatively uncommon endocrine disorder resulting from excessive secretion of growth hormone, are described. In patients with acromegaly, increased quantities of circulating growth hormone may cause hypertrophy of multiple bodily structures, including components of the phonatory and articulatory apparatus. Speech recordings of 11 patients with acromegaly (six women and five men) were subjected to fundamental frequency and articulation analysis. Despite clinically apparent lingual hypertrophy in each of the patients studied, no speech articulation errors were found. In contrast, acromegaly appeared to produce a lowering of voice fundamental frequency (fo) characteristics in some, but not all, patients. Women exhibited more striking changes in fo than did men.

Acromegaly↗
PubMed1976

[Urinary excretion of hydroxyproline in acromegaly (author's transl)].

Urinary excretion of hydroxyproline was examined with the Hypronosticon test in 25 patients with acromegaly (13 men, 12 women) and 15 healthy persons. At the same time, plasma levels and urinary excretion of phosphorus and calcium were also measured. Patients with active acromegaly had a significantly higher urinary hydroxyproline output (32.55 +/- 8.68 mg/24 h m2) than healthy persons (12.12 +/- 2.33 mg/24 h-m2). They also excreted considerably more hydroxyproline than patients with successfully treated acromegaly. Effective treatment was proved by STH levels and good suppressibility by 100 mg glucose. Unsucessfully treated patients, on the contrary, had a raised urinary excretion of hydroxyproline (31.23 +/- 16.61 mg/24 h-m2) and high fasting plasma levels of somatotropic hormone. Hydroxyprolinuria proved, therefore, of value in assessing the development and treatment of acromegaly.

Acromegaly↗
PubMed1979

Immunoreactive somatomedin B in acromegaly and in Turner's syndrome.

Serum somatomedin B was measured by radioimmunoassay in forty-seven normal subjects, twenty-nine patients with acromegaly before and twenty-four after treatment, and eighteen patients with Turner's syndrome. Somatomedin B levels were significantly elevated in untreated acromegaly and in Turner's syndrome compared with the control group; they decreased following treatment of acromegaly. Because of the overlap between the groups, little information could be obtained from single somatomedin B estimations, which could, therefore, not replace dynamic tests of growth hormone secretion. No correlation between growth hormone and somatomedin B in acromegaly was detected; however, somatomedin B appeared to be related to the insulin response during the oral glucose tolerance test. In Turner's syndrome, no relationship between somatomedin B and insulin production, urinary oestrogen excretion, growth hormone secretion, gonadotrophin levels, age or height was found. The reason for the raised somatomedin B levels in Turner's syndrome remains at present unknown.

Acromegaly↗
PubMed1978

Diabetic retinopathy in acromegaly.

A study was made of diabetic retinopathy in acromegaly. 10 of 15 patients with acromegaly had diabetes mellitus, and 3 of the 10 showed diabetic retinopathy. 2 of them had a diabetic family history. 1 patient with a diabetic family history had retinopathy of state IIIa in Scott's classification, and the other 2 showed a few microaneurysms and/or punctate hemorrhages in the macula. Diabetes mellitus and diabetic retinopathy in acromegaly showed no correlation with the duration of acromegaly and diabetes mellitus, age, or growth hormone level. No diabetic cataract was found in the present series. It was concluded that diabetic retinopathy due to secondary diabetes mellitus is usually slight or moderate. Diabetes mellitus with severe retinopathy is probably primary diabetes due to a genetic defect, and secondary diabetes may be different in nature from the primary disease.

Acromegaly↗
PubMed1977

Cardiac size and function in acromegaly.

Sixteen acromegalic patients underwent echocardiography, phonocardiography, stress electrocardiography with Thallium perfusion scanning and gated radioisotope left ventricular angiocardiograms. Abnormalities consisting of increased echo left ventricular mass index, low velocity of circumferential fiber shortening or elevated pre-ejection period to left ventricular ejection time ratio were found in six patients with coexistent hypertension or coronary disease. Concentric left ventricular hypertrophy was also found in three patients with no known etiology other than acromegaly of greater than thirteen years' duration or with fasting growth hormone concentrations greater than 100 ng/ml. One of these three also had left ventricular dysfunction. Neither hypertrophy nor ventricular dysfunction was found in other acromegalics with shorter duration of disease or lower growth hormone concentrations or with normal growth hormone concentrations after therapy. A high prevalence of coronary artery and hypertensive heart disease is associated with acromegaly. A few patients with acromegaly have a specific, potentially reversible cardiomyopathy probably related to prolonged acromegaly or very high growth hormone concentrations.

Acromegaly↗
PubMed1976

The diurnal rhythm of plasma aldosterone, plasma renin activity, plasma cortisol and serum growth hormone and subnormal responsiveness of aldosterone to angiotensin-II in the patients with normotensive acromegaly.

The diurnal rhythm of plasma aldosterone concentration (PA), plasma renin activity (PRA), plasma cortisol (PC) and serum growth hormone (GH) were examined in 5 cases of normotensive acromegaly and the results were compared with the observations in normal subjects. Moreover, the response of PA to angiotensin-II infusion was studied in 6 cases of normotensive acromegaly. A normal diurnal rhythm with the lowest values in the evening or midnight and the highest values in the morning was observed in 3 of 5 cases in PA and 3 of 4 cases in PC. On the other hand, no apparent rhythm of GH was observed in any cases and that of PRA in 4 of 5 cases. Although there was a significant positive correlation between PA and PC, no significant correlation was demonstrated between PA and PRA. The response of PA to angiotensin-II fusion was significantly suppressed in normotensive acromegaly as compared to the normal subjects in spite of normal levels of PRA except for 1 case. The above observations were interpreted to suggest that the aldosterone regulation system is slightly altered in a certain number of patients with normotensive acromegaly in contrast to the normal subjects in which PRA is the main contributing factor. The low PA and suppressed response of PA toangiotensin-II infusion may suggest the defective action of angiotensin-II infusion on the adrenal gland.

Acromegaly↗
PubMed1976

Thyroid function in acromegaly before and after transsphenoidal hypophysectomy followed by cryoapplication.

Thyroid function was studied in acromegaly before and after transsphenoidal hypophysectomy followed by cryoapplication. The clinical material comprised 36 euthyroid, 1 hypothyroid and 3 hyperthyroid patients. In addition to the usual thyroid parameters a standard thyrotrophin-releasing hormone (TRH) stimulation test using 200 mug of synthetic TRH given iv was used. In untreated acromegaly with euthyroidism the response of serum TSH to TRH was significantly less than in normal controls, the increment being 7.1 mU/1 vs. 12.5 mU/1. In 23% of the patients the response was subnormal (less than 3.0 mU/1). The total thyroxine was significantly higher than in controls. Goitre occurred in 53% of the patients. After operation 3 patients became hypothyroid. In 30% of the patients remaining euthyroid the response to TRH was subnormal and the mean response in this group was close to the lower normal limit of 3.0 mU/1. In 7 patients who showed a subnormal response to TRH before or shortly after the operation there was a gradual increase and normalization of the response during the next few years. A subnormal, and also a low normal response to TRH before or after hypophysectomy does not necessarily indicate an increased risk for the development of hypothyroidism, and indeed the pituitary remnant seems to have a remarkable capacity for regeneration. In the hypothyroid patient there was a low normal response to TRH, the reason being unknown. In one of the hyperthyroid patients the basal TSH level was 6.5 and 8.9 mU/1 on two occasions in the thyrotoxic phase, showing a small response to TRH. The possibility that hyperthyroidism was due to increased secretion of TSH is discussed but not claimed proven. The incidence of hyperthyroidism in a large material of acromegaly from this department equals 9% which is above the prevalence of hyperthyroidism in the general population in Finland, indicating that acromegaly in one way or another seems to increase the incidence of manifest thyrotoxicosis.

Acromegaly↗
PubMed1992

[Acromegaly and bronchial carcinoid tumor. Apropos of a case].

Acromegaly due to ectopic secretion of growth hormone-releasing hormone (GHRH) is rare. A 29-year-old woman with acromegaly secondary to ectopic GHRH secretion by a bronchial carcinoid tumor is presented. Normalization of GHRH levels, reversal of pituitary hyperplasia and regression of acromegaly followed resection of the bronchial tumor. The authors stressed the interest of GHRH dosage in patients with acromegaly and pituitary hyperplasia.

Acromegaly↗
PubMed1977

Failure of selective pituitary adenomectomy to cure acromegaly.

Complete selective pituitary adenomectomy for acromegaly may fail to cure the underlying endocrinopathy. A 40-year-old man who had acromegaly of ten-years duration was initially treated with pituitary irradiation eight years prior to surgery. Three years after irradiation his mean GH concentration decreased from 53 to 9.0 ng/ml, then subsequently increased, and was associated with development of severe hyperglycemia. A transsphenoidal microdissection was performed, and a discrete pituitary adenoma was visualized and totally removed at surgery. GH concentrations decreased from 46 to 5.0 ng/ml one week after surgery and to 3.0 ng/ml 10 months after surgery. Despite improvement postoperatively, the patient still demonstrated abnormal GH dynamics and responses to the GTT, abnormal nocturnal and random GH sampling, and abnormal responses to the L-dopa, apomorphine, and TRH stimulation tests. Acromegaly could be caused by either hypothalamic hyperfunction, an autonomous pituitary tumor, or both; but the latter would not explain the results obtained in this patient. This suggests that reduction of GH to normal concentrations following selective pituitary adenomectomy is not synonomous with curing acromegaly.

Acromegaly↗
PubMed1978

[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↗