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PubMed1976

Hypoglobulinemia in acromegaly.

We have observed an apparent hypoglobulinemia in 17 of 35 patients (48.6%) with acromegaly. This unexpected finding was persistent and reproducible up to six years for five acromegalic patients, and more than one year for nine other patients. Serum globulin was analyzed by three different methods, and the deficiency was most noticeable in the alpha globulin fraction (alpha1 greater than alpha2). When hypoglobulinemia occurred in control hospital in-patients (11%) it was associated with chronic or severe illnesses, and limited nutritional intake, but similar medical problems were absent in the acromegalic patients. There was no correlation of the hypoglobulinemia in the 35 acromegalic patients to their growth hormone (GH) concentration (r = 0.07), ages, sex, treatment status, or to the seriousness or duration of the acromegaly. The pathophysiology of the apparent hypoglobulinemia in acromegaly is unknown, but may be related to transport and/or disposal of excess growth hormone, or a defect in protein synthesis.

Acromegaly↗

PubMed1977

Pulmonary function in acromegaly.

The lung volumes of 12 female and eight male patients with acromegaly, chosen because of the absence of associated cardiorespiratory disease, were determined physiologically and radiographically. Enlarged lung volumes were found in half the males but in none of the females, due allowance being made for the presence of a significant thoracic kyphosis. Upper airway narrowing was suggested by an increase in the expiratory-inspiratory flow rate ratio in six patients, four of whom were male, and acromegaly of the larynx was confirmed in the three subjects who consented to laryngoscopy. Upper airway obstruction is more likely to account for respiratory death in acromegaly than disordered pulmonary function in enlarged acromegalic lungs. Neither of these respiratory findings could be correlated with the fasting level of growth hormone but there was a suggestion that they were more likely to occur when the duration of the disorder was longer.

Acromegaly↗

PubMed1979

Acromegaly associated with a bronchial carcinoid tumor: evidence for ectopic production of growth hormone-releasing activity.

A patient with acromegaly, pituitary enlargement, and elevated plasma GH levels also had a bronchial carcinoid tumor. Signs and symptoms of active acromegaly along with elevated GH levels persisted for 11 yr after hypophysectomy and pituitary stalk section. Resection of the bronchial carcinoid reduced plasma GH to barely detectable levels. Extracts of the frozen carcinoid tumor were devoid of significant GH, but when added to isolated pituitary cells of estrogen-primed male rats in 4-day primary culture exhibited specific GH-releasing activity in vitro. These findings strongly suggest that the patient's acromegaly resulted from continual stimulation of pituitary somatotrophs by a GH-releasing factor secreted by the bronchial carcinoid.

Acromegaly↗

PubMed1975

[Comparison with growth hormone responses to various drugs or substances in patients with active acromegaly (author's transl)].

Growth hormone (GH) responses to L-dopa, 2-Br-alpha-ergocryptine (CB-154), thyrotropine-releasing hormone (TRH), luteinizing hormone-releasing hormone (LH-RH), glucagon and glucose were investigated in six patients with active acromegaly. The following results were obtained. 1) Subcutaneous injection of 1 mg glucagon caused a clear-cut decrease in plasma GH levels in 5 out of 6 active acromegalic patients at 30 minutes after the injection. In 2 out of 6 patients a rebound of plasma GH was observed. 2) In three out of six patients with active acromegaly, oral administration of 0.5 g L-dopa caused a significant suppression of plasma GH levels. 3) CB-154 (2.5mg) administered orally elicited a marked decrease in plasma GH levels in the same three patients who showed a significant suppressive GH reponse to L-dopa, and the inhibitory effect of CB-154 on GH secretion lasted for 6 hours. These patients who had a GH response to L-dopa or CB-154 were named "responders". 4) Intravenous administration of TRH resulted in a significant increase in plasma GH in 4 patients 3 of whom were responders and the other a non-responder. 5) Pretreatment with CB-154 did not modify the TRH-induced GH increase in all patients who had a positive response to TRH. 6) A significant increase in plasma GH was elicited by the intravenous injection of 100 mug LH-RH in 3 out of 6 patients with acromegaly. 7) When oral administration of CB-154 had been given 2 hours before LH-RH, the GH response to LH-RH was blunted in two of three patients who had a LH-RH-induced increase in plasma GH levels.

Acromegaly↗

PubMed1979

Abnormal growth hormone responses to CB-154 and thyrotropin-releasing hormone (TRH) in patients with acromegaly.

CB-154 (2-Br-alpha-ergocriptine) stimulates growth hormone (GH) release in normal subjects. In acromegaly, however, this agent often decreases plasma GH level paradoxically. In order to examine the mechanism of the so-called "paradoxical decrease" in plasma GH with CB-154, GH responses to CB-154 were compared with GH responses to thyrotropin-releasing hormone (TRH), arginine, and luteinizing hormone-releasing hormone (LH-RH) in 20 cases of acromegaly. CB-154, as well as L-dopa, elicited decrease in GH in those patients whose GH secretion was more responsive to TRH and less responsive to arginine. These results suggest that, like L-dopa, CB-154 has similar dual actions of TRH antagonistic GH decrease and GH-RF (GH-releasing factor) facilitative GH increase. Moreover, it was speculated from this study that CB-154 has no significant effect on LH-RH release. The value of (increase ratio of GH on TRH)/(increase ratio of GH on arginine) can be used as an index for the indication of chronic CB-154 therapy in patients with acromegaly.

Acromegaly↗

PubMed1979

Acromegaly with normal growth-hormone levels and pituitary histology. Case report.

In rare cases, acromegalic patients have normal basal concentrations of growth hormone, and their acromegaly results from abnormal growth-hormone secretory patterns. A patient is reported with the clinical features of acromegaly, who had elevated somatomedin levels and an enlarged sella turcica, but whose serum growth-hormone levels on continuous monitoring were in the normal range, with levels of 2.8 to 8.9 ng/ml. Dynamic studies of growth hormone revealed normal responses to hypo- and hyperglycemia, but abnormal responses to L-dopa and thyroid-releasing hormone. At surgery, neither a pituitary adenoma nor eosinophilic hyperplasia was present. It is likely that this patient's acromegaly resulted from the presence of chronically high normal levels of growth hormone.

Acromegaly↗

PubMed1976

Insulin secretion and glucose tolerance in acromegaly.

Thirty patients with active acromegaly were divided into five groups according to the results of their IRI and blood glucose curves in the course of oral glucose tolerance test. Young acromegalics with short duration of acromegaly had grossly exaggerated IRI response with the peak in the first half-an-hour and the flat blood glucose curve. In the second group the peak of IRI response was in the first hour and the blood glucose curve rose to high values in the early stage after the glucose load. The IRI response in the third group was still exaggerated but delayed and the diabetic type of blood glucose curve was found in some of these patients. Acromegalics with overt diabetes mellitus lost their exaggerated IRI response and the IRI curves were flat in those with more advanced disturbance of glucose tolerance. It was suggested that the groups described might represent individual stages in the development of diabetes mellitus in acromegaly. Unclear position in this scheme is kept by the group of active acromegalics with IRI response in normal limits and glucose tolerance unimpaired.

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.

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PubMed1976

Prolactin concentrations in patients with acromegaly: clinical significance and response to surgery.

Basal serum prolactin and growth hormone (GH) concentrations were measured by radioimmunoassay in forty patients with acromegaly. GH concentrations were elevated in all patients studied before treatment and prolactin levels were raised in seven of twenty-six patients. Of the thirty-two patients reviewed after treatment (which in most cases was transsphenoidal hypophysectomy) twenty-five had GH concentrations below 5 ng/ml and twenty-nine had normal prolactin levels. In eighteen patients hormone measurements were made both before and after hypophysectomy: though GH levels fell in all but one, prolactin fell in only six patients. They were not significantly changed in eleven patients. There was no correlation of GH and prolactin either before or after surgery. Seven patients had greatly elevated prolactin levels and in four of these there was evidence of upward extension of a pituitary tumour on air encephalogram (AEG). Only one patient with a normal prolactin level had an abnormal AEG. Two patients with elevated prolactin concentrations and normal AEGs had a parallel fall of prolactin and GH in response to surgery. Four of the five hyperprolactinaemic men complained of loss of libido: in three gonadotrophin concentrations before and after treatment were normal. We conclude that there is no overall correlation of GH and prolactin levels in patients with acromegaly. Seven of twenty-six untreated patients (27%) had hyperprolactinaemia. We suggest that in these patients a raised prolactin level may be due either to interference with the normal inhibitory control mechanism of prolactin by suprasellar extension or, more rarely, to secretion of both GH and prolactin by the tumour itself. A high prolactin concentration may be the cause of the impotence of which some patients with acromegaly complain.

Acromegaly↗

PubMed1975

The Jewish Hospital of St. Louis therapeutic grand rounds no. 9. Diagnosis and therapy of acromegaly.

Acromegaly, the clinical expression of chronic hypersecretion of growth hormone, develops insidiously and is too often not recognized until the disease is advanced. However, a useful screening procedure, the measurement of serum growth hormone after an oral glucose load, is available. Though evidence suggesting that acromegaly may be a disorder of defective hypothalamic regulation of pituitary growth hormone secretion has accumulated, the pathogenesis of the diease is not sufficiently understood to permit consistently effective medical therapy. Current therapy, therefore, is directed toward destruction of growth hormone producing pituitary tissue. Patients with major suprasellar extension and chiasmal compression usually require transfrontal surgery. Patients without major suprasellar extension can be treated with external irradiation or with transsphenoidal surgery. It is our current practice to limit the former to young patients withe relatively modest elevation of the serum growth hormone concentration.

Acromegaly↗

PubMedDate not supplied

Hypoproteinemia in acromegaly.

Although it is well known that growth hormone may influence protein metabolism, few investigations have been undertaken on serum protein levels in acromegaly; recently hypoglobulinemia has been observed in this endocrine disorder. In 28 acromegalic patients and 56 control subjects sera have been analyzed for total protein determination and for electrophoretic protein separation. The results have shown that in acromegalic there is a slight but statistically highly significant decrease of serum total protein (mean +/- SE 6.66 +/- 0.07 g/100 ml vs 7.10 +/- 0.07 g/100 ml), albumin, alpha 1 and alpha 2-globulins. Since growth hormone stimulates protein synthesis, the pathophysiological significance of hypoproteinemia of acromegaly is at present obscure.

Acromegaly↗

PubMed1975

Serum lipids in acromegaly.

Serum cholesterol and triglyceride concentrations were determined in 46 patients with active acromegaly but with otherwise intact pituitary function. The mean serum-cholesterol level of the patients was lower and the mean serum-triglyceride higher than in the basic population of comparable age. The incidence of hypercholesterolemia was similar to that in general population, whereas the incidence of type IV hypertriglyceridemia was almost three times higher than in control population. The serum triglyceride level was not related to relative body weight, basal serum growth hormone, or insulin concentrations, nor did it correlate with glucose tolerance or with plasma-insulin response to oral glucose. However, the patients with highest plasma-insulin response had significantly higher serum triglyceride than the rest of the acromegalic group. The endogenous serum-triglyceride turnover rate showed no consistent changes, but increased serum triglyceride was associated with increased production rate. Upon successful surgical treatment of the acromegaly, serum-triglyceride level decreased in most of the cases who initially had hypertriglyceridemia. It is concluded that acromeagaly can give rise to moderate secondary hypertriglyceridemia.

Acromegaly↗

PubMed1978

Acromegaly and the temporal bone.

Acromegaly is a chronic disease of middle life resulting from excessive secretion of growth hormones by the acidophil cells of the anterior pituitary. The typical clinical features include enlargement of the skull, thorax, hands and feet. Recently, three patients with acromegaly have been operated upon for active otologic disease. In spite of massive mastoid cortex bone, the structures of the otic capsule were found to be of normal dimensions and in the usual relationships.

Acromegaly↗

PubMed1978

Surgical correction of the facial deformities of acromegaly.

The neurosurgical treatment of acromegaly is well established, but little has been written about correction of the facial deformities of this disease. Although hypertrophy of the skin and subcutaneous tissues may decrease after successful treatment of the pituitary tumor, there is no reversal of the bony changes. An acromegalic patient is presented whose facial deformities were repaired in stages by mandibular osteotomy and soft tissue excision. The history and pathology of acromegaly are reviewed.

Acromegaly↗

PubMed1975

Hypothalamic hormone interaction in acromegaly.

The growth hormone response to the administration of the currently available synthetic hypothalamic hormones was assessed in eleven patients with acromegaly. Eight of them showed a positive GH response to thyrotrophin releasing hormone and three showed no response. The GH response to TRH was shown to be unrelated to the thyrotrophin response to TRH. The GH response to TRH was inhibited by the administration of growth hormone release inhibiting hormone. Luteinizing hormone/follicle stimulating hormone releasing hormone (LHRH) caused a positive GH response in four patients, but this was trivial in three. The TRH mediated GH release in acromegaly is not mediated via TSH and appears to be attributable to loss of specificity of the receptor sites on the somatotroph to the hypothalamic hormones.

Acromegaly↗

PubMed1978

Growth hormone modulation of arginine-induced glucagon release: studies of isolated growth hormone deficiency and acromegaly.

Plasma glucagon and insulin responses to L-arginine were compared in normal controls and patients with isolated growth hormone deficiency and acromegaly. Patients with isolated growth hormone deficiency were characterized by high plasma glucagon response and low plasma insulin response, whereas acromegalic patients showed exaggerated plasma glucagon response and almost normal insulin response. These results suggest that growth hormone is probably required for optimum function of the islets, and since hyperglucagonaemia was observed in both growth hormone deficiency and acromegaly, metabolic disturbances stemming from the respective primary diseases may affect glucagon secretion.

Acromegaly↗

PubMed1978

Acromegaly: insensitivity of the pancreatic alpha cell to hyperglycaemia.

Plasma glucagon levels were determined after 50 g of oral glucose loading in eleven acromegalics and fourteen normal subjects. Basal plasma glucagon levels were significantly elevated in patients with acromegaly, as compared with those in normal subjects. Oral glucose loading caused a decrease in plasma glucagon in normal subjects but not in acromegalics. Since this non-suppressibility of plasma glucagon by orally administered glucose was observed even in acromegalics without diabetes, it is concluded that insensitivity of the pancreatic alpha cell to hyperglycaemia exists in patients with acromegaly as well as in diabetics.

Acromegaly↗

PubMed1978

Evaluation of the results of trans-sphenoidal surgery in acromegaly by assessment of the growth hormone response to thyrotrophin-releasing hormone.

Eighteen acromegalic patients GH-responsive to TRH were reinvestigated following trans-sphenoidal surgery and radiotherapy. Basal serum GH decreased below 10 microgram/1 in thirteen cases; nine of them became GH-unresponsive to TRH 1 month after operation, and another one following conventional pituitary irradiation. Four of these ten patients also showed a normal GH response to L-Dopa after treatment, and five responded normally to insulin-induced hypoglycaemia; two patients had a normal GH secretory pattern after both these stimuli. No recurrences were observed over a follow-up period of 15-80 months among the ten patients who became GH-unresponsive to TRH following operation, while one of the three subjects still responsive to TRH in spite of normalized basal serum GH concentration relapsed 10 months after surgery. Three patients with normalized TRH test following operation were repeatedly reinvestigated over a 3-6 years period and always found unresponsive. The present study shows that the 'paradoxical' GH responses to TRH and L-Dopa frequently disappear after surgery, that complete normalization of GH secretory pattern may rarely be attained, and that the disappearance of GH response to TRH probably indicates satisfactory treatment of acromegaly. These data suggest that the 'paradoxical' GH responses frequently found in acromegaly are dependent on the adenoma per se and not on hypothalamic dysfunction.

Acromegaly↗