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PubMed1998

Heart failure in 3 patients with acromegaly: echocardiographic assessment.

We evaluated 3 patients with acromegaly who developed heart failure. Heart failure appeared to be due to acromegalic cardiomyopathy in 2 patients who did not have hypertension or evidence of coronary artery disease, and it was possibly due to acromegalic cardiomyopathy combined with familiar hypertrophic cardiomyopathy in 1 patient. The common echocardiographic findings in the present three cases were: 1) enlargement of the left atrium, 2) markedly dilated left ventricular cavity with diffuse hypokinesis, 3) decrease of indices of the left ventricular systolic function, and 4) no evidence of left ventricular hypertrophy. Echocardiographic findings in acromegaly with congestive heart failure resemble those of idiopathic dilated cardiomyopathy.

Acromegaly↗
PubMed2003

Acromegaly with multiple cardiovascular complications--cardiomyopathy, chordae rupture of mitral valve, myocardial infarction and sick sinus syndrome.

A 62-year-old woman had acromegaly and developed congestive heart failure with cardiomyopathy, mitral regurgitation due to chordae rupture, coronary artery disease and sick sinus syndrome. Since congestive heart failure was resistant to medical therapy, mitral valve replacement, aortocoronary bypass surgery and implantation of permanent pacemaker were performed one month after her admission. Although acromegalic patients with cardiomyopathy are usually resistant to therapy, we successfully treated the patient by the surgeries. It appears that all these diseases resulted from an elevated plasma concentration of growth hormone. Untreated acromegaly for more than ten years may contribute to multiple complications such as those in the present patient.

Acromegaly↗
PubMedDate not supplied

Follow-up study of the heart in acromegaly: pre- and post-operative evaluation.

Pre-operative and post-operative echocardiographic data were analyzed from 8 patients with acromegaly. Pre-operatively, end-diastolic diameter was greater than 55 mm in 5 patients (63%) and concentric left ventricular hypertrophy was observed in 3 patients (38%). However, left ventricular function was normal (fractional shortening of the left ventricle greater than 28%) in all patients except 1. All patients had increased left ventricular mass. There was no significant correlation between left ventricular mass and basal plasma growth hormone concentration. An average of 23.9 months after hypophysectomy, growth hormone concentration was significantly decreased. However, the abnormal echocardiographic findings remained. In conclusion, echocardiographic abnormalities (left ventricular dilatation and hypertrophy) are common in patients with acromegaly, but systolic function is, in general, maintained. These cardiac abnormalities persist after reduction of plasma growth hormone concentration.

Acromegaly↗
PubMed1990

Mixed pituitary adenoma and gangliocytoma associated with acromegaly--case report.

A gangliocytoma in the sellar region is very rare. We report a case of an intrasellar gangliocytoma complicated by pituitary adenoma presenting with acromegaly. A 52-year-old female was admitted to our hospital with headache, mild acromegaly, and bitemporal hemianopsia, and endocrinological study found a high serum level of growth hormone (GH). A computed tomographic scan revealed a tumor in the sellar region, which was almost totally removed by trans-sphenoidal surgery. Histological examination of the resected specimen showed diffuse, chromophobe-type pituitary adenoma, partially containing cholesterin clefts. Areas of clusters of dysmorphic neurons, adjacent to or mixed with pituitary adenoma, were diagnosed as gangliocytoma. The immunohistochemical examination showed GH-releasing hormone (GRH)-positive dysmorphic neurons and GH-positive pituitary adenoma. We consider that the trophic effect of GRH secreted by the neurons of GRH-producing intrasellar gangliocytoma probably caused the GH-producing pituitary adenoma.

Acromegaly↗
PubMedDate not supplied

Heredity and symptoms in acromegaly.

The author has performed clinical and follow-up studies of 80 acromegalic patients treated by transanthro-sphenoidal removal of the pituitary adenoma. Heredity for acromegaly or gigantism was recorded in 3.8% of the patients and other hereditary factors in 13.8%. Head trauma, meningitis or encephalitis was recorded in the case histories in 18.8%. The predominant symptoms were sweating, paraesthesiae, headache and joint pain. Acromegaly was in 37.6% associated with goitre, parathyroid adenoma, gastric or duodenal ulcer, parotid tumours of submandibular swelling. The fecundity among the married patients was good, 34.4% having three or more children. Successful pregnancies occurred after the transanthro-sphenoidal removal of the adenoma.

Acromegaly↗
PubMed1986

Somatostatin octapeptide (SMS 201-995) in the medical treatment of acromegaly.

Parenteral somatostatin has been used to suppress growth hormone secretion in acromegalic patients, but long-term treatment is hampered by its short half-life of a few minutes in the circulation. An octapeptide analogue of somatostatin (SMS 201-995) has recently been developed that has greater potency and selectivity in suppressing growth hormone than the native hormone. In this study somatostatin and somatostatin octapeptide infusions were compared in 13 patients with active acromegaly. The octapeptide had a longer duration of action in the suppression of growth hormone than native somatostatin. A twice daily dose of 100 micrograms significantly suppressed growth hormone during the day. Prolactin was not suppressed, even in hyperprolactinaemic patients, and suppression of insulin was of short duration. Two patients had diarrhoea, but this disappeared when treatment with the octapeptide was stopped. Somatostatin is known to suppress pancreatic exocrine function, and it is therefore important to look for evidence of malabsorption during long-term treatment with the octapeptide. Somatostatin octapeptide is therefore useful in the treatment of acromegaly, but evidence of malabsorption should be watched for; nonparenteral routes of administration need to be assessed.

Acromegaly↗
PubMed1985

The pathogenesis of acromegaly. Clinical and immunocytochemical analysis in 75 patients.

A series of 75 patients with acromegaly and immunocytochemically characterized pituitary adenomas has been analyzed. Tumors secreting growth hormone (GH) only were found in 21% of cases. The remainder had tumors immunoreactive for more than one pituitary hormone: GH and prolactin in 31%; GH, prolactin, and glycoprotein in 40%; and GH and glycoprotein in 8%. Microadenomas were surgically treated in 17 patients with a success rate of 82%. Overall, normalization of basal GH secretion (to less than or equal to 5 ng/ml) was achieved in 54% of cases. The implications of these findings for the pathogenesis and neurosurgical management of acromegaly are discussed.

Acromegaly↗
PubMed1986

Familial acromegaly with pituitary adenoma. Report of three affected siblings.

The authors report the cases of three brothers with pituitary adenomas who had classical findings of acromegaly and gigantism. Two had irreducibly elevated growth hormone (GH) values and underwent transsphenoidal microsurgical extirpation of their tumors. The third acromegalic brother had a normal GH value and evidence of panhypopituitarism; he had a small intrasellar tumor and a partially empty sella. The pattern of inheritance was probably autosomal recessive. A review of literature indicated that familial incidence of isolated acromegaly with pituitary adenomas is rare.

Acromegaly↗
PubMed1986

Therapeutic efficacy of a somatostatin analogue (SMS 201-995) in active acromegaly.

Twelve patients with active acromegaly, six of whom had not responded to previous combined surgery, radiotherapy, and bromocriptine administration, were treated with an octapeptide long-acting somatostatin analogue, SMS 201-995, given subcutaneously for up to 1 year. Growth hormone (GH) levels decreased by 50% to 90% after a single 25-micrograms SMS 201-995 injection in all patients, including two who were resistant to bromocriptine therapy. After GH values reached a nadir, they returned to preinjection values over a 12-hour period and no rebound was seen. Assessment of the GH-lowering effect of the drug at weekly intervals for the first 6 weeks and monthly thereafter disclosed no tachyphylaxis. Gradual increase of the dose from 50 to 150 micrograms daily led to a significant increase in clinical improvement. Shrinkage of the size of the pituitary tumor was documented in three of nine evaluated cases. Abdominal cramps of a transient nature not associated with diarrhea were noted in two patients but there were no other side effects. Hematological and biochemical blood and urine tests, including serum thyroxine and cortisol levels, did not reveal any abnormality during chronic treatment. This study demonstrates the safety and efficacy of SMS 201-995 in the short-term treatment of acromegaly.

Acromegaly↗
PubMed1995

Acromegaly, diabetes insipidus, and visual loss caused by metastatic growth hormone-releasing hormone-producing malignant pancreatic endocrine tumor in the pituitary gland. Case report.

The case of a 52-year-old woman with acromegaly, diabetes insipidus, and visual impairment caused by a metastatic growth hormone-releasing hormone (GRH)-produced pancreatic tumor is reported. Serum growth hormone (GH) and somatomedin C levels were elevated to 14 ng/ml (normal < 5 ng/ml), and 3.20 U/ml (normal < 1.88 U/ml), respectively. Paradoxical increases were observed in GH levels after glucose tolerance and thyrotropin-releasing hormone-stimulation tests. Biopsy of a pituitary tumor observed on computerized tomography scans and magnetic resonance studies revealed a metastatic cancer. When circulating GRH levels were measured, a marked increase in plasma GRH (1145 pg/ml; normal < 4-1 pg/ml) was observed. The patient died of cachexia due to metastases. Postmortem examination revealed that a primary tumor, a malignant endocrine lesion, was present in the pancreas, with metastatic tumors in the pituitary, lung, liver, and adrenal glands. Synthesis and production of GRH by the tumor was demonstrated by Northern blotting and immunohistochemical analysis. The pituitary gland showed hyperplastic, but not adenomatous changes. The authors stress the importance of both exploration for an ectopic source of GRH and the search for a GH-producing pituitary adenoma when unusual signs and symptoms are seen in patients with acromegaly.

Acromegaly↗
PubMedDate not supplied

New options for diagnosing and treating acromegaly.

Insulin-like growth factor 1 (IGF-1) is the final pathway of the growth hormone cascade, and is a better clinical measure of acromegaly than growth hormone itself. In patients with acromegaly, medical treatment with a somatostatin analog normalizes growth hormone and IGF-1 levels and produces clinical improvement quickly.

Acromegaly↗
PubMedDate not supplied

Acromegaly and pheochromocytoma: report of a rare coexistence.

OBJECTIVE: To describe a patient with the rare coexistence of acromegaly and pheochromocytoma. METHODS: We report a case of a 57-year-old woman, who was initially examined because of polyarthritis, she was also diagnosed with type 2 diabetes mellitus and hypertension at age 56 years. Her history, clinical findings, laboratory results, and management are summarized, and etiologic hypotheses are discussed. RESULTS: The patient had recurrent headaches and reported an increasing size of her shoes and gloves during the previous 4 years. Enlargement of her hands and feet and a bilateral temporal field defect were noted on examination. Laboratory studies revealed high levels of insulin-like growth factor I (IGF-I) and growth hormone (GH). Magnetic resonance imaging (MRI) showed a 3-cm sellar mass with impingement on the optic chiasm. The plasma level of growth hormone-releasing hormone (GHRH) was normal. She underwent transsphenoidal adenomectomy. Histologic examination confirmed a pituitary adenoma, immunoreactive for GH. Postoperatively, her headaches and arthritic pain diminished, and her levels of IGF-I and GH normalized; however, labile hypertension persisted. The urinary metanephrines and plasma catecholamines were increased. A 3-cm left adrenal mass, seen on abdominal MRI, was removed laparoscopically, after which urinary metanephrines normalized and both the diabetes and the hypertension resolved. Histopathologic analysis confirmed the diagnosis of pheochromocytoma. Immunohistochemical staining was negative for GHRH. CONCLUSION: The finding of a pheochromocytoma and acromegaly could be a fortuitous coexistence of two separate endocrine tumors; however, the probability of such an event is extremely low. A cause-and-effect relationship has been suggested because of previous reports of GHRH production by pheochromocytomas. Some investigators have also suggested that this coexistence might be a multiple endocrine neoplasia variant. Our patient had no evidence of GHRH production, nor did we document any familial autosomal dominant transmission pattern.

Acromegaly↗
PubMed1986

Treatment of resistant acromegaly with a long-acting somatostatin analogue (SMS 201-995).

Six patients with resistant acromegaly were given a long-acting somatostatin analogue (SMS 201-995) for 5 to 12 months. The clinical response was dramatic; relief of headache occurred within minutes of the injection. The mean 24-hour growth hormone levels fell acutely after the administration of 50 or 100 micrograms every 12 hours, especially in four patients with small tumors (p less than 0.001). Dosages of up to 1500 micrograms/d were necessary to produce maximum lowering of growth hormone secretion in some patients. On long-term treatment, plasma somatomedin-C levels fell in all patients and became normal in four. Plasma immunoreactive levels of SMS 201-995 related inversely to growth hormone concentration: A reproducible threshold for growth hormone inhibition in five of the patients, ranging from 70 to 1200 pg/mL, was maintained for 6 to 8 hours after the injections. This somatostatin analogue is effective in the treatment of acromegaly, has no major side effects, and causes only transient changes in carbohydrate metabolism.

Acromegaly↗
PubMed1992

Rapid reduction of left ventricular hypertrophy in acromegaly after suppression of growth hormone hypersecretion.

OBJECTIVE: To examine the possible role of growth hormone as a pathogenetic factor in the development of myocardial hypertrophy in acromegaly. DESIGN: An uncontrolled clinical trial. SETTING: Tertiary-care medical center. PATIENTS: Sixteen patients with acromegaly were stratified into two groups: Group I (n = 10) had left ventricular hypertrophy (LVH), and group II (n = 6) did not have LVH. INTERVENTION: Therapy with octreotide acetate (SMS 201-995), a long-acting somatostatin analog (mean dose, 538 micrograms/d), was administered for 2 months. MEASUREMENTS: Plasma growth hormone and insulin-like growth factor I (IGF-I) concentrations, hand volume, and echocardiographic left ventricular dimensions and mass were measured at baseline and at 1 week and 2 months after the start of therapy. RESULTS: Before octreotide therapy, both groups had similar hand volumes and similar growth hormone and IGF-I hypersecretion. Both groups showed a reduction in growth hormone at 2 months (mean reduction, 13.7 micrograms/L in patients with LVH [P < 0.01] and 14.1 micrograms/L in patients without LVH [P < 0.05]). Plasma IGF-I was also decreased (mean reduction, 305 micrograms/L in patients with LVH [P < 0.01] and 304 micrograms/L in patients without LVH [P < 0.05]). Reduction of growth hormone and IGF-I hypersecretion in patients with LVH was associated with a rapid decrease in left ventricular mass (339 g to 299 g, P < 0.01) within 1 week, which was sustained at 2 months (274 g, P < 0.04). Patients without LVH showed no statistical change in left ventricular mass. In patients with LVH, the decrease in left ventricular mass correlated with the octreotide-induced decrease in growth hormone (r = 0.79, P less than 0.05) but not with blood pressure. Blood pressure, left ventricular dimensions, and percent of fractional shortening were not altered by therapy in either group. Hand volume decreased in both groups. CONCLUSIONS: Normalization of growth hormone secretion is associated with reduction of left ventricular mass in acromegalic patients with LVH within 1 week of initiating therapy with octreotide.

Acromegaly↗
PubMed1978

Acromegaly and galactorrhea-amenorrhea with two pituitary adenomas secreting growth hormone or prolactin. A case report.

A prolactinoma was removed from a nulliparous woman who had acromegaly, galactorrhea-amenorrhea, elevated serum growth hormone and prolactin, and hypogonadotropinism. Postoperatively galactorrhea decreased and cyclic vaginal bleeding ensued; serum prolactin concentration was normal but growth hormone remained elevated and the acromegalic complex was unchanged, even after subsequently administered bromocriptine. At a second transsphenoidal operation, an adenoma of somatotropes was removed; improvement in symptoms and signs and normalisation of pituitary function, including growth hormone, followed. The possible presence of distinctly separate pituitary adenomas should be considered in patients with galactorrhea associated with acromegaly.

Acromegaly↗
PubMed1998

Morphologic analysis of dentofacial structure in patients with acromegaly.

The purpose of this study was to investigate the morphologic changes of the oral and maxillofacial skeletal structure in patients with acromegaly and the correlation between growth hormone, age at onset, and duration. Fifty-four acromegalic patients (28 men and 26 women) were compared with 45 normal adults (23 men and 22 women) using casts and cephalometric analysis. The incisor relationship was classified into four types: edge-to-edge bite, crossbite, maxillary incisor protrusion, and normal bite. Many cases of edge-to-edge bite and crossbite were observed in acromegalic patients. The most characteristic craniofacial skeletal differences in patients with acromegaly were protruded glabella and increased anterior face height. Enlargement of the ascending ramus and prominence of the mandible, chin, and mouth were the most noticeable profile characteristics of acromegalic patients. Male patients tended to demonstrate downward mandibular advancement and crossbite, while females showed extension of the ascending ramus, downward displacement of mandible, bimaxillary alveolar protrusion, and edge-to-edge bite.

Acromegaly↗
PubMedDate not supplied

Management and treatment of patients with acromegaly.

Untreated acromegaly causes substantial morbidity and mortality, and results in a marked reduction in quality of life. For this reason, the treatment goals need to be well defined and therapy optimised. This article describes the clinical approach to acromegaly, including: Pathophysiology of growth hormone secretion; Clinical features; Biochemical and radiological diagnosis; Treatment goals and therapeutic options; Prognosis.

Acromegaly↗
PubMed1999

[The role of insulin-like-growth-factor-binding protein 3 in the evaluation of disease activity in acromegaly].

Studied the diagnostic value of measurements of insulin-like growth factor binding protein-3 compared to insulin-like growth factor-1 as a parameter of disease activity in patients with active (n = 12, 8 females, 4 males, 29-69 years old) and inactive (n = 14, 11 females, 3 males, 28-58 years old) acromegaly. Patients were assigned to the active group if they had GH levels > or = 2 ng/ml, to the inactive group if they had growth hormone levels < 2 ng/ml after 75 g glucose challenge. The absolute serum insulin-like growth factor-1 concentration (526 +/- 66 ng/ml vs. 272 +/- 61 ng/ml, p = 0.015; mean +/- SE) and the insulin-like growth factor-1 standard deviation score (3.23 +/- 0.33 vs. 0.67 +/- 0.58, p = 0.0013) was higher in the active than in the inactive group, but no significant difference was seen between the corresponding insulin-like growth factor binding protein-3 values (7270 +/- 1500 vs. 5340 +/- 1050 ng/ml). Positive significant correlation was found between insulin-like growth factor-1 and insulin-like growth factor binding protein-3 both in the active (n = 12, r = 0.55, p < 0.05) and in the inactive (n = 14, r = 0.61, p < 0.05) group. A significant negative correlation existed between insulin-like growth factor binding protein-3 and age in the inactive (r = 0.58, n = 14; p < 0.05), but not in the active (r = 0.35, n = 12) group. The diagnostic value of insulin-like growth factor binding protein-3 is less than that of the insulin-like growth factor-1. Conclude that the insulin-like growth factor binding protein-3 has smaller suitability to determine the activity of acromegaly than the insulin like-growth factor-1 measurement.

Acromegaly↗