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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a prospective study aimed at evaluating objectively the compliance with nasal continuous positive airway pressure (CPAP) treatment, 233 obstructive sleep apnea (OSA) (apnea index, > 10 apneas/hour) patients and 36 nonapneic snorers were studied. The compliance to treatment was measured by the mean rate of use of the CPAP device, obtained from a built-in time counter. The follow-up period was 874 +/- 48 in OSA patients and 675 +/- 83 in snorers. CPAP was proposed to all OSA patients but only to those snorers who felt improved after an initial laboratory night on CPAP. Nineteen OSA patients refused CPAP. Of the 214 OSA patients who accepted CPAP, 181 are still on treatment, with a mean daily rate of use of 5.6 +/- 0.1 hours (mean +/- SEM); 22 patients stopped CPAP after a variable period of time; 10 patients died and one acromegalic patient was considered cured after hypophysectomy for a pituitary adenoma. Depending upon the definition of acceptable compliance, the compliance rate in this group was between 77% and 89%. The mean rate of use was correlated with indices of disease severity (apnea index, apnea+hypopnea index, minimal SaO2 during sleep, daytime PaO2, pulmonary artery pressure). Thirty-six nonapneic snorers accepted CPAP. In this group, 26 are still on CPAP, with a mean daily rate of use of 5.4 +/- 0.5 hours; one patient died; one underwent uvolopalatopharyngoplasty without follow-up; and eight stopped CPAP. The compliance rate in this group was between 58% and 78%. This study shows that CPAP is reasonably accepted by OSA patients as well as by nonapneic snorers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term compliance with nasal continuous positive airway pressure (CPAP) in obstructive sleep apnea patients and nonapneic snorers. 147 Aug 8

Subjects with Cushing's disease have diminished growth hormone (GH) response to growth hormone-releasing hormone (GHRH). The aim of our study was to investigate the underlying mechanism of this diminished GH response in these patients using pyridostigmine (PD), an acetylcholinesterase inhibitor, which is reported to increase GH secretion by reducing somatostatin tone. Eight subjects with untreated Cushing's disease (caused by a pituitary adenoma) and 6 control subjects received GHRH 100 micrograms in 1 ml of saline, as intravenous bolus injection 60 min after (1) placebo (2 tablets, p.o.) or (2) PD (120 mg, p.o.). After GHRH plus placebo, the GH peak (mean +/- SEM) was significantly lower in subjects with Cushing's disease (2.4 +/- 0.5 micrograms/l) compared to control subjects (25.1 +/- 1.8 micrograms/l, p less than 0.05). After GHRH plus PD, the GH peak was significantly enhanced both in subjects with Cushing's disease (7.1 +/- 2.3 micrograms/l, p less than 0.05) and in control subjects (42.3 +/- 4.3 micrograms/l, p less than 0.05). In patients with Cushing's disease, the GH response to GHRH plus PD was lower with respect to the GH response to GHRH alone in normal subjects. We conclude that hypercortisolism may cause a decrease in central cholinergic tone which is in turn hypothesized to be responsible of an enhanced somatostatin release from the hypothalamus. However, other metabolic or central nervous system alterations may act synergistically with hypercortisolism in causing GH inhibition in patients with Cushing's disease.
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PMID:Pyridostigmine enhances even if it does not normalize the growth hormone responses to growth hormone-releasing hormone in patients with Cushing's disease. 180 75

We studied the sequential changes of plasma levels of immunoreactive '7B2' (IR-7B2), a neuroendocrine polypeptide, after a subcutaneous injection of 50 micrograms of synthetic octapeptide somatostatin analogue (SMS 201-995) in seven patients with acromegaly due to GH-producing pituitary adenoma. Compared to the basal levels, mean plasma IR-7B2 and GH levels significantly decreased, until 5 and 10 h respectively after the administration of SMS 201-995. The mean (+/- SEM) nadir levels of plasma IR-7B2 and GH were 68.1 +/- 10.1 and 13.1 +/- 6.9%, respectively, compared to mean plasma levels before treatment (100%). Plasma IR-7B2 as well as GH levels did not change significantly when saline was administered subcutaneously to three acromegalic patients. In addition, plasma IR-7B2 levels did not change significantly after the administration of SMS 201-995 in normal subjects or in patients with primary hypothyroidism in whom SMS 201-995 induced a decrease of plasma TSH levels. These results strongly suggest that SMS 201-995 has an unequivocal suppressive effect on the synthesis and/or the secretion of 7B2 in human somatotroph adenoma cells.
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PMID:Effect of octapeptide somatostatin analogue (SMS 201-995) on plasma 7B2 (a neuroendocrine polypeptide) levels in patients with acromegaly. 233 11

Specific somatostatin (SRIH) receptors on human pituitary adenoma cell membranes were characterized using [125I]Tyr11-SRIH as the radioligand. Specific binding of [125I] Tyr11-SRIH to adenoma cell membranes reached a steady state within 30 min at 25 C, and semilogarithmic analysis of the data revealed that the rate of the binding was linear at 25 C with a t1/2 of 13.2 min. Specific binding increased linearly with 5-160 micrograms plasma membrane protein. SRIH-14 and SRIH-28 inhibited [125I]Tyr11-SRIH binding to adenoma cell membranes with ID50S of 0.32 and 0.50 nM, respectively, while secretin, glucagon, gastrin, cholecystokinin-8, bombesin, TRH, LHRH, human GH-releasing factor-(1-44)-NH2, D-Ala2-met-enkephalin, gamma-aminobutyric acid and taurine did not significantly inhibit binding. All of 13 GH-secreting adenomas investigated had specific and high affinity SRIH receptors, with a dissociation constant (Kd) of 0.80 +/- 0.15 nM (mean +/- SEM) and a maximal binding capacity (Bmax) of 234.2 +/- 86.9 fmol/mg protein (mean +/- SEM). Among five of the nonsecreting pituitary adenomas examined, two had SRIH receptors with Kd values of 0.18 and 0.32 nM and Bmax values of 17.2 and 48.0 fmol/mg protein, respectively. In the remaining three, SRIH receptors were not detected. These results indicate that GH-secreting adenomas as well as some nonfunctioning adenomas have specific SRIH receptors, and hence, the function of the adenomas could be altered by SRIH.
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PMID:Specific somatostatin receptors on human pituitary adenoma cell membranes. 286 81

The plasma GH response to somatostatin (SRIH) infusion and SRIH receptors in pituitary adenoma cell membranes were investigated in six acromegalic patients. Infusion of 0.3 and 1.0 microgram/kg . h SRIH increased plasma SRIH concentrations in these patients in a dose-related manner. In five of the six patients, mean plasma GH levels decreased to 65.5 +/- 5.0% (+/- SEM) and 43.7 +/- 3.1% of the basal level when 0.3 or 1.0 microgram/kg . h SRIH was infused, respectively. In the remaining patient, plasma GH levels did not change, even when a larger dose of SRIH was infused. High density and specific SRIH receptors, with a mean dissociation constant of 0.92 +/- 0.17 nM and a mean maximal binding capacity of 523.8 +/- 174.6 fmol/mg protein, were identified in GH-secreting adenomas from the five SRIH-responsive patients. On the other hand, in the adenoma from the SRIH-nonresponsive patient, the maximal binding capacity (40.5 fmol/mg protein) was as low as those of nonfunctioning adenomas, as reported previously (undetectable to 48.0 fmol/mg protein). We conclude that the differential responses of plasma GH to SRIH in acromegalic patients may be related to variations in the binding capacity for SRIH in adenoma cell membranes.
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PMID:Plasma growth hormone responses to somatostatin (SRIH) and SRIH receptors in pituitary adenomas in acromegalic patients. 286 49

Dopamine receptors on human pituitary adenoma membranes were characterized using [3H] spiperone as the radioligand. The specific [3H]spiperone binding sites on prolactin (PRL)-secreting adenoma membranes were recognized as a dopamine receptor, based upon the data showing high affinity binding, saturability, specificity, temperature dependence, and reversibility. All of 14 PRL-secreting adenomas had high affinity dopamine receptors, with a dissociation constant (Kd) of 0.85 +/- 0.11 nmol/l (mean +/- SEM) and a maximal binding capacity (Bmax) of 428 +/- 48.6 fmol/mg protein. Among 14 growth hormone (GH)-secreting adenomas examined, 8 (57%) had dopamine receptors with a Kd of 1.90 +/- 0.47 nmol/l and a Bmax of 131 +/- 36.9 fmol/mg protein. Furthermore, 15 of 24 (58%) nonsecreting pituitary adenomas also had dopamine receptors with a Kd of 1.86 +/- 0.37 nmol/l and a Bmax of 162 +/- 26.0 fmol/mg protein. These results indicate that some GH-secreting adenomas as well as some nonsecreting pituitary adenomas contain dopamine receptors. But their affinity and number of binding sites are significantly lower (P less than 0.05) and fewer (P less than 0.001) respectively, than those in PRL-secreting adenomas.
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PMID:Demonstration of specific dopamine receptors on human pituitary adenomas. 357 89

This study reports the clinical and biological follow-up 5-11 yr after transsphenoidal selective adenomectomy in 25 patients with acromegaly. Eight patients had microadenomas, and 17 had macroadenomas. Initial normalization of plasma GH levels (basal values, less than 5 ng/ml; glucose-suppressed concentrations, less than 2.5 ng/ml) was achieved in all 8 patients with microadenomas and in 13 patients with macroadenomas. Of these, 3 patients with normal GH levels and dynamics had relapse of GH hypersecretion after intervals between 1-6 yr after microadenoma removal. Recurrence of pituitary adenoma was documented by surgery in 1 patient and by computed tomographic scanning in 2 others. Normal basal and glucose-suppressed plasma GH concentrations were maintained 7.4 +/- 0.5 (+/- SEM) yr after adenomectomy in 7 patients with microadenomas and in all 10 patients with macroadenomas. Thus, 88% of the patients with microadenomas and 59% of the patients with macroadenomas were cured, and the overall cure rate was 68%. We conclude that recurrence of acromegaly after successful surgery may occur late after adenoma removal and that it cannot be predicted by normal postoperative GH levels and dynamics. However, in view of the overall cure rate, transsphenoidal adenomectomy remains a most valuable treatment for acromegaly.
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PMID:Acromegaly: biochemical assessment of cure after long term follow-up of transsphenoidal selective adenomectomy. 405 86

It is commonly accepted that hypothalamic dopamine has an inhibitory role not only on prolactin but also on TSH secretion. To study the hypothalamic dopaminergic participation in TSH secretion in various hypothalamo-pituitary disorders, we examined the effect of sulpiride, a dopamine antagonist. Using a commercially available human TSH radioimmunoassay (RIA) kit and improving it, we developed a high sensitivity RIA for human TSH (assay sensitivity: 0.15 micro Units/ml, 50% B/B0 values: 3.47 micro Units/ml). In 18 normal controls, plasma TSH increased significantly after intramuscular injection of sulpiride of 1.01 +/- 0.17 micro Units/ml (Mean +/- SEM). In 61 patients with pituitary adenoma, plasma TSH responses to sulpiride were significantly greater than those of normal controls, and the mean maximal increments were as follows: 1.65 +/- 0.24 micro Units/ml in acromegaly (n = 21), 2.63+/- 0.55 micro Units/ml in non-functioning pituitary adenoma (n = 23), and 4.49 +/- 0.70 micro Units/ml in prolactin producing pituitary adenoma (n = 17), respectively. The maximal TSH responses to sulpiride in prolactin-producing pituitary adenoma were significantly greater than those in non-functioning pituitary adenoma (p less than 0.05) and those in acromegalic patients (p less than 0.001). On the other hand, we could observe no TSH responses to sulpiride in 9 cases of hypothalamic tumor with hyperprolactinemia. These results suggest that the dopaminergic inhibitory influence on TSH secretion is increased in patients with pituitary adenoma, and that it is especially dominant in patients with prolactin producing pituitary adenoma. It is concluded that hypothalamic dopaminergic tone can be evaluated indirectly by the sulpiride test, and that the test is useful in the differential diagnosis of hypothalamo-pituitary disorders.
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PMID:[Effect of sulpiride on plasma TSH secretion in various hypothalamo-pituitary disorders (author's transl)]. 709 11

Seven patients with growth hormone (GH)-secreting pituitary adenoma were treated preoperatively with octreotide (Sandostatin or SMS 201-995; a somatostatin analogue), and were compared with 18 non-treated patients in their clinical courses and adenoma analyses. Octreotide treatment improved the endocrinological data in all 7 cases. The octreotide-treated adenomas were soft and easily removed by suction and curettage. The postoperative normalization of endocrinological data was encountered more often in the octreotide-treated cases than in the non-treated, although the statistical significance was not observed by the limited number of cases. The adenoma tissues were examined with conventional histology and immunohistochemistry, and the amount of GH messenger ribonucleic acid (mRNA) was quantitatively assessed. The studies demonstrated: 1) No fibrosis nor necrosis was observed in the adenomas from the octreotide-treated patients. 2) Immunohistochemistry for human GH revealed no remarkable differences between the octreotide-treated and the non-treated adenomas. 3) The amounts of GH mRNA in the adenoma from the octreotide-treated patients were 4.2 +/- 1.8 (mean +/- SEM; expressed in an arbitrary unit) and were significantly less than those from the non-treated (33.6 +/- 9.1). These data suggest that octreotide inhibits not only GH release from the adenoma but also its biosynthesis.
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PMID:Octreotide treatment results in the inhibition of GH gene expression in the adenoma of the patients with acromegaly. 852 60

Plasma levels of chromogranin A (CgA) were measured by ELISA in 22 patients with pheochromocytoma (18 non-metastatic, 3 metastatic, and 1 mixed neuroendocrine-neural tumor), 9 patients with primary hyperparathyroidism, and 9 patients with pituitary adenoma. The plasma levels of CgA were compared with norepinephrine, epinephrine, parathyroid hormone and pituitary hormones, i.e., growth hormone and prolactin. In pheochromocytoma, CgA in preoperative plasma of the patients without metastasis was 228 +/- 38 U/L (mean +/- SEM) and significantly higher than healthy controls (30 +/- 11 U/L, n = 40). Plasma CgA was decreased after removal of the tumors (28 +/- 6.0 U/L), except in three patients with metastatic pheochromocytoma and a mixed neuroendocrine neural tumor. The concentration of CgA in the patients with non-metastatic pheochromocytoma was significantly correlated with that of plasma norepinephrine (P < 0.005, r = 0.68) and urinary norepinephrine (P < 0.05, r = 0.65), but not with that of epinephrine. There was an exceptional case in which CgA was extremely high, but the CA level was normal. This tumor was a highly malignant pheochromocytoma with extensive metastases composed of small tumor cells which were occasionally positive for tyrosine hydroxylase immunohistochemically. These cells were considered to be poorly differentiated tumor cells and synthesized a very small amount of norepinephrine. Plasma levels of the patients with primary hyperparathyroidism and the patients with pituitary adenoma were 44 +/- 4 U/L and 48 +/- 8 U/L, respectively. Only one patient with a growth hormone-producing pituitary adenoma had a high level of CgA. Plasma CgA is a useful tumor marker for pheochromocytoma, even for malignant pheochromocytoma without elevated CA level, but not for hyperparathyroidism, or pituitary adenoma.
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PMID:Plasma chromogranin A in pheochromocytoma, primary hyperparathyroidism and pituitary adenoma in comparison with catecholamine, parathyroid hormone and pituitary hormones. 922 69


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