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PubMed1995

Desensitization to somatostatin analogue (Octreotide) observed in a patient with acromegaly.

We encountered a 33-year-old female patient with a pituitary growth hormone (GH)-secreting macroadenoma. The patient was treated with somatostatin analogue (Octreotide) in combination with bromocriptine for 2 months before a transsphenoidal adenomectomy was carried out. Octreotide (300-800 micrograms/day) in combination with bromocriptine was effective in reducing the size of the adenoma by 36%, but produced only a marginal decrease in serum GH. After the operation, bromocriptine alone (15 mg/day) did not lower the level of GH which was produced by residual adenoma tissue. When octreotide (200 micrograms/day) was resumed along with the bromocriptine one year after the operation, it effectively lowered serum GH for 6 months. Thereafter, octreotide therapy became ineffective with a concomitant rise in serum GH and somatomedin C, which was not accompanied by an increase in tumor size. This was a rare case of acromegaly that showed desensitization to octreotide after long-term treatment.

Acromegaly↗
PubMed1995

Scalp hair loss caused by octreotide in a patient with acromegaly: a case report.

We used octreotide to treat a woman with acromegaly and observed pituitary adenoma shrinkage after 5 months. Diffuse scalp hair loss occurred after 5 months, resulting in the discontinuation of treatment. After the cessation of octreotide, the hair loss stopped and hair growth resumed. Since bromocriptine did not effectively decrease the GH level of the patient, we decided to perform transsphenoidal surgery. After resection of the pituitary adenoma, her GH and IGF-1 levels were normalized. Although octreotide-induced scalp hair loss has not been well recognized, we should pay more attention to this side effect.

Acromegaly↗
PubMed1995

Short-term effects of octreotide on glucose tolerance in patients with acromegaly.

To elucidate the short-term effects of octreotide, a somatostatin analogue, on glucose tolerance in acromegaly, the plasma glucose and insulin responses to a 75-g oral glucose tolerance test (75-g OGTT) were examined in 6 patients. The glucose disposal rate (GDR) was also measured by the hyperinsulinemic euglycemic clamp method before and after the administration of octreotide. Before octreotide therapy, 2 patients had normal responses of plasma glucose and insulin to 75-g OGTT (normal glucose tolerance: NGT) and 4 showed hyperinsulinemia or glucose intolerance (glucose intolerance: GIT). GDR-insulin dose-response curves showed a normal pattern in patients with NGT and pattern of insulin resistance in patients with GIT. After 2-3 weeks of octreotide administration, plasma growth hormone (GH) levels decreased in all of the patients. The plasma glucose response to 75-g OGTT was not changed in any patient. In contrast, the plasma insulin response to 75-g OGTT was enhanced in patients with NGT but lessened in patients with GIT. Patients with NGT showed no significant change in GDR-insulin dose-response curves. Patients with GIT showed improvement in GDR at low levels of plasma insulin, but did not show complete improvement at high levels. These results indicate that octreotide improves insulin resistance at the insulin receptor site by lowering plasma levels of GH and insulin in acromegalic patients with glucose intolerance.

Acromegaly↗
PubMed1996

Heterogeneous responses to the long-term treatment of active acromegaly with octreotide.

To study GH response to the long-acting somatostatin analogue, we treated 11 actively acromegalic patients with octreotide (Sandostatin), 100 micrograms, sc, tid, for six months. Their endocrinological outcomes and clinical improvements varied. The 11-h GH secretory profiles on pretreatment day confirmed the hypersecretion of GH in all patients. Three hours after the first dose of octreotide, serum GH declined rapidly to levels below 5 ng/ml in all but two patients who failed to normalize their serum GH. In spite of the subsequent doses, there was no further suppression in serum GH. Drug resistance with GH rebound developed in some patients after three months of continued treatment. The paradoxical serum GH rises in response to oral glucose or iv TRH detected before the treatment in all patients attenuated or disappeared after the 6-month octreotide therapy; an exceptional case was one of the above-mentioned two patients, whose serum GH was stimulated more than before by glucose and TRH at the end of therapy. Serum insulin-like growth factor I (IGF-I) levels of all patients showed a significant reduction after 6-month treatment, but their mean values remained abnormally high. There were no intolerable adverse side effects; some patients, however, experienced pain at the injection site, passage of loose stool, and incidence of new gall stone or intrahepatic lesions on octreotide therapy. We concluded that octreotide was a useful long-term adjunctive therapeutic agent for patients with active acromegaly, but that a high degree of response heterogeneity including total refractoriness would be expected.

Acromegaly↗
PubMed1997

Assessment of insulin resistance in acromegaly associated with diabetes mellitus before and after transsphenoidal adenomectomy.

With a euglycemic hyperinsulinemic clamp method, whole-body insulin resistance was assessed in 6 cases with acromegaly associated with diabetes mellitus before and after transsphenoidal adenomectomy. The glucose infusion rate (GIR) correlated well with the plasma IGF-I level but poorly with that of GH. Further improvement in insulin sensitivity occurred 3-4 months after operation without substantial changes in plasma levels of both GH and IGF-I or glycemic control. These results indicate that GH excess can induce insulin resistance in association with plasma IGF-I and also through undefined secondary effect.

Acromegaly↗
PubMed2003

Mortality in 154 surgically treated patients with acromegaly--a 10-year follow-up survey.

To determine the effects of surgery and adjuvant therapy on the mortality rate of Japanese patients with acromegaly, 154 surgically treated patients were followed until death or December 2000. Mean follow-up period was 10.0 +/- 6.5 (SD) years. Postoperative GH levels, mean values of GH levels measured in the first postoperative month, were <2.5 ng/mL in 73 (47.4%), 2.5-5.0 ng/mL in 50 (32.5%), and >5.0 ng/mL in 31 patients (20.1%). Three of 123 patients with postoperative GH levels <5.0 ng/mL underwent a second transsphenoidal surgery (TSS), the other 120 received no further treatment. Additional treatments, including second TSS, medical treatment, and gamma-knife irradiation for residual tumor, were administered to 25 of 31 patients whose postoperative GH was >5.0 ng/mL. Among the total 154 patients surveyed, 11 (7.1%) died during the follow-up period. The standard mortality ratio (SMR) was 1.17, not different from age- and sex-matched controls. The SMR of the 72 patients with postoperative GH <2.5 ng/mL was better than that of the 51 patients whose postoperative GH was 2.5-5.0 ng/mL (1.09 vs. 1.64); however, the difference was not statistically significant. In conclusion, TSS and adequate adjuvant treatment decreased the excess mortality rate of acromegalics to nearly the same level as that of the general Japanese population.

Acromegaly↗
PubMed2003

Acromegaly with fibrous dysplasia: McCune-Albright Syndrome -- clinical studies in 3 cases and brief review of literature--.

The McCune-Albright syndrome (MAS) is characterized by a triad of poly/monostotic fibrous dysplasia, café-au-lait macules and hyperfunctioning endocrinopathies including growth hormone (GH) excess. Polyostotic bone lesions and café-au-lait macules are common while monostotic bone lesions are rare. Similarly, acromegaly as a manifestation of endocrine hyperfunction with MAS is uncommon and in most of the instances somatotropinoma has not been documented. We report 3 patients, two of them had monostotic lesion, none had café-au-lait macules and all had GH secreting pituitary macroadenoma. All of them underwent transfrontal pituitary adenomectomy and had histopathological confirmation of GH secreting pituitary adenoma. A brief review of literature is also presented.

Acromegaly↗
PubMed2004

Serum levels of 20 kilodalton human growth hormone (20K-hGH) in patients with acromegaly before and after treatment with octreotide and transsphenoidal surgery.

Circulating human GH (hGH) consists of several molecular isoforms. It was previously reported that the proportion of 20 kilodalton hGH (20K-hGH) was elevated in the serum of patients with active acromegaly. In this study, we investigated the effects of octreotide and transsphenoidal adenomectomy on the proportion of 20K-hGH in the serum of 7 acromegalic patients. To achieve an acute effect, octreotide (100 microg) was subcutaneously injected as a bolus. To observe the chronic effects of octreotide therapy and surgery, serum samples were obtained by repetitive blood sampling before and 3 to 8 weeks after treatment. Serum levels of 20K-hGH and 22 kilodalton hGH (22K-hGH) were determined by specific enzyme-linked immunosorbent assay. A bolus injection of octreotide elicited a parallel decrease in serum 22K-hGH and 20K-hGH, resulting in an unchanged proportion of 20K-hGH to total circulating hGH. The proportion of 20K-hGH was decreased in 4 of 4 patients 4 to 7 weeks after surgery and in 2 of 4 patients after chronic treatment with octreotide for 3 to 8 weeks. The proportion of serum 20K-hGH was positively related to mean serum 20K-hGH as well as serum total hGH levels, but not with serum IGF-I levels. These findings suggest that high serum levels of 20K-hGH or total hGH per se might elicit a chronic change in the clearance kinetics of 20K-hGH and increase the proportion of 20K-hGH in acromegalic patients.

Acromegaly↗
PubMed1975

Suppression of serum growth hormone levels by glucagon in patients with active acromegaly.

One mg of glucagon was given subcutaneously to eight patients with active acromegaly. Seven out of eight patients had a rapid decrease in serum growth hormone (GH) levels at 30 min after the glucagon injection. In two out of seven patients a rebound increase in serum GH following the early GH reduction was observed. On the other hand, oral administration of 50 g glucose which caused a comparable increase in blood glucose to that after the glucagon injection elicited no early suppression in serum GH levels in the same patients. These data suggest that the inhibition of GH release induced by glucagon could not be related to the increase in blood glucose by glucagon.

Acromegaly↗
PubMed1984

Acromegaly and HLA.

The frequencies of HLA-antigens in A, B, C and DR loci were examined in 34 Japanese patients with acromegaly. The frequency of DRW9 was slightly higher and the frequency of DR4 was slightly, but not significantly, lower than the controls.

Acromegaly↗
PubMed1984

Modulation of postinhibitory rebound rise in plasma GH by hypothalamic hormones in patients with acromegaly.

To evaluate the GH regulating mechanism in acromegalic patients, post-inhibitory rebound rise in GH secretion induced by somatostatin was studied in these cases and normal subjects, and was compared with the rebound GH rise induced by dopamine. After somatostatin infusion (500 micrograms/75 min) both 5 normal and 9 acromegalic subjects showed prompt GH decreases during the infusion (% decrease: 69.1 +/- 10.4 vs 74.4 +/- 5.1) and showed rebound rises after its termination. However, the rebound rises occurred more promptly and markedly in normal controls than in acromegalic patients, i.e. the rebound peak appeared at 45 min in normal controls and at 75 min in acromegalic patients after the cessation of somatostatin infusion. Dopamine (DA) infusion (5 micrograms/kg/min for 90 min) also induced similar inhibition and postinhibitory rebound rises in GH secretion in 7 patients with acromegaly. Although the maximum inhibition (65.6 +/- 6.4% vs 74.4 +/- 5.1%) and the inhibitory area (4338.0 +/- 481.5% X min vs 3682.5 +/- 295.5% X min) during the DA or somatostatin infusion were not different, the rebound at 15 min was significantly greater after DA than after somatostatin (p less than 0.02). When TRH was injected at the termination of somatostatin infusion, the rebound increase was significantly enhanced and the rebound peak appeared 45 min earlier than after a single somatostatin administration. Similarly, hp GRF (1-44)-NH2 enhanced the postinhibitory rebound rises in 4 patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

A case of acromegaly associated with Graves' disease. A possible role of endogenous TRH and an effect of bromocriptine on GH and TSH secretion.

A 44-year-old man subjected to Hardy's operation for a treatment of acromegaly developed hyperthyroidism right after surgery. He had a normal thyroid function with a slightly suppressed TSH response to TRH before operation. Sudden onset of hyperthyroidism after surgery and suppressed TSH were compatible with Graves' disease. Hyperthyroidism was effectively treated with propylthiouracil (PTU) with slightly increased basal TSH level and normal response of TSH to TRH. Plasma GH level also increased after he attained euthyroidism, but inappropriate GH response to TRH persisted. It is suggested that increased endogenous TRH stimulated both TSH and GH release, but inappropriate GH response to TRH occurred irrespective of endogenous hypothalamic TRH. Bromocriptine, 5.0 mg/day, suppressed plasma GH level to a normal range with a concomitant suppression of PRL and TSH, both basal levels and responses to TRH.

Acromegaly↗
PubMed1986

Effect of a single administration of somatostatin analogue (SMS 201-995) on GH, TSH and insulin secretion in patients with acromegaly.

The effect of a long-acting somatostatin analogue SMS 201-995 on GH secretion was investigated. Eleven acromegalic patients received a single dose of 50 micrograms SMS 201-995 administered subcutaneously, and plasma GH, IGF-I, GRF, TSH, IRI and blood glucose were determined at regular intervals. Nine of 11 patients had elevated basal plasma GH levels above 5 ng/ml. In all patients, plasma GH levels fell immediately from 39.5 +/- 17.3 ng/ml (mean +/- SEM) to 4.3 +/- 1.6 ng/ml (P less than 0.05) with a maximal inhibition of 82.9 +/- 3.3% of the basal levels and the suppression persisted for about 6 h of the observation period. IGF-I and GRF levels were not apparently altered. TSH and IRI levels also rapidly fell. Blood glucose levels fell slightly by 0.5 h. Ten of 11 patients had pain at injection sites. Except for this, no side effects were observed. Our results show that the new somatostatin analogue SMS 201-995 may inhibit GH hypersecretion in acromegalic patients for significant periods, suggesting that this agent can be a useful clinical tool for the treatment of acromegaly.

Acromegaly↗
PubMed1988

A case of active acromegaly with reduced height and type 1 renal tubular acidosis.

A 41-year-old man with acromegaly was suffering from chronic, progressive backache and aware of reduction in his body height. Endocrine studies revealed increased glucose non-suppressible serum growth hormone (GH) and serum prolactin (PRL). Pituitary microadenoma was detected by a computerized axial tomogram and subsequently resected by trans-sphenoidal adenomectomy. The tumor proved to be a mixed GH- and PRL-secreting adenoma by electron microscopy and immunoperoxidase staining. Concurrent investigation of backache and reduced height disclosed markedly reduced radiodensity of the spinal bones, bilateral nephrocalcinosis, and hypercalciuria, which were ascribed to renal tubular acidosis (RTA) demonstrated by reduced urinary excretion of acids and insufficient reduction of urinary pH following oral administration of ammonium chloride. From the analogy to certain endocrinopathies, it appears likely that enhanced calcium metabolism and resultant hypercalciuria due to excess GH and PRL have led to the development of RTA, which further enhanced calciuria. Such enhanced calcium metabolism and consequent hypercalicuria conceivably led to accelerated demineralization of the spine and resulted in the reduced height of this patient in his early forties.

Acidosis, Renal Tubular↗
PubMed1988

Treatment of acromegaly with long acting somatostatin analogue SMS 201-995.

Ten acromegalic patients were treated with the somatostatin analogue SMS 201-995 (SMS) for 3-38 weeks in various doses and by different administration routines (thrice daily or multiple sc injection). Plasma GH daily profiles, plasma IGF-I, urinary GH, serum TSH, IRI and fasting blood glucose (FBG) concentrations were measured before and during SMS treatment. Plasma GH rapidly decreased within one hour in all patients and was suppressed for at least 4 h after a 50 micrograms sc injection of SMS in 8 patients. Multiple injections of 300-600 micrograms/day SMS (25-50 micrograms X 12) suppressed GH throughout the day. Plasma IGF-I was completely normalized in 4 patients, and, in all but one of the others, decreased markedly. Urinary GH decreased within the first week of treatment in all patients and normalization was obtained in 3 patients. Shrinkage of the pituitary tumor, as determined by CT or MRI, was observed in 7 of 9 patients. Other clinical improvements, such as diminution or complete disappearance of swelling of soft tissues, excessive perspiration, and headache, were observed in 7 of 8 patients. Changes in serum TSH, IRI and FBG were seen in 3-4 patients, but without any apparent clinical problems. In conclusion, SMS is a useful clinical tool for treatment of acromegaly, and a multiple sc injection method seems to be preferable.

Acromegaly↗
PubMed1989

Comparative in vivo and in vitro studies on abnormal GH secretion in patients with acromegaly.

Eight patients with active acromegaly due to GH-producing pituitary adenoma were studied. GH secretory dynamics in vitro was evaluated by adding GRF, CRF, or a somatostatin analog, SMS 201-995 to the perifusate of dispersed cells from tumors. A comparison was made between the data obtained in preoperative tests for GH secretion and those obtained in experiments in vitro. Before operation, the GRF test (100 micrograms, iv) resulted in no GH response in three of six patients examined. The CRF test (100 micrograms, iv) resulted in a paradoxical GH increase in two of the same six patients. In vitro studies performed on adenoma cells revealed that exposure to GRF (100 ng/ml) elicited an increase in GH in seven of eight patients examined. Exposure to CRF (100 ng/ml) caused an enhanced GH secretion in four of the same eight patients. There were cases in which GH response to these hypothalamic hormones was observed in vitro but not in vivo, whereas there was only one case in which CRF caused an increase in GH in vivo but not in vitro. Thus, GH secretory dynamics was not always the same in vivo and in vitro. The discrepancy could be ascribed to the different secretory status of hypothalamic hormone (e.g., GRF or somatostatin) in vivo in each acromegalic patient.

Acromegaly↗
PubMed1989

Growth hormone releasing hormone-sensitive adenylate cyclase activity in growth hormone-producing pituitary adenoma: correlation to the response of plasma growth hormone to growth hormone releasing hormone in patients with acromegaly.

The correlation between response of plasma GH to GHRH and the GHRH-induced stimulation of the intracellular adenylate cyclase (AC) activity in pituitary adenoma cell membranes in acromegalic patients was investigated. Each peak plasma GH level after iv administration of GHRH ranged from 1.1 to 13.8 times the basal level in 13 acromegalic patients. On the other hand, the maximal stimulation of intracellular AC activity (cAMP production) induced by GHRH varied from 1.4 to 6.4 times the control level in each GH-producing pituitary adenoma cell membrane. A significant positive correlation (r = 0.89, P less than 0.005) between plasma GH response to GHRH and intracellular cAMP production stimulated by GHRH was observed in nine of the acromegalic patients. In contrast, the response of plasma GH to GHRH was significantly blunted, despite a fairly large production of intracellular cAMP stimulated by GHRH, in the other four acromegalic patients. These results suggest that GHRH-induced GH release from GH-producing pituitary adenomas of patients with acromegaly may be regulated not only by GHRH receptor-adenylate cyclase system but also modified by several other factors including somatostatin and Sm-C.

Acromegaly↗
PubMed1989

The combination therapy with bromocriptine and cyproheptadine in patients with acromegaly.

The therapeutic efficacy of the combination of cyproheptadine and bromocriptine was studied in 15 patients with active acromegaly showing incomplete GH suppression in response to bromocriptine therapy alone. The mean basal plasma GH was 31.3 +/- 5.5 micrograms/L, and it decreased to 19.0 +/- 3.9 micrograms/L during the single bromocriptine therapy (10 to 20 mg for 2 to 21 months). When cyproheptadine (12 to 16 mg for 8 to 52 months) was added to bromocriptine therapy, plasma GH decreased further (9.4 +/- 3.0 micrograms/L: vs pretreatment, P less than 0.001; vs bromocriptine treatment, P less than 0.005), and GH normalization was obtained in 8 patients. The plasma somatomedin-C levels in these 8 patients (0.3-1.8 U/ml) were within the normal range during the combination therapy. Plasma GH responses to TRH or GHRH were markedly suppressed in 6 patients during the combination therapy compared to pretreatment or during bromocriptine treatment. In addition, a clear reduction in the tumor size was observed in 4 of 7 previously untreated patients during the combination therapy. In conclusion, cyproheptadine has therapeutic efficacy in acromegalic patients who showed incomplete GH suppression in response to treatment with bromocriptine alone. Following the cyproheptadine and bromocriptine combination therapy tumor shrinkage was observed in some patients.

Acromegaly↗