Aggravation of hypoglycemia in insulinoma patients by the long-acting somatostatin analogue octreotide (Sandostatin®)

1989 ◽  
Vol 121 (1) ◽  
pp. 34-40 ◽  
Author(s):  
C. D. A. Stehouwer ◽  
W. F. Lems ◽  
H. R. A. Fischer ◽  
W. H. L. Hackeng ◽  
M. A. B. Naafs
Keyword(s):  
Blood Glucose ◽  
Hormone Secretion ◽  
Somatostatin Analogues ◽  
Serum Glucose ◽  
Somatostatin Analogue ◽  
Transient Decrease ◽  
Glucoregulatory Hormones ◽  
Octreotide Therapy ◽  
Long Acting ◽  
Analogue Octreotide

Abstract. Recently somatostatin analogues were successfully used to control insulin-induced hypoglycemia in patients with insulinoma. We observed a transient decrease in glucose levels and symptomatic hypoglycemia after administration of the long-acting somatostatin analogue octreotide (Sandostatin®) in two insulinoma patients. We studied the acute effects of octreotide (administered before breakfast) on blood glucose and glucoregulatory hormones in these patients. In one patient, we studied the effects of glucagon replacement and changing the time of breakfast (relative to octreotide administration) on octreotide-associated changes in blood glucose and glucoregulatory hormones. Compared with control levels, octreotide therapy reduced insulin levels. During hypoglycemia glucagon and growth hormone levels were suppressed, but cortisol levels appropriately increased. The increase in catecholamine levels was normal in one patient, but markedly attenuated in the other. A transient decrease in serum glucose after octreotide was absent after glucagon replacement, but present when breakfast was taken before administration of octreotide. We conclude that in patients with insulinoma, octreotide therapy may be associated with clinically important hypoglycemia, during which counterregulatory hormone secretion may be attenuated.

Resistant Paediatric Somatotropinomas due to AIP Mutations: Role of Pegvisomant

2018 ◽  
Vol 90 (3) ◽  
pp. 196-202 ◽  
Author(s):  
Kriti Joshi ◽  
Adrian F. Daly ◽  
Albert Beckers ◽  
Margaret Zacharin
Keyword(s):  
Combined Therapy ◽  
Somatostatin Analogues ◽  
Somatostatin Analogue ◽  
Tumour Mass ◽  
Residual Tumour ◽  
Control Disease ◽  
Long Acting ◽  
Analogue Octreotide

Background: Somatotropinomas are rare in childhood and frequently associated with genetic mutations. AIP mutations are found in 20–25% cases and cause aggressive somatotropinomas, often resistant to somatostatin analogues. Aims: To assess responses to multimodal therapy including pegvisomant in 2 children with sporadic somatotropinomas due to AIP mutations. Case Description: We report 2 children, a boy aged 13 and a girl aged 10, with rapid growth, visual impairment, and growth hormone hypersecretion. Magnetic resonance imaging confirmed a pituitary macroadenoma with parasellar extension in both. Despite multiple surgical attempts to debulk tumour mass, residual tumour persisted. Genetic analysis showed two different AIP mutations (patient 1: c.562delC [p.Arg188Glyfs*8]; patient 2: c.140_ 163del24 [p.Gly47_Arg54del8]). They were initially treated with a long-acting somatostatin analogue (octreotide LAR 30 mg/month) and cabergoline as a dopamine agonist, with the later addition of pegvisomant titrated up to 20 mg/day and with radiotherapy for long-term control. Somatostatin analogue was ceased due to patient intolerance and lack of control. Patient 1 had normalization of insulin-like growth factor-1 (IGF-1) after 5 months of combined therapy with pegvisomant and cabergoline. For patient 2, normalization of IGF-1 was achieved after 2 months of cabergoline and pegvisomant. Conclusion: AIP-associated tumours can be resistant to management with somatostatin analogues. Pegvisomant can safely be used, to normalize IGF-1 levels and help control disease.

Shrinkage of a primary thyrotropin-secreting pituitary adenoma treated with the long-acting somatostatin analogue octreotide (SMS 201-995)

1991 ◽  
Vol 124 (5) ◽  
pp. 487-491 ◽  
Author(s):  
André Warnet ◽  
Elisabeth Lajeunie ◽  
Françoise Gelbert ◽  
Michèle Duet ◽  
Philippe Chanson ◽  
...  
Keyword(s):  
Adverse Reactions ◽  
Pituitary Tumour ◽  
Somatostatin Analogue ◽  
Line Treatment ◽  
First Line ◽  
Sustained Improvement ◽  
Octreotide Therapy ◽  
Long Acting ◽  
Analogue Octreotide ◽  
First Line Treatment

Abstract. The long-acting somatostatin agonist octreotide can control TSH hypersecretion from most thyrotropic adenomas. Octreotide therapy has even been shown to improve chiasmal dysfunction. We report another patient in whom octreotide therapy was associated with gradual suppression of TSH hypersecretion, which escaped partially, dramatic and very rapid and sustained improvement of chiasm compression, and dramatic and sustained shrinkage of an unresectable TSH-secreting pituitary tumour. Unusual and prolonged gastrointestinal adverse reactions eventually disappeared except for steatorrhea. In conclusion, octreotide may be considered as first line treatment in patients with unresectable thyrotropic adenomas.

scholarly journals Somatostatin and gastrointestinal tract. Clinical experiences

2013 ◽  
Vol 154 (39) ◽  
pp. 1535-1540 ◽  
Author(s):  
László Herszényi ◽  
Emese Mihály ◽  
Zsolt Tulassay
Keyword(s):  
Gastrointestinal Tract ◽  
Gastrointestinal Hormones ◽  
Gastrointestinal Diseases ◽  
Somatostatin Analogues ◽  
Therapeutic Modality ◽  
Exocrine Function ◽  
Somatostatin Analogue ◽  
Clinical Experiences ◽  
Pancreatic Fistulas ◽  
Long Acting

The effect of somatostatin on the gastrointestinal tract is complex; it inhibits the release of gastrointestinal hormones, the exocrine function of the stomach, pancreas and bile, decreases motility and influences absorption as well. Based on these diverse effects there was an increased expectation towards the success of somatostatin therapy in various gastrointestinal disorders. The preconditions for somatostatin treatment was created by the development of long acting somatostatin analogues (octreotide, lanreotide). During the last twenty-five years large trials clarified the role of somatostatin analogues in the treatment of various gastrointestinal diseases. This study summarizes shortly these results. Somatostatin analogue treatment could be effective in various pathological conditions of the gastrointestinal tract, however, this therapeutic modality became a part of the clinical routine only in neuroendocrine tumours and adjuvant treatment of oesophageal variceal bleeding and pancreatic fistulas. Orv. Hetil., 2013, 154, 1535–1540.

Long-acting somatostatin analogue (Sandostatin) reduces late night insulinopenic ketogenesis in diabetic teenagers

1987 ◽  
Vol 116 (4_Suppla) ◽  
pp. S45-S53 ◽  
Author(s):  
R.S.R. Aarsen ◽  
G.J. Bruining ◽  
W.F.A. Grose ◽  
R. van Strik ◽  
S.W.J. Lamberts ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Insulin Pump ◽  
Movement Analysis ◽  
Early Morning ◽  
Insulin Pump Therapy ◽  
Rank Test ◽  
Somatostatin Analogue ◽  
Late Night ◽  
Free Insulin ◽  
Long Acting

Abstract. Ten diabetic teenagers were admitted into our hospital for two nights, separated by one week. In a double-blind cross-over randomized study they received either 50 μg of the new long-acting somatostatin analogue Sandostatin sc or placebo. All patients were between 12 and 16 years of age, C-peptide negative with a duration of diabetes of at least four years. They had either conventional therapy or insulin pump therapy. Insulin doses and diets were kept unchanged. Blood samples were taken half hourly from 17.00 h until 09.30 h the next morning from an indwelling venous catheter. Hormonal and metabolic profiles on the two nights were evaluated by means of a distribution free time sequential co-movement analysis and by the paired Wilcoxon's signed rank test. After Sandostatin was given at 22.00 h, GH levels were significantly suppressed during 4 h. During that period blood glucose was slightly but significantly lower than after placebo. The free-insulin profiles from both nights were very comparable. Co-movement analysis showed a significant correlation between glucose and free insulin variations with a 30-min backward shift of the glucose curve. However, after Sandostatin administration this relation was lost in the period between 22.00 and 07.00 h, indicating a different effect of insulin on glucose levels during the nights Sandostatin was given. Early morning glucose rises were associated with free insulin levels below 20 mU/l. This association was not altered during the Sandostatin nights. Glucagon was not suppressed by Sandostatin except at 120 min after injection, and remained unchanged during the rest of the observation period. Triglyceride levels as well as 3-OH-butyrate values were significantly lower after Sandostatin. Plasma levels of FFA, free glycerol, alanine and cortisol were not significantly reduced. It is concluded that a single sc injection of 50 μg of Sandostatin given at 22.00 h is a potent GH inhibitor and lowers blood glucose concentrations for up to 4 h after injection. Early morning blood glucose rise is not prevented, but overnight hepatic ketogenesis as reflected by 3-OH--butyrate levels appears suppressed by Sandostatin up to the next morning injection of insulin.

PHARMACOKINETICS OF THE LONG-ACTING SOMATOSTATIN ANALOGUE OCTREOTIDE (SMS 201-995) IN ACROMEGALY

1990 ◽  
Vol 32 (5) ◽  
pp. 545-550 ◽  
Author(s):  
J. NICHOLLS ◽  
D. WYNICK ◽  
J. DOMIN ◽  
L. M. SANDLER ◽  
S. R. BLOOM
Keyword(s):  
Somatostatin Analogue ◽  
Long Acting ◽  
Analogue Octreotide

Clinical use of the long acting somatostatin analogue octreotide in pediatrics

1994 ◽  
Vol 153 (5) ◽  
pp. 304-310 ◽  
Author(s):  
M. T. Tauber ◽  
A. G. Harris ◽  
P. Rochiccioli
Keyword(s):  
Somatostatin Analogue ◽  
Clinical Use ◽  
Long Acting ◽  
Analogue Octreotide

Clinical and pathophysiological aspects of somatostatin and the gastrointestinal tract

1987 ◽  
Vol 116 (4_Suppla) ◽  
pp. S19-S25 ◽  
Author(s):  
C. B.H.W. Lamers
Keyword(s):  
Gastrointestinal Tract ◽  
Gastrointestinal Haemorrhage ◽  
Somatostatin Analogues ◽  
Exocrine Secretion ◽  
Somatostatin Analogue ◽  
Cell Hyperplasia ◽  
Secretory Diarrhoea ◽  
D Cell ◽  
Long Acting ◽  
Clinical Conditions

Abstract. Somatostatin is present in the gastrointestinal tract in appreciable amounts. The highest concentrations of the polypeptide are found in the stomach, the upper small intestine, and the pancreas. Within the gastrointestinal tract, somatostatin inhibits various functions, including endocrine and exocrine secretion, motility, blood flow, absorption, and growth. The polypeptide regulates these functions by endocrine, paracrine, neurocrine or luminal mechanisms. Abnormalities of endogenous somatostatin have been implicated in several gastrointestinal disorders, including the somatostatinoma syndrome, antroduodenal D-cell hyperplasia, peptic ulcer, obesity, and liver cirrhosis. Because of its potent inhibitory effects, somatostatin or somatostatin-analogues have been used as therapeutic agents in various clinical conditions, such as upper gastrointestinal haemorrhage, endocrine pancreatic tumours, gastrointestinal and pancreatic fistulas, pancreatitis, secretory diarrhoea, and dumping syndrome. The recent availability of the synthetic long-acting somatostatin-analogue SMS 201-995 (Sandostatin) has greatly facilitated the therapeutical application of somatostatin-polypeptides.

Disappearance half-life times of exogenous and growth hormone-releasing factor-stimulated endogenous growth hormone in normal rats

1991 ◽  
Vol 128 (3) ◽  
pp. 369-374 ◽  
Author(s):  
I. M. Chapman ◽  
A. Helfgott ◽  
J. O. Willoughby
Keyword(s):  
Growth Hormone ◽  
Endogenous Growth ◽  
Half Life ◽  
Somatostatin Analogue ◽  
Blood Samples ◽  
Growth Hormone Releasing Factor ◽  
Hypothalamic Hormones ◽  
Significant Difference ◽  
Long Acting ◽  
Analogue Octreotide

ABSTRACT This study was performed to determine the disappearance half-life times of endogenous and exogenous rat GH in conscious normal rats and to compare these with the decay characteristics of GH at the end of spontaneous normal bursts. The endogenous half-life was determined in five rats by giving an i.v. injection of rat GH-releasing factor followed after 10 min by an i.v. injection of long-acting somatostatin analogue (octreotide) and taking blood samples for 85 min. The half-lives (mean ± s.e.m.) were 3·4±0·4 min and 13·2±1·1 min for the first and second exponential respectively as determined by bi-exponential analysis. The exogenous GH half-life was determined in ten rats by giving i.v. octreotide followed after 10 min by i.v. rat GH and sampling for 85 min. The half-lives of exogenous GH were 3·3±0·2 min and 17·5±1·4 min by bi-exponential analysis and there was no significant difference between the half-lives of endogenous and exogenous GH. The half-life of the decline of GH levels at the end of spontaneous bursts in nine rats was 14·4±0·9 min, not different from the half-life of endogenous GH, the secretion of which was terminated by octreotide. This suggests that the end of spontaneous GH bursts is marked by sudden cessation of GH release and may provide an indication of the rapidity of change in the levels of the underlying hypothalamic hormones which control GH release. Journal of Endocrinology (1991) 128, 369–374

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