Normalization of glucose homeostasis by a long-acting somatostatin analog SMS 201-995 in a newborn with nesidioblastosis

Bruining, G. J.; Bosschaart, A.N; Aarsen, R. S. R.; Lamberts, Steven W. J.; Sauer, Pieter J. J.; Pozo, E. Del

doi:10.1530/acta.0.112s334

Cited by 21 publications

(11 citation statements)

References 7 publications

(11 reference statements)

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“…In addition, SMC levels were in agreement with adequate induction by circulating GH, whereas children with retarded growth have exhibited low values in another trial [13], although high variability has also been stated [14]. The data reported here are also in angreement with recent observations concerning the ef fect of SMS on similar cases treated for longer periods of time [5][6][7][8][9], but no GH analysis was made.…”

Section: Discussionsupporting

confidence: 87%

“…Hyperplasia of pancreatic islet cells leads to persistent hyperinsulin emia and, in most instances, to uncontrollable hypogly cemia. The potent inhibitory effect of SMS on B cell function has now been studied in this condition in acute trials [2][3][4] and in a few long-term observations [5][6][7][8][9], In the latter, normal growth progression despite somatotro pin suppression has been reported, but no sequential growth hormone (GH) measurements have been con ducted and the time relationship between the effect of SMS on GH and somatomedin C (SMC) generation has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

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Growth Progression and 24-Hour Hormone Profile in an Infant Treated Chronically with a Long-Acting Somatostatin Derivative

Rodrı́guez

Pozo²,

Rodríguez-Arnao³

et al. 1991

Horm Res

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The diagnosis of nesidioblastosis was established in a 9-month-old male child with a history of recurrent convulsive seizures and hypoglycemia. After unsuccessful subtotal pancreatectomy, treatment was started with the long-acting somatostatin derivative Sandostatin® (Octreotide, Sandoz) at a dosage of 25 µg t.i.d. spaced between carbohydrate-enriched meals. With this regime, blood glucose was maintained at the low normal range and seizures ceased. During a 30-month observation period, growth velocity and weight progression were well within the predicted limits. A 24-hour hormone profile recorded at the end of the observation period revealed the following: (1) failure to improve blood glucose with carbohydrate-enriched food due to reactive hyperinsulinemia; (2) hyperglycemic reaction after administration of Sandostatin caused by a reduction of plasma insulin; this effect was particularly marked during sleep; (3) low mean GH, decreased spiking frequency and reduced area covered by the nocturnal peaks by recognized standards, and (4) normal somatomedin C levels for age. Interpretation of growth hormone (GH) data is hindered by the lack of pertinent information from the patient’s age group. Recording of normal growth progression in the case illustrated here can only be explained by the capability of a reduced GH secretory rate to maintain full biological activity as shown by the normal plasma level of somatomedin C. Indeed, recent evidence has been provided elsewhere for normal growth progression in the presence of low GH secretion, although other factors unrelated to this hormone may also be operative at this early age. Further reports concerning the treatment of non-GH-dependent conditions with somatostatin derivatives will certainly contribute to the better understanding of the mechanisms governing growth in the postnatal period.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Growth Progression and 24-Hour Hormone Profile in an Infant Treated Chronically with a Long-Acting Somatostatin Derivative

Rodrı́guez

Pozo²,

Rodríguez-Arnao³

et al. 1991

Horm Res

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“…The success¬ ful use of Sandostatin in the treatment of acute (neonatal) hypoglycaemia in children with nesi¬ dioblastosis has been reported now in 3 children by several groups of investigators (Bruining et al 1986;Hindmarsh et al 1987;Delemarre-van de Waal et al 1987). Nesidioblastosis of the newborn.…”

mentioning

confidence: 95%

A guide to the clinical use of the somatostatin analogue SMS 201-995 (Sandostatin)

Lamberts

1987

Acta Endocrinologica

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SMS 201-995 (Sandostatin) is an octapeptide which differs in its action from native somatostatin in four ways: 1) it inhibits GH hormone secretion in preference to insulin secretion; 2) it can be administered subcutaneously or even orally; 3) it is long-acting (t1/2 after sc administration 113 min), and 4) there is no rebound hypersecretion of hormones when the effect of the analogue lingers off. In this paper a guide is offered for the use of Sandostatin in the treatment of acromegaly (after unsuccessful operation and/or radiotherapy) and of metastatic endocrine pancreatic tumours and carcinoids. A dose regimen for these two types of patients is suggested and the adverse reactions which can be expected are summarized. In addition, preliminary data are shown and the limitations are discussed of possible future indications of the analogue in the treatment of cancer, diabetes mellitus and gastrointestinal diseases. (1985): Treatment of patients with pancreatic endo¬ crine tumours using a new long-acting somatostatin analogue SMS 201-995: symptomatic and peptide responses. Gut 26: 438-444.

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“…The ratio of insulin and blood glucose concentration is considered to be indicative for hyperinsulinism when the value is higher than 5. In newborns this ratio rarely exceeds 1 [3]. Noteworthy is that at the time of blood sampling to determine the insulin concentration, the mean blood glucose level was 3.8 + 1.3 mmol/1 (range 1.7-6.4 mmol/1).…”

Section: Resultsmentioning

confidence: 98%

Glucose metabolism in a term infant with transient hyperinsulinism and high carbohydrate intake

et al. 1993

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Transient hyperinsulinaemia is a well-known cause of hypoglycaemia in newborn infants. The hypoglycaemia may be caused by a decreased glucose production and/or an increased glucose uptake. Whether the increased uptake is caused by increased glucose oxidation or increased non-oxidative disposal is not known. The aim of this study was to investigate the fate of the large amount of glucose infused in a term infant who developed hypoglycaemia due to transient hyperinsulinaemia shortly after birth and was treated with high glucose infusions. On day 6 an indirect calorimetry study was performed, together with a glucose turnover study. Carbohydrate intake was 13.6 mg/kg per minute (19.6 g/kg per day). Both studies were repeated on day 11, when carbohydrate intake was normalised to 7.8 mg/kg per minute (11.2 g/kg per day). Glucose oxidation was 28% higher and non-oxidative glucose disposal was 257% higher on day 6 as compared to day 11. Our results indicate that hypoglycaemia during hyperinsulinism is the result of increased non-oxidative disposal of glucose and not increased glucose oxidation. The results indicate a remarkable capacity of the newborn for lipogenesis during high carbohydrate intake.

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Normalization of glucose homeostasis by a long-acting somatostatin analog SMS 201-995 in a newborn with nesidioblastosis

Cited by 21 publications

References 7 publications

Growth Progression and 24-Hour Hormone Profile in an Infant Treated Chronically with a Long-Acting Somatostatin Derivative

Growth Progression and 24-Hour Hormone Profile in an Infant Treated Chronically with a Long-Acting Somatostatin Derivative

A guide to the clinical use of the somatostatin analogue SMS 201-995 (Sandostatin)

Glucose metabolism in a term infant with transient hyperinsulinism and high carbohydrate intake

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