Somatostatin treatment of insulin excess due to β-cell adenoma in a neonate

Kitson, Hilary; McCrossin, Robert; Jimenez, Marlene; Middleton, Aliya; Silink, Martin

doi:10.1016/s0022-3476(80)80353-2

Cited by 31 publications

(6 citation statements)

References 7 publications

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“…Nevertheless, efforts have been made to counteract excessive insulin secretion by non-invasive me¬ thods. Diazoxide has been administered to hypoglycémie children (Crowder et al, 1976) and more recently, somatostatin has also been tried with variable success alone or combined with glucagon (Hirsch et al (1977), Kitson et al (1980), Roti et al (1981) Petrus et al (1981), Bloomgarden et al (1980). The naturai peptide has been injected to hypoglycémie neonates in hourly do¬ ses of 44 to 120 ug.…”

Section: Discussionmentioning

confidence: 99%

“…The lacking capacity of adaptation to very low glucose levels and the difficulty in compensating for carbohydrate demands by exogenous administration of glucose may render the management of newborn hypoglycemia problematic. In certain instances, the in¬ travenous infusion of native somatostatin, which inhibits insu¬ lin secretion by the beta-cells, has been proven useful in the short term treatment of this condition (Hirsch et al (1977), Kitson et al (1980), Roti et al (1981), Petrus et al (1981)). The present report illustrates the effect of a new long acting somatostatin derivative, SMS 201-995 (Bauer et al, 1982), in a case of a newborn with nesidioblastosis.…”

Section: Introductionmentioning

confidence: 99%

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

Bruining¹,

Bosschaart²,

Aarsen³

et al. 1986

Acta Endocrinologica

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A female child was admitted to the hospital few days after birth with severe hypoglycemia and convulsive episodes. Plasma insulin levels were elevated and oral and intravenous administration of glucose were unable to keep blood glucose above 2 mmol/l limit. Intravenous infusion of a long acting somatostatin analog, SMS 201-995, at a dosage gradually increasing from 2 to 50 \g=m\g/24hr, was accompanied by a dramatic fall in circulating insulin levels. Normality of glucose homeostasis was restored and convulsive spells ceased. Fasting blood glucose levels stabilized between 3.4 and 4.7 mmol/l. No rebound phenomenon was observed during short term interruptions of the SMS 201-995 infusion. A subtotal pancreatectomy was performed during SMS treatment, and the diagnosis of nesidioblastosis was confirmed by immunocytologic and electron-microscopic studies. It is concluded that this new potent and long acting somatostatin derivative may be useful in the management of hyperinsulinism in the neonate.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Bruining¹,

Bosschaart²,

Aarsen³

et al. 1986

Acta Endocrinologica

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“…Diazoxide is usually the first drug to be tried, but it is often not effective, especially in severe hyperinsulinemic hypoglycemia of neonatal onset. Somatostatin has also been recommended and, with the arrival of long acting analogs, pancreatectomy or further resections have been avoided in certain patients (24,26,28,33). When medical treatment fails, surgery is unavoidable to prevent permanent brain damage.…”

mentioning

confidence: 99%

Neonatal Hyperinsulinemic Hypoglycemia: Heterogeneity of the Syndrome and Keys for Differential Diagnosis1

Sempoux¹,

Guiot²,

Lefevre³

et al. 1998

The Journal of Clinical Endocrinology &Amp; Metabolism

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The two major forms of infantile persistent hyperinsulinemic hypoglycemia require different treatments, but are difficult to differentiate during surgery. Indeed, one is characterized by focal adenomatous hyperplasia often macroscopically invisible, whereas the other consists of a diffuse, but discreet, ␤-cell abnormality. We evaluated, in a large series of persistent hyperinsulinemic hypoglycemia, the reliability of two criteria in differentiating these two forms: the mean ␤-cell nuclear radius (MNR) and the ␤-cell nuclear crowding, i.e. the number of nuclei per 1000 m 2 ␤-cell (BCNC). The values of the largest MNR and of BCNC in cases bearing a focal lesion (respectively, 3.27 m Ϯ 0.25 and 14.62 Ϯ 1.78) were significantly different from those in the diffuse pathology (4.25 m Ϯ 0.43 and 10.00 Ϯ 1.55). Setting the threshold value of MNR at 3.70 m and that of BCNC at 12.00 enabled correct classification of 90.9% of the diffuse and 100% of the focal forms.␤-Cell nuclear analysis can thus contribute to a subclassification of the syndrome, not allowed by clinical or biological data. If performed during surgery it could help in determining the extent of pancreatectomy necessary to cure the patient, as the diffuse form, with abnormal nuclei in the whole pancreas, requires subtotal to near-total pancreatectomy, whereas the focal form, devoid of abnormal insular ␤-cell nuclei, can be cured by partial pancreatectomy.

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“…The treatment is difficult, based on dextrose infusions and inhibition of insulin secretion with Diazoxide, or more recently with glucagon, somatostatine or steroids [2,3].…”

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confidence: 99%

Pancreatic venous samplings in infants and children with primary hyperinsulinism

et al. 1989

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The authors present 19 cases of hyperinsulinism in children worked up with selective pancreatic venous samplings (PVS). Focal lesions were found in 7, diffuse secretion in 8 and normal insulin levels in 4. In three patients with focal hypersecretion less extensive surgery could be performed and confirmed the presence of focal lesions in two. These preliminary results are encouraging and PVS seems to be a valuable technic for detection of focal lesions in the pancreas of children with hyperinsulinism.

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Somatostatin treatment of insulin excess due to β-cell adenoma in a neonate

Cited by 31 publications

References 7 publications

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

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

Neonatal Hyperinsulinemic Hypoglycemia: Heterogeneity of the Syndrome and Keys for Differential Diagnosis1

Pancreatic venous samplings in infants and children with primary hyperinsulinism

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