ArticleAnnals of pediatric endocrinology & metabolism2021
Pasireotide treatment for severe congenital hyperinsulinism due to a homozygous ABCC8 mutation.
Article in Annals of pediatric endocrinology & metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- A case of congenital hyperinsulinism withClinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2026Article
- Somatostatin and Its Analogues as Second-Line Treatments in Non-Neoplastic Conditions.International journal of molecular sciences · 2026Review
- Case Report: Pasireotide treatment in neonatal congenital hyperinsulinism due to a homozygousFrontiers in endocrinology · 2026Article
- Advances in Pharmacotherapy for Congenital Hyperinsulinism.Paediatric drugs · 2026Review
- A selective nonpeptide somatostatin receptor 5 agonist effectively decreases insulin secretion in hyperinsulinism.The Journal of biological chemistry · 2023Article
- Congenital hyperinsulinemic hypoglycemia (HH) requiring treatment as the presenting feature of Kabuki syndrome.Clinical case reports · 2023Article
- Standardised practices in the networked management of congenital hyperinsulinism: a UK national collaborative consensus.Frontiers in endocrinology · 2023Review
- Pasireotide-a novel somatostatin receptor ligand after 20 years of use.Reviews in endocrine & metabolic disorders · 2022Review
- Somatostatin receptors in congenital hyperinsulinism: Biology to bedside.Frontiers in endocrinology · 2022Review
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ABCC8 and KCJN11 mutations cause the most severe diazoxide-resistant forms of congenital hyperinsulinism (CHI). Somatostatin analogues are considered as secondline treatment in diazoxide-unresponsive cases. Current treatment protocols include the first-generation somatostatin analogue octreotide, although pasireotide, a second-generation somatostatin analogue, might be more effective in reducing insulin secretion. Herein we report the first off-label use of pasireotide in a boy with a severe therapy-resistant form of CHI due to a homozygous ABCC8 mutation. After partial pancreatectomy, hyperinsulinism persisted; in an attempt to prevent further surgery, off-label treatment with pasireotide was initiated. Short-acting pasireotide treatment caused high blood glucose level shortly after injection. Long-acting pasireotide treatment resulted in more stable glycemic control. No side effects (e.g., central adrenal insufficiency) were noticed during a 2-month treatment period. Because of recurrent hypoglycemia despite a rather high carbohydrate intake, the boy underwent near-total pancreatectomy at the age of 11 months. In conclusion, pasireotide treatment slightly improved glycemic control without side effects in a boy with severe CHI. However, the effect of pasireotide was not sufficient to prevent near-total pancreatectomy in this case of severe CHI.
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