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Related Experiment Videos

Nesidioblastosis and persistent neonatal hyperinsulinism

C Sempoux1, F Poggi, F Brunelle

  • 1Department of Pathology, University Hospital St Luc, Brussels, Belgium, USA.

Diabete & Metabolisme
|December 1, 1995
PubMed
Summary

Diffuse neonatal hyperinsulinism, causing severe hypoglycemia, may stem from beta-cell functional abnormalities rather than increased cell mass. Histological examination reveals potential clues to this condition.

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Area of Science:

  • Pediatric Endocrinology
  • Cell Biology
  • Surgical Pathology

Background:

  • Neonatal hyperinsulinism (NH) presents with severe hypoglycemia, potentially leading to neurological damage.
  • Pancreatic abnormalities in NH include focal or diffuse lesions; diffuse forms often necessitate subtotal pancreatectomy due to uncertain pathogenesis.
  • Investigating the underlying causes of diffuse NH is crucial for improving treatment strategies.

Purpose of the Study:

  • To explore hypotheses regarding the pathogenesis of diffuse neonatal hyperinsulinism.
  • To re-evaluate the role of nesidioblastosis and beta-cell mass in diffuse NH.
  • To identify the most probable cause of diffuse NH, focusing on cellular function.

Main Methods:

  • Histological examination of pancreatic tissue from hyperinsulinemic infants.

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  • Immunohistochemical analysis using specific antibodies to detect proinsulin.
  • Microscopic evaluation of beta-cell mass and D-cell volume density.
  • Assessment of nuclear and cytoplasmic morphology in pancreatic cells.

    • Main Results:

    • Nesidioblastosis is not specific and does not represent continuous endocrine cell proliferation.
    • Increased beta-cell mass was not consistently observed in hyperinsulinemic infants compared to controls.
    • While a decrease in D cells was inconsistently noted, increased proinsulin in the Golgi and abnormal cell morphology suggest a functional beta-cell abnormality.

    Conclusions:

    • The pathogenesis of diffuse neonatal hyperinsulinism is unlikely due to increased beta-cell mass or consistently decreased D cells.
    • Beta-cell functional abnormality, indicated by proinsulin processing and cellular morphology, appears to be the most likely explanation for diffuse NH.
    • Intraoperative morphological examination and proinsulin messenger RNA studies may offer insights into functional activity.