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Pancreatic islet cell function and metabolic control in an infant with permanent neonatal diabetes
Insights
Neonatal diabetes involves immature pancreatic beta- and alpha-cell function. This study shows partial recovery of beta-cell function, suggesting potential reversibility in permanent neonatal diabetes.
Area of Science:
- Endocrinology
- Neonatal medicine
- Diabetes research
Background:
- Neonatal diabetes mellitus (NDM) is a rare condition requiring careful monitoring of pancreatic islet cell function.
- Understanding the dynamics of beta-cell and alpha-cell function is crucial for managing NDM.
- Assessing metabolic control via Hemoglobin A1c is standard practice in diabetes management.
Observation:
- A patient with typical neonatal diabetes was observed for 16 months.
- Evaluations included pancreatic beta- and alpha-cell function and metabolic control.
- Plasma insulin and C-peptide levels were initially inappropriate for hyperglycemia, with C-peptide falling below detection limits twice.
Findings:
- Endogenous insulin secretion was less than 10% of non-diabetic infants.
- Plasma immunoreactive glucagon normalized, while glucagon-like immunoreactivity increased above the reference range.
- Beta-cell function showed partial recovery on two occasions despite initial damage.
Implications:
- The findings suggest immature islet cell function at diagnosis, with alpha-cells maturing within the first month.
- Partial beta-cell recovery indicates that the damage in permanent neonatal diabetes may be at least partially reversible.
- This highlights the importance of continued monitoring and potential therapeutic interventions for NDM.
Abstract:
A girl with typical clinical manifestations of neonatal diabetes was observed for 16 months with consecutive evaluations of pancreatic beta- and alpha-cell function and metabolic control. At the diagnosis both the plasma immunoreactive insulin (IRI) and C-peptide concentrations were inappropriate for the contemporaneous hyperglycemia. During the follow-up, the C-peptide fell twice below the detection limit but the beta-cell function recovered partially on both occasions. Based on 24-hour urinary C-peptide excretion, the endogenous insulin secretion was less than 10% of that in non-diabetic infants. When diagnosed the patient had plasma immunoreactive glucagon (IRG) and glucagon-like immunoreactivity (GLI) concentrations below the reference range for normal neonates. The IRG normalised within the first month, while the GLI increased to a level exceeding the reference range. Hemoglobin A1 had already risen at the time of diagnosis and subsequently rose to a level indicating poor metabolic control. The findings indicate an immature function of both beta- and alpha-cells at the diagnosis with the alpha-cells maturing within the first month. The recovery of the beta-cell function, after two failures in this patient with permanent neonatal diabetes, suggests that the beta-cell damage was at least partially reversible.