Paeds Vivas · endocrinology-diabetes-and-growth
Monogenic diabetes and neonatal diabetes — branching viva
Branching viva from the six-week-old with persistent hyperglycaemia, through the antibody-negative twelve-year-old mislabelled type 1, the glucokinase-MODY child found on a screening glucose, and the multi-system HNF1B-MODY with renal cysts, to the genetic testing pathway and the genotype-matched drug choice.
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Branch 1 — The six-week-old with persistent hyperglycaemia
Stage 1. A six-week-old, small for gestational age, has persistent insulin-requiring hyperglycaemia found during a febrile illness. What is the diagnostic principle that governs any diabetes at this age? [1]
Diabetes under six months is almost never autoimmune type 1, so the working diagnosis is monogenic neonatal diabetes until a genetic test says otherwise; the work-up is molecular, not antibody-based. [1]
Stage 2 (release). The baby has mild developmental delay and hypotonia. Which gene group rises up your differential, and what is the clinical syndrome called? [2] [5]
The combination of neonatal diabetes with developmental delay and hypotonia points to an activating KCNJ11 or ABCC8 potassium-channel mutation with a DEND syndrome (developmental delay, epilepsy and neonatal diabetes). [2] [5]
Stage 3 (release). The panel confirms an activating KCNJ11 mutation. How does this change the treatment and why does it work? [3]
The child is switched from insulin to oral glibenclamide. The activating mutation holds the KATP channel open so the beta cell cannot depolarise; a sulfonylurea closes the channel directly, bypassing the faulty ATP-sensing step and restoring insulin release, which usually improves both glycaemia and the neurological features. [3]
References5ShowHide
- [1]Hattersley AT; Greeley SAW; Polak M; et al ISPAD Clinical Practice Consensus Guidelines 2018: The diagnosis and management of monogenic diabetes in children and adolescents. Pediatr Diabetes, 2018.PMID 30225972
- [2]Gloyn AL; Pearson ER; Antcliff JF; et al Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med, 2004.PMID 15115830
- [3]Pearson ER; Flechtner I; Njølstad PR; et al Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations. N Engl J Med, 2006.PMID 16885550
- [4]Pihoker C; Gilliam LK; Ellard S; et al Prevalence, characteristics and clinical diagnosis of maturity onset diabetes of the young due to mutations in HNF1A, HNF4A, and glucokinase: results from the SEARCH for Diabetes in Youth. J Clin Endocrinol Metab, 2013.PMID 23771925
- [5]Edghill EL; Bingham C; Ellard S; Hattersley AT Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11. Rev Endocr Metab Disord, 2010.PMID 20922570