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Prolonged honeymoon phase in an adolescent with diabetes and thyrotoxicosis provides support for the accelerator hypothesis
Author(s) -
Abdullah Nadeem,
AlKhalidi Omer,
Brown Kathryn J,
Reid Judith,
Cheetham Tim D
Publication year - 2008
Publication title -
pediatric diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.678
H-Index - 75
eISSN - 1399-5448
pISSN - 1399-543X
DOI - 10.1111/j.1399-5448.2008.00347.x
Subject(s) - medicine , carbimazole , euthyroid , endocrinology , diabetes mellitus , beta cell , insulin , insulin resistance , thyroid function tests , hormone , thyroid function , beta (programming language) , thyroid , graves' disease , islet , computer science , programming language
A 14‐yr‐old female presented with diabetes and Graves’ disease. Eighteen months later, she was euthyroid on carbimazole, and her haemoglobin A1c (HbA1c) was normal (5.2%) on a small insulin dose (0.3–0.4 units/kg/day). An assessment of her pancreatic beta‐cell reserve, determined by comparing HbA1c and insulin dose, suggested that this was greater than other patients with type 1 diabetes in our service 18 months postdiagnosis (n = 185). We suspect that excess thyroid hormone led to an insulin‐resistant state and accelerated her presentation with hyperglycaemia. Insulin resistance fell once normal thyroid function was restored and helped to attenuate further beta‐cell destruction when beta‐cell mass was relatively well preserved.