In response

We thank Bering and Devendra for their comments. We agree that further research into preservation of β-cell function is highly relevant to patients with LADY though, of course, it is no more important than that in any other area of diabetes.

While we agree that early insulin therapy may preserve β-cell function, we would argue that progressive decline due to T-cell mediated destruction in type 1 diabetes is the norm. Extrapolation from the data of Weng et al based on type 2 diabetes and published only recently in 2008 does not allow the comment that the patient's β-cell function may have ‘been left to deteriorate on sulfonylureas’.¹ Nor would we accept that automatic early treatment with insulin is more likely to ‘prevent catastrophic outcomes such as diabetic ketoacidosis’ than proper patient education and a supply of Ketostix®. Indeed, the psychosocial gains for a teenager (and other family members) treated with oral agents while maintaining excellent glycaemic control (as judged by the HbA_1c values stated) for four years should not be underestimated.²

It is clear that the patient's family history would have allowed her inclusion into research studies on the progression to type 1 diabetes and that, had she been so involved, she may well have been discovered earlier and, thus, have had a milder initial clinical course. We doubt, though, whether this justifies the cost of HLA typing outside of research studies especially when, as Bering and Devendra point out, the results are only as good as tossing a coin.³ With regard to antibody testing we concur with the views expressed but feel that the role of ZnT8 only recently described needs to be explored in additional studies.⁴

• © 2009 Royal College of Physicians