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Should we screen children with type 1 diabetes for Addison's disease?
  1. Amir Babiker,
  2. Emily R Leach,
  3. Vipan Datta
  1. Norfolk and Norwich University Hospital, Norwich, UK
  1. Correspondence to Dr Vipan Datta, Norfolk and Norwich University Hospital, Norwich, UK; vipan.datta{at}

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Children with type 1 diabetes mellitus (T1DM) are at a higher risk of developing other autoimmune diseases. The National Institute of Clinical Excellence guidance in 2009 included recommendations about screening for thyroid disease (TD) and coeliac disease (CD) in children with T1DM, but there was no guidance regarding screening for autoimmune Addison's disease (AD).1

Symptoms of AD in children with T1DM include recurrent hypoglycaemia with falling insulin requirements and/or salt craving. Eight per cent of patients with AD require annual hospital treatment for adrenal crisis.2 This risk is increased when diabetes is concomitantly present with AD.3 This suggests the importance of screening for AD in patients with T1DM. However, there are contradicting views in the literature about this screening.4 5 At our institution the practice is to screen all children with T1DM at diagnosis for TD, CD and AD. We look at the antiadrenal antibodies (AAA) results in children with T1DM at diagnosis to determine whether this helps in the early diagnosis of AD. We also looked at the AAA results in children who tested positive for thyroid peroxidase (TPO) and/or tissue transglutaminase (TTG) antibodies, to determine whether those who have other organ-specific antibodies should have targeted screening for AD.

Over a period of 7 years (2003–2009), 223 children were diagnosed with T1DM. Of the 150 children for whom the results of AAA were available, only 3 (2%) were positive (table 1). These three children do not have biochemical evidence of AD on short synacthen test (peak cortisol >550 nmol/l) (table 1) and are clinically well after 38–82 months follow-up.

Table 1

Children with T1DM who tested positive for AAA

Sixteen (10.6%) of the 150 children whose AAA results were available had positive TPO and/or TTG antibodies. All three AAA-positive children had positivity for another autoimmune antibody, but this did not affect the clinical outcome as described above (table 1). These three children also do not have clinical features to suggest a diagnosis of polyendocrine syndrome type II which includes T1DM, AD, hypothyroidism, vitiligo and less commonly hypogonadism.

Children with T1DM often have intensive annual blood investigations. Each AAA test costs £7.20 in our institute. The potential cost saving would have been £1080.00 over 7 years if we had not performed these tests, not taking into account the hidden cost of manpower time.

Our data do not favour routine screening for autoimmune AD and we propose that the AAA test should be requested in children with T1DM only when AD is clinically suspected.


Dr Mariana Abdelsaid helped in data collection and Dr K K Dhatariya helped in editing.



  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed