Letter: follow‐up practices in coeliac disease – intestinal biopsy after child‐to‐adult transition might be useful

Abstract

We are grateful to Sharkey et al. for illustrating their approach to adult coeliac disease (CD) follow-up protocol.1 In accordance with standard practice, they diagnosed CD on the basis of anti-tissue transglutaminase antibodies (anti-tTg) seropositivity and of the presence of villous atrophy at duodenal biopsy. After roughly 1 year from the initiation of the gluten-free diet (GFD), they performed a follow-up biopsy to distinguish patients still showing villous atrophy from those who were somewhat healed. Sharkey et al. found that 47% of patients still showed villous atrophy at histological re-evaluation. These patients were advised to undergo a stricter dietary intervention, beyond the current recommendations for a safe GFD - that is, eliminating codex-allowed gluten-free wheat starches and barley malt extracts, as well as pure oats. After 12 months, this dietary intervention achieved a success rate of 50% in mucosal healing. It is evident that follow-up biopsy yielded a key element in clinical decision-making. Although this study clearly mirrors common clinical scenarios rather than research settings, some limitations should have been further pointed out. It is surprising and not clear why the quite high number of anti-tTG negative patients (15%) were not further studied by determining anti-endomysial antibodies (EmA). A systematic review considering all available studies has already shown that EmA sensitivity is comparable to anti-tTg (93% vs. 92.8%).2 Therefore, criticisms could be raised for those patients diagnosed with negative anti-tTg and regardless their EmA (and also their HLA status): this issue is very debatable, most of all for those seronegative patients who had persistent villous atrophy on a GFD and for whom other diagnoses must be ruled out.3 Another questionable issue is the definition of Marsh 2: in the article it is stated that Marsh 2 corresponds to an increased lymphocytic infiltrate in the lamina propria, but this does not match with the original and widely accepted definition of crypt hyperplasia coupled to intraepithelial lymphocytosis.4 With regard to the follow-up strategy adopted by the authors, patients without villous atrophy at 1-year biopsy reassessment were finally discharged to their primary care physicians after one more clinical and laboratory check-up, instead of being still seen yearly at the referral centre. Albeit this shift can be perceived by patients as a lesser disease burden, inadequately informed and trained primary care physicians might not provide satisfactory follow-up.5 It would have been interesting to read more details on how their referral centre and the primary care share follow-up protocols and ensure best practices. In conclusion, their case records highlighted some important issues which are of great interest for both adult and paediatric gastroenterologists managing patients with CD, such as histological diagnosis and follow-up strategies. Due to the recent publication of the new ESPGHAN guidelines for the diagnosis of CD, a milestone for the ‘non-biopsy’ diagnosis in some paediatric selected cases has been reached.6 However, as no better tool other than duodenal biopsy is available, so far, to predict complications of uncontrolled CD,7 we wonder whether a follow-up biopsy should be routinely run by adult gastroenterologists at some point after the transition from the paediatric referral centre. Declaration of personal and funding interests: None.