LAUSR

to allow accurate prognostication and therapy planning in children; (ii) provision of EB-specific growth charts as more feasible assessment tools in daily practice that consider EB peculiarities; and (iii) data on scheduling gastrostomy and nutritional interventions to counteract profound nutritional deficits that in this cohort were shown to start before the age of 2 years. The retrospective nature of the single-centre study harbours some limitations as mentioned by the authors: laboratory analyses were rarely performed within the first year of life; concomitant nutritional intakes, wound extent and compliance were not systematically recorded; the socioeconomic impact of resource-limited settings was not further delineated; and there was no further stratifying analyses of EB subtypes. Notably, translating weight and height measurements (the latter may be challenging in affected individuals because of immobility or joint contractures) or distinct laboratory values into supplementary dosing regimens, accurate time points to start enteral nutrition and, more importantly, sustainable clinical benefit in patients with EB is as much critical as complex, and requires a highly individual approach. The latter depends on a broad spectrum of key variables being considered, including disease severity and extent of organ involvement, the presence of infection and an inflammatory state as well as the clinical milestones that alter an individual’s nutritional requirements and daily feeding modalities such as weaning, teething, childhood diseases or start of school. Prospective studies are highly warranted, in particular to assess modalities and effects of nutritional interventions and supplementation in affected individuals – a challenging task in clinical research on rare diseases. Against this background, the paper by Reimer et al. provides relevant information and further evidence for the EB community that is valuable and that can be incorporated into clinical practice guidelines to target better wound healing, inflammatory pathways and anaemia as pathogenic traits in EB.