More than 20 years of serological approach to diagnosis of celiac disease (CD) has deeply changed the classical clinical presentation of the disease, and some reports indicate that CD and obesity can coexist in both childhood and adolescence. We reviewed clinical records of 149 children with CD followed in our institution between 1991 and 2007, considering weight, height and body mass index (BMI), both at diagnosis and after at least 12 months of gluten-free diet (GFD). In all, 11% of patients had BMI z-score >+1 and 3% were obese (z-score >+2) at presentation. In our population, there was a significant (P=0.008) increase in BMI z-score after GFD and the percentage of overweight (z-score >+1) subjects almost doubled (11 vs 21%, P=0.03). Our data suggest the need for a careful follow-up of nutritional status after diagnosis of CD, especially addressing those who are already overweight at presentation.
More than 20 years of serological approach to diagnosis of celiac disease (CD) has deeply changed the classical clinical presentation of failure to thrive, malnutrition, diarrhea and abdominal pain that we used to face (Telega et al., 2008). New extraintestinal symptoms have gained importance and case-finding strategy in high-risk groups (subjects with refractory iron-deficiency anemia, osteoporosis, increased transaminase levels, autoimmune disease, family history and other associated conditions) often leads to diagnosis before overt malnutrition can take place. Some reports in the literature also suggest that CD and obesity can coexist in both childhood and adolescence (Conti-Nibali et al., 1987; Franzese et al., 2001; Oso and Fraser, 2006; Arslan et al., 2009). Furthermore, patients with CD who have normal nutritional status, or are overweight at presentation, would be at further risk of obesity after gluten-free diet (GFD) because of improved intestinal absorption and unbalanced diet rich in lipids and proteins (Mariani et al., 1998; Dickey and Kearney, 2006).
Materials and methods
Clinical records of 149 children (57 males) with CD, among those followed in our institution between 1991 and 2007, were reviewed. All patients had at least one positive determination of IgA antigliadin, antiendomysium or antitransglutaminase antibodies according to the availability of laboratory tests during the considered period. IgG antigliadin and antitransglutaminase antibodies were employed to support clinical decisions in subjects with IgA deficiency. The diagnosis of CD was always established after endoscopic duodenal biopsy and histological grading according to the Marsh criteria (Marsh, 1990). All patients were regularly (every 12–24 months) followed up at the outpatient clinic and only those who had normal antitransglutaminase antibodies at the last visit were considered. Weight, height and body mass index (BMI) were collected both at diagnosis and after at least 12 months of GFD, and z-score for BMI was calculated according to the 2007 WHO Child Growth Standards. Every subject was assigned to one of six BMI z-score subgroups as follows: <−2; −1/−2; 0/−1; 0/+1;+1/+2; and >+2. Comparisons between class assignment at diagnosis and after GFD were made using Wilcoxon signed-rank and χ2 tests with significance level at P<0.05.
CD was diagnosed at a median age of 6.2 years (range 0.7–17) and the median follow-up was 4.5 years (range 1–16.3). Our data (Figure 1) show that 23% of children had a poor weight gain at diagnosis (BMI z-score <−1) but only 5% were severely malnourished (z-score <−2). On the other side, 11% of them had a BMI z-score >+1 and 3% were obese (z-score >+2). After GFD, there was a significant (P=0.008) increase in the BMI z-score and the percentage of overweight (z-score >+1) subjects almost doubled (11 vs 21%, P=0.03). The proportion of obese patients remained unchanged (3 vs 4%). Because of the economic support to CD patients offered by the Italian Health System, almost all our children had a mixed dietary regimen including both commercial and naturally gluten-free food.
Our experience is consistent with the increasing awareness that malnutrition today is quite an unusual presentation in both adults and children with CD. About 80% of children diagnosed in our institution showed a good or fairly good nutritional status and some of them were clearly overweight. Possible explanations of such a finding include early serological diagnosis, interindividual variability in intestinal sensitivity to gluten, prevalent expression of the disease outside the intestine and compensatory absorption in distal small bowel (Arslan et al., 2009). GFD seems to increase the risk of overweight or obesity, and concerns have been raised about the nutritional imbalance and hypercaloric content of commercial or natural gluten-free food. There is a trend, both in adults and in children, on a GFD to replace gluten-derived carbohydrates with an increased consumption of fats, proteins and hypercaloric beverages and to decrease fiber intake (Mariani et al., 1998; Dickey and Kearney, 2006; Ferrara et al., 2009). Incorrect dietary habits can be induced by unpalatability and expense of commercial gluten-free products or by the availability of commercial gluten-free snacks and biscuits with a high content of lipids. Adolescents are likely to be at a higher risk of inappropriate and potentially harmful alimentary habits (Mariani et al., 1998). Dietary modifications are more troublesome in countries such as Italy, where people have a high gluten-containing diet (bread, pizza and pasta), but similar dietary imbalances have also been described in Dutch children with CD (Hopman et al., 2006). In conclusion, we would suggest the need for a careful follow-up of nutritional status after the diagnosis of CD, as new morbidities could also emerge in children strictly compliant with GFD. Nutritional advice should be especially directed to those who were already overweight at the presentation of the disease.
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The authors declare no conflict of interest.
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Cite this article
Valletta, E., Fornaro, M., Cipolli, M. et al. Celiac disease and obesity: need for nutritional follow-up after diagnosis. Eur J Clin Nutr 64, 1371–1372 (2010). https://doi.org/10.1038/ejcn.2010.161
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