Coeliac disease tied to a threefold increase in NAFLD risk
Coeliac disease patients have a threefold risk of nonalcoholic fatty liver disease (NAFLD) despite adherence to a gluten-free diet, a study has found. This risk is especially higher in the lean population.
The case–control study included 202 CD outpatients (median age 45 years; 72.8 percent female) following a gluten-free diet and 202 non-CD controls (median age 46 years; 65.3 percent female). NAFLD had a raw prevalence of 34.7 percent vs 21.8 percent, respectively (p=0.006).
Logistic regression analysis confirmed an elevated NAFLD risk in the CD group (adjusted odds ratio, 2.90; 95 percent CI, 1.64–5.15; p<0.001). Of note, the risk was more pronounced in normal weight CD patients (adjusted odds ratio, 5.71; 2.30–14.19; p<0.001).
While not fully understood, the markedly increased NAFLD risk observed in lean CD patients may be explained by a gut‐liver axis alteration in CD. Specifically, altered intestinal permeability and small intestinal bowel overgrowth are common and have also been described in NAFLD, suggesting a possible pathogenic link. [Aliment Pharmacol Ther 2015;41:352‐359; Minerva Gastroenterol Dietol 2013;59:89‐95]
Another possible explanation is that the contents of the gluten-free diet paired with the hyperphagic compensatory status that usually follows malabsorption is known to induce weight gain and increased lipid intake, which are key factors in the development of NAFLD. [Aliment Pharmacol Ther 2018;47:192‐202]
Therefore, the gut microbiome might represent a future therapeutic target in the pathogenesis and treatment of the concurrent NAFLD, researchers said.
In light of the current findings, researchers recommended that clinicians provide a dietary advice using a patient‐tailored approach to assist CD patients with NAFLD in achieving an appropriate nutritional intake while cutting the risk of long‐term liver‐related events.
Additional studies are warranted to clarify whether the risk of NAFLD is attributable to a gluten-free diet alone or to persistent gut‐liver axis alterations, they added.