Alimentary Pharmacology and Therapeutics Letter to the Editors tified patients whose outcomes may be improved by management strategies that combine corticosteroids (with or without azathioprine) and ursodeoxycholic acid.7, 8 The experience of Drs Yilmaz and Dayanan suggests that immunosuppressive therapy alone may be effective as an anti-fibrotic regimen in some patients. Furthermore, outcomes may be better than in those with classical AIH or PBC. The overlap syndromes are clinical descriptions based largely on clinical judgments, and the AIH/PBC overlap syndrome described by Drs Yilmaz and Dayanan exists within a clinical spectrum that is bounded by patients with mainly AIH and weak manifestations of PBC and by patients with mainly PBC and inflammatory features reminiscent of AIH.8 Immunosuppressive therapy has a role across the spectrum, but outcomes may differ depending on the predominant component.8 The absence of relapse after drug withdrawal suggests that PBC may have been the predominant disease in this experience. The observations of Drs Yilmaz and Dayanan indicate that immunosuppressive therapy can have anti-fibrotic effects in immune-mediated liver diseases outside the classical phenotype of AIH. Future objectives must be to characterise those patients who are likely to respond, validate non-invasive methods to monitor fibrosis, and rigorously evaluate site-specific anti-fibrotic interventions that might supplement or replace current strategies.9

Letter: metabolic syndrome in patients with coeliac disease on a gluten-free diet G. Chiarioni*,†, S. De Marchi‡, M. Prior‡ & E. Arosio‡ *Division of Gastroenterology, University of Verona, Verona, Italy. † Division of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ‡ Division of Vascular Rehabilitation of the University of Verona, Azienda Ospedaliera Universitaria Integrata di Verona, Verona, Italy. E-mail: [email protected] doi:10.1111/apt.13125

SIRS, We appreciated reading the study by Tortora et al. on potential metabolic risk of gluten-free diet (GFD) in coeliac disease (CD).1 The authors reported in an observational study that GFD in CD might facilitate de novo metabolic syndrome, questioning the potential full benefit of a dietetic intervention in this immune disease. For the first time, such impressive data are provided in a large-sized sample. Aliment Pharmacol Ther 2015; 41: 789–796 ª 2015 John Wiley & Sons Ltd

ACKNOWLEDGEMENT The author’s declarations of personal and financial interests are unchanged from those in the original article.9 REFERENCES 1. Yilmaz B, Dayanan R. Letter: reversibility of hepatic fibrosis and immunosuppression withdrawal in patients with autoimmune hepatitis/primary biliary cirrhosis overlap syndrome. Aliment Pharmacol Ther 2015; 41: 794. 2. Czaja AJ, Carpenter HA. Decreased fibrosis during corticosteroid therapy of autoimmune hepatitis. J Hepatol 2004; 40: 646–52. 3. Mohamadnejad M, Malekzadeh R, Nasseri-Moghaddam S, et al. Impact of immunosuppressive treatment on liver fibrosis in autoimmune hepatitis. Dig Dis Sci 2005; 50: 547–51. 4. Czaja AJ. Hepatic inflammation and progressive liver fibrosis in chronic liver disease. World J Gastroenterol 2014; 20: 2515–32. 5. Leuschner M, Guldutuna S, You T, et al. Ursodeoxycholic acid and prednisolone versus ursodeoxycholic acid and placebo in the treatment of early stages of primary biliary cirrhosis. J Hepatol 1996; 25: 49–57. 6. Chazouilleres O, Wendum D, Serfaty L, et al. Long term outcome and response to therapy of primary biliary cirrhosis-autoimmune hepatitis overlap syndrome. J Hepatol 2006; 44: 400–6. 7. Boberg KM, Chapman RW, Hirschfield GM, et al. Overlap syndromes: the International Autoimmune Hepatitis Group (IAIHG) position statement on a controversial issue. J Hepatol 2011; 54: 374–85. 8. Czaja AJ. Cholestatic phenotypes of autoimmune hepatitis. Clin Gastroenterol Hepatol 2014; 12: 1430–8. 9. Czaja AJ. Review article: prevention and reversal of hepatic fibrosis in autoimmune hepatitis. Aliment Pharmacol Ther 2014; 39: 385–406.

However, these data are at variance with the existing literature, and our own experience, where plasma triglycerides and LDL cholesterol were substantially unaffected by GFD.2, 3 On the contrary, in our sample of young CD patients, a number of blood and instrumental parameters of cardiovascular risk, including HDL cholesterol, were benefitted by GFD.3 In addition, our data are consistent with the low-grade inflammatory aetiology hypothesis of the metabolic syndrome, potentially improved by the treatment of a comorbid immune condition (i.e. CD).2 However, we would like to highlight some potential pitfalls of the valuable paper by Tortora et al. The authors apparently grouped a mixed population sample in their report. Potential CD is commonly not considered a mandatory indication for dietetic intervention.4 We feel that including potential CD patients in the data analysis might have biased the results, provided the percentage was relevant. In addition, the Marsh 2 histology grade used in the paper to diagnose classical CD may 795

Letter to the Editors indicate patients without evidence of partial villous atrophy.4 Finally, we acknowledge that there are no universally accepted guidelines to monitor adherence to dietary advice in CD.4 We assume that all the patients were compliant with GFD at follow-up. However, we feel that limiting the follow-up to the measurement of anti-tissue transglutaminase antibodies and dietetic consultation makes it hard to allow for full response of the disease to GFD.5 In conclusion, one may wonder whether metabolic syndrome was associated with the prescription of a GFD in patients where it was not mandatory, or simply the tale of an immune condition poorly responding to mandatory dietetic treatment, as an alternative. Eventually, this paper might raise concerns on the potential harm of a GFD when the prescription is not mandatory.

Letter: metabolic syndrome in patients with coeliac disease on a gluten-free diet – authors’ reply R. Tortora & A. Rispo Gastroenterology – Department of Clinical Medicine and Surgery, University Federico II of Naples, Naples, Italy. E-mail: [email protected] doi:10.1111/apt.13137

SIRS, First, we sincerely appreciated the interest and comments on our paper by Chiarioni and Colleagues.1, 2Our work (and the final statistical analysis) included only patients affected by “classical” and “non-classical” coeliac disease according to the Oslo definitions.3 So, even if the definition of ‘potential’ coeliac disease was reported in the Methods, no subject with potential coeliac disease (Marsh 0-1) was considered in the analysis. Starting from this consideration, our group of patients with coeliac disease can be considered ‘homogeneous’ and gluten-free diet (GFD) was prescribed in the context of a ‘mandatory’ indication. The previous experience by Chiarioni and De Marchi,4 reporting different results with respect to ours, in terms of lipid profile pre- and post-GFD, was very clear in our

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ACKNOWLEDGEMENT Declaration of personal and funding interests: None. REFERENCES 1. Tortora R, Capone P, de Stefano G, et al. Metabolic syndrome in patients with coeliac disease on a gluten-free diet. Aliment Pharmacol Ther 2015; 41: 352–9. 2. Rybak A, Cukrowska B, Socha J, Socha P. Long term follow up of celiac disease—is atherosclerosis a problem? Nutrients 2014; 6: 2718–29. 3. de Marchi S, Chiarioni G, Prior M, Arosio E. Young adults with coeliac disease may be at increased risk of early atherosclerosis. Aliment Pharmacol Ther 2013; 38: 162–9. 4. Ludvigsson JF, Lefner DA, Bai JC, et al. The Oslo definitions for celiac disease and related terms. Gut 2013; 62: 43–52. 5. Lanzini A, Lanzarotto F, Villanacci V, et al. Complete recovery of intestinal mucosa occurs very rarely in adult coeliac patients despite adherence to gluten-free diet. Aliment Pharmacol Ther 2009; 29: 1299–308.

minds and, in effect, we (briefly) discussed it in the paper. However, we think that the wide population included in our study tends to give more robust results compared with that of previous papers, including small series. Finally, we are not surprised by our results showing that GFD (even after considering its high glycaemic index) returns the risk of metabolic syndrome of patients with coeliac disease almost to that reported in the general population.

ACKNOWLEDGEMENT The authors’ declarations of personal and financial interests are unchanged from those in the original article.2 REFERENCES 1. Chiarioni G, De Marchi S, Prior M, Arosio E. Letter: metabolic syndrome in patients with coeliac disease on a gluten-free diet: the old story of chicken and egg? Aliment Pharmacol Ther 2015; 41: 795–6. 2. Tortora R, Capone P, De Stefano G, et al. Metabolic syndrome in patients with coeliac disease on a gluten-free diet. Aliment Pharmacol Ther 2015; 41: 352–9. 3. Ludvigsson JF, Leffler DA, Bai JC, et al. The Oslo definitions for coeliac disease and related terms. Gut 2013; 14: 43–52. 4. De Marchi S, Chiarioni G, Prior M, et al. Young adults with coeliac disease may be at increate risk of early atherosclerosis. Aliment Pharmacol Ther 2013; 38: 162–9.

Aliment Pharmacol Ther 2015; 41: 789–796 ª 2015 John Wiley & Sons Ltd

Letter: metabolic syndrome in patients with coeliac disease on a gluten-free diet.

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