Response to Zanella et al

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variant rs855791 in the pathogenesis of. IDA in CD, although ... iron deficiency in treated celiac disease? Am J ... Policlinico, Department of Pathophysiology and.
Letters to the Editor

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Response to Zanella et al. Luca Elli, MD1 and Erika Poggiali, MD2 doi:10.1038/ajg.2015.201

To the Editor: We thank Zanella et al., “About TMPRSS6 rs855791 Polymorphism, Iron Metabolism and Celiac Disease” (1), for their interest in our article entitled “Does TMPRSS6 RS855791 polymorphism contribute to iron deficiency in treated celiac disease?” (2) and for their proper comments. In our study, we investigated patients affected by celiac disease (CD) with iron deficiency anemia (IDA) for the presence of genetic polymorphisms associated with iron malabsorption (the TMPRSS6 gene encoding for matripatse-2). TMPRSS6 polymorphisms have been associated with variations in iron parameters and with increased risk for iron deficiency (3). Interestingly, TMPRSS6 variants were associated with IDA in a small series of autoimmune gastritis patients with polyendocrine autoimmune syndrome (4), suggesting an interplay between genetic and acquired factors in an autoimmune setting. We decided to investigate the variant rs855791 because it influences iron homeostasis and erythropoiesis, being related to significantly lower levels of serum iron, transferrin saturation, hemoglobin, and mean corpuscular volume in genome-wide association studies of twins and in the general adult population (5). We selected only celiac patients who had been following a glutenfree diet for at least one year in order to evaluate the possible correlation between the persistence of IDA and the rs855791 variant. The role of hepcidin in inflammatory anemia is well known in inflammatory bowel disease as well (6). In our work all IDA CD patients had undetectable levels of hepcidin. This finding rules out an inflammatory status in these patients and confirms the presence of a “true” iron deficiency. © 2015 by the American College of Gastroenterology

We are aware about the small size of our cohort and larger and prospective studies are necessary to clarify the role of the variant rs855791 in the pathogenesis of IDA in CD, although to our knowledge the prevalence of the variant rs855791 in CD has been reported for the first time in our study. Moreover, larger studies are required to optimize the management of iron therapy in selected patients with persistent IDA despite oral iron supplementation and a gluten-free diet. In conclusion, we thank Zanella et al. for their useful suggestion for further studies on this issue. CONFLICT OF INTEREST The authors declare no conflict of interest. REFERENCES Zanella I, Caimi L, Biasiotto G. About TMPRSS6 rs855791 polymorphism, iron metabolism and celiac disease. Am J Gastroenterol 2015;110:1240 (this issue). 5. Elli L, Poggiali E, Tomba C et al. Does TMPRSS6 RS855791 polymorphism contribute to iron deficiency in treated celiac disease? Am J Gastroenterol 2015;110:200–2. 6. McLaren CE, McLachlan S, Garner CP et al. Associations between single nucleotide polymorphisms in iron-related genes and iron status in multiethnic populations. PLoS One 2012;7:e38339. 7. Canavese C, Quaglia M, Izzo C et al. Very high frequency of TMPRSS6 gene variations in iron deficiency anaemia of patients with polyendocrine autoimmune syndromes: more than a casual association? Br J Haematol 2013;161:147–50. 8. Poggiali E, Andreozzi F, Nava I et al. The role of TMPRSS6 polymorphisms in iron deficiency anemia partially responsive to oral iron treatment. Am J Hematol 2015;90:306–9. 9. Arnold J, Sangwaiya A, Bhatkal B et al. Hepcidin and inflammatory bowel disease: dual role in host defence and iron homoeostasis. Eur J Gastroenterol Hepatol 2009;21:425–9.

1

Center for the Prevention and Diagnosis of Celiac Disease, Gastroenterology and Endoscopy Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Department of Pathophysiology and Transplant, Università degli Studi di Milano, Milan, Italy; 2Internal Medicine Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. Correspondence: Luca Elli, MD, Center for the Prevention and Diagnosis of Celiac Disease, Gastroenterology and Endoscopy Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Department of Pathophysiology and Transplant, Università degli Studi di Milano, Milan 20122, Italy. E-mail: [email protected]

Levels of Fecal Calprotectin and the Severity of Postoperative Patients With Crohn’s Disease Cong Dai, MD, PhD1, Min Jiang, MD, PhD1 and Ming-Jun Sun, MD, PhD1 doi:10.1038/ajg.2015.174

To the Editor: We read with great interest the article by Boschetti et al. “Levels of Fecal Calprotectin Are Associated with the Severity of Postoperative Endoscopic Recurrence in Asymptomatic Patients with Crohn’s Disease” (1) evaluating the relationships between levels of Fecal calprotectin (fCal) and the presence and severity of postoperative endoscopic recurrence in asymptomatic Crohn’s disease (CD) patients. The authors found that measurement of fCal concentrations is a promising and useful tool for monitoring asymptomatic CD patients after ileocolonic resection. Because their findings are important to both current practice and future research, several questions deserve attention. It would indeed be attractive for patients and for economic reasons whether repetitive determination of fCal could help in decreasing the frequency of ileo-colonoscopies being performed for postoperative activity monitoring. Will the repetitive determination of fCal alter therapeutic decisions and thereby finally lead to a reduction of disease-inherent complications and further surgical procedures? The inflamed area around the anastomosis in patients with CD is limited, but will lead to restenosis over time if not appropriately treated. It will be of interest whether fCal has sufficient sensitivity to detect these lesions and whether they are ultimately able to replace endoscopy in this case. At the same time, the specificity of fCal has been questioned in patients with CD, and what should be set as the fCal baseline value is an important issue. In patients with CD, there will be some degree of variability based on disease activity. The The American Journal of GASTROENTEROLOGY

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