Scandinavian Journal of Gastroenterology. 2014; 49: 255–256
RESPONSE TO LETTER
Response to Letter: Folate deficiency in Crohn’s disease FERNANDO BERMEJO1, ALICIA ALGABA1, IVÁN GUERRA1 & JAVIER P. GISBERT2 1
Gastroenterology Units, Hospital Universitario de Fuenlabrada, Madrid, Spain, and 2Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IP) and Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain
Abstract Folate deficiency in patients with Crohn’s disease may be due to a combination of factors: poor diet, malabsorption, increased requirements due to inflammation of the mucosa, and the taking of certain drugs as sulfasalazine and methotrexate. A significant proportion of patients with Crohn’s disease suffer from folate deficiency, suggesting that regular screening should be performed.
We appreciate the interest shown in our study [1] by Dr Onal and thank him for his insightful comments [2]. Regarding the first question, we think that the relatively high prevalence of folate deficiency in our series (22.2%) was due to the combination of several factors that included: i) inflammation of the mucosa (37% of our patients had disease activity), ii) concomitant upper gastrointestinal disease (7%), iii) poor folate intake (although it is difficult to be screened, the reserves of folate in the body are not high, and a lack of intake of foods rich in folate may cause a relatively quick decrease in plasma levels), and iv) treatment with sulfasalazine or methotrexate (low percentage in our patients). Nevertheless, the prevalence observed in our patients was similar to that previously reported by other authors, for example, 28.8% in the article of Yakut et al. [3]. With respect to the second question, although Harvey and Bradshaw published their clinical disease index in an original paper, a cut-off point for considering the disease as inactive was not established [4]. Vermeire et al. described the correlation between the Crohn’s disease activity index (CDAI) and Harvey–Bradshaw index in assessing Crohn’s disease severity [5]. According to these authors, a Harvey– Bradshaw score £ 4 points corresponded to a CDAI
£ 150 points (clinical remission). In our study, we decided to set the cut-off below that point and to consider patients with Harvey–Bradshaw scores of 3 or 4 as having mild activity (e.g. a patient with moderate abdominal pain and a mild or moderate affectation of general well-being by an active ileitis). We agree that this decision is arbitrary; so, a repeated analysis, considering Harvey–Bradshaw index score £ 4 points as clinical remission, has now been carried out. We have obtained similar results to those described with the previous criteria, and Crohn’s disease activity continued being a risk factor for folate deficiency (OR = 2.5; 95% CI: 1.2–5.5; p = 0.014). Finally, the folate levels according to Crohn’s disease activity were as follows. Patients in remission: 8 ± 5.1 ng/ml; patients with mild activity: 7.5 ± 5.4 ng/ml; and patients with moderate activity: 6 ± 3.5 ng/ml. No cases of severe disease were included just because subjects were included consecutively during their scheduled visit to the outpatient clinic. References [1] Bermejo F, Algaba A, Guerra I, Chaparro M, De-La-Poza G, Valer P, et al. Should we monitor vitamin B12 and folate levels in Crohn’s disease patients? Scand J Gastroenterol 2013;48:1272–7.
Correspondence: Fernando Bermejo, Gastroenterology Units, Hospital Universitario de Fuenlabrada, Ríos Rosas 17, 28003 Madrid, Spain. Tel: +34 916006175. Fax: +34 916006175. E-mail: [email protected]
(Received 23 November 2013; accepted 24 November 2013) ISSN 0036-5521 print/ISSN 1502-7708 online 2014 Informa Healthcare DOI: 10.3109/00365521.2013.869829
256
Response to Letter
[2] Onal IK. Folate deficiency in Crohn’s disease. Scand J Gastroenterol; Epub ahead of print, DOI: 10.3109/00365521. 2013.865260. [3] Yakut M, Ustun Y, Kabacam G, Soykan I. Serum vitamin B12 and folate status in patients with inflammatory bowel diseases. Eur J Intern Med 2010;21:320–3.
[4] Harvey RF, Bradshaw JM. A simple index of Crohn’s disease activity. Lancet 1980;1:514. [5] Vermeire S, Schreiber S, Sandborn WJ, Dubois C, Rutgeerts P. Correlation between the Crohn’s disease activity and Harvey-Bradshaw indices in assessing Crohn’s disease severity. Clin Gastroenterol Hepatol 2010;8:357–63.
Copyright of Scandinavian Journal of Gastroenterology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
RESPONSE TO LETTER
Response to Letter: Folate deficiency in Crohn’s disease FERNANDO BERMEJO1, ALICIA ALGABA1, IVÁN GUERRA1 & JAVIER P. GISBERT2 1
Gastroenterology Units, Hospital Universitario de Fuenlabrada, Madrid, Spain, and 2Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IP) and Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain
Abstract Folate deficiency in patients with Crohn’s disease may be due to a combination of factors: poor diet, malabsorption, increased requirements due to inflammation of the mucosa, and the taking of certain drugs as sulfasalazine and methotrexate. A significant proportion of patients with Crohn’s disease suffer from folate deficiency, suggesting that regular screening should be performed.
We appreciate the interest shown in our study [1] by Dr Onal and thank him for his insightful comments [2]. Regarding the first question, we think that the relatively high prevalence of folate deficiency in our series (22.2%) was due to the combination of several factors that included: i) inflammation of the mucosa (37% of our patients had disease activity), ii) concomitant upper gastrointestinal disease (7%), iii) poor folate intake (although it is difficult to be screened, the reserves of folate in the body are not high, and a lack of intake of foods rich in folate may cause a relatively quick decrease in plasma levels), and iv) treatment with sulfasalazine or methotrexate (low percentage in our patients). Nevertheless, the prevalence observed in our patients was similar to that previously reported by other authors, for example, 28.8% in the article of Yakut et al. [3]. With respect to the second question, although Harvey and Bradshaw published their clinical disease index in an original paper, a cut-off point for considering the disease as inactive was not established [4]. Vermeire et al. described the correlation between the Crohn’s disease activity index (CDAI) and Harvey–Bradshaw index in assessing Crohn’s disease severity [5]. According to these authors, a Harvey– Bradshaw score £ 4 points corresponded to a CDAI
£ 150 points (clinical remission). In our study, we decided to set the cut-off below that point and to consider patients with Harvey–Bradshaw scores of 3 or 4 as having mild activity (e.g. a patient with moderate abdominal pain and a mild or moderate affectation of general well-being by an active ileitis). We agree that this decision is arbitrary; so, a repeated analysis, considering Harvey–Bradshaw index score £ 4 points as clinical remission, has now been carried out. We have obtained similar results to those described with the previous criteria, and Crohn’s disease activity continued being a risk factor for folate deficiency (OR = 2.5; 95% CI: 1.2–5.5; p = 0.014). Finally, the folate levels according to Crohn’s disease activity were as follows. Patients in remission: 8 ± 5.1 ng/ml; patients with mild activity: 7.5 ± 5.4 ng/ml; and patients with moderate activity: 6 ± 3.5 ng/ml. No cases of severe disease were included just because subjects were included consecutively during their scheduled visit to the outpatient clinic. References [1] Bermejo F, Algaba A, Guerra I, Chaparro M, De-La-Poza G, Valer P, et al. Should we monitor vitamin B12 and folate levels in Crohn’s disease patients? Scand J Gastroenterol 2013;48:1272–7.
Correspondence: Fernando Bermejo, Gastroenterology Units, Hospital Universitario de Fuenlabrada, Ríos Rosas 17, 28003 Madrid, Spain. Tel: +34 916006175. Fax: +34 916006175. E-mail: [email protected]
(Received 23 November 2013; accepted 24 November 2013) ISSN 0036-5521 print/ISSN 1502-7708 online 2014 Informa Healthcare DOI: 10.3109/00365521.2013.869829
256
Response to Letter
[2] Onal IK. Folate deficiency in Crohn’s disease. Scand J Gastroenterol; Epub ahead of print, DOI: 10.3109/00365521. 2013.865260. [3] Yakut M, Ustun Y, Kabacam G, Soykan I. Serum vitamin B12 and folate status in patients with inflammatory bowel diseases. Eur J Intern Med 2010;21:320–3.
[4] Harvey RF, Bradshaw JM. A simple index of Crohn’s disease activity. Lancet 1980;1:514. [5] Vermeire S, Schreiber S, Sandborn WJ, Dubois C, Rutgeerts P. Correlation between the Crohn’s disease activity and Harvey-Bradshaw indices in assessing Crohn’s disease severity. Clin Gastroenterol Hepatol 2010;8:357–63.
Copyright of Scandinavian Journal of Gastroenterology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
