Deficiency In Inflammatory Bowel Disease Research Articles

The management of iron deficiency in inflammatory bowel disease - an online tool developed by the RAND/UCLA appropriateness method

BackgroundIron deficiency is a common and undertreated problem in inflammatory bowel disease (IBD).AimTo develop an online tool to support treatment choice at the patient-specific level.MethodsUsing the RAND/UCLA Appropriateness Method (RUAM), a European expert panel assessed the appropriateness of treatment regimens for a variety of clinical scenarios in patients with non-anaemic iron deficiency (NAID) and iron deficiency anaemia (IDA). Treatment options included adjustment of IBD medication only, oral iron supplementation, high-/low-dose intravenous (IV) regimens, IV iron plus erythropoietin-stimulating agent (ESA), and blood transfusion. The panel process consisted of two individual rating rounds (1148 treatment indications; 9-point scale) and three plenary discussion meetings.ResultsThe panel reached agreement on 71% of treatment indications. ‘No treatment’ was never considered appropriate, and repeat treatment after previous failure was generally discouraged. For 98% of scenarios, at least one treatment was appropriate. Adjustment of IBD medication was deemed appropriate in all patients with active disease. Use of oral iron was mainly considered an option in NAID and mildly anaemic patients without disease activity. IV regimens were often judged appropriate, with high-dose IV iron being the preferred option in 77% of IDA scenarios. Blood transfusion and IV+ESA were indicated in exceptional cases only.ConclusionsThe RUAM revealed high agreement amongst experts on the management of iron deficiency in patients with IBD. High-dose IV iron was more often considered appropriate than other options. To facilitate dissemination of the recommendations, panel outcomes were embedded in an online tool, accessible via http://ferroscope.com/.

Anemia and iron deficiency in inflammatory bowel disease: an open, prospective, observational study on diagnosis, treatment with ferric carboxymaltose and quality of life

Objective. Iron deficiency and anemia are being increasingly recognized as a complication of inflammatory bowel disease (IBD). The aim of this study was to observe, in a non-interventional way, how Swedish gastroenterologists adhere to guidelines in IBD outpatients treated with intravenous ferric carboxymaltose (FCM), and the result of treatment. Material and methods. Altogether 394 IBD patients (Crohn's disease (CD) 60%, ulcerative colitis (UC) 40%) from 14 centers were included. Group A (n = 216) was observed from November 2008 and group B (n = 178) from March 2010. Time of observation ranged from 12 to 29 months. Results. S-Ferritin (µmol/l) and transferrin saturation (T-Sat; %) were recorded at baseline in 62% and 50% in group A. Median values for Hb, ferritin and T-Sat at baseline were 111 g/l, 10 µmol/l and10%, respectively, and 134 g/l, 121 µmol/l and 20% after iron treatment (p < 0.001 for all three parameters). Similar results were found in group B. Approximately three-quarters of all patients had only one iron infusion during the study period. Median time to reinfusion was 6 (1–25) months. Only previously described infusion reactions occurred in 27 (7%) patients. Conclusions. Adherence to European guidelines was rather poor and needs to be improved. The effect on iron parameters of intravenous FCM was significant, and resulted in a ferritin level that indicates an effect on the iron stores. The effect was mostly sustained for a year since only one-quarter of the patients were given repeated iron infusions. No unforeseen safety concerns emerged during the observation period.

Mo1954 DNA Mismatch Repair Deficiency in Inflammatory Bowel Disease Associated Colorectal Carcinomas

Mo1954 DNA Mismatch Repair Deficiency in Inflammatory Bowel Disease Associated Colorectal Carcinomas

A Shift From Oral to Intravenous Iron Supplementation Therapy Is Observed Over Time in a Large Swiss Cohort of Patients With Inflammatory Bowel Disease

In 2007, leading international experts in the field of inflammatory bowel disease (IBD) recommended intravenous (IV) iron supplements over oral (PO) ones because of superior effectiveness and better tolerance. We aimed to determine the percentage of patients with IBD undergoing iron therapy and to assess the dynamics of iron prescription habits (IV versus PO). We analyzed anonymized data on patients with Crohn's disease and ulcerative colitis extracted from the Helsana database. Helsana is a Swiss health insurance company providing coverage for 18% of the Swiss population (1.2 million individuals). In total, 629 patients with Crohn's disease (61% female) and 398 patients with ulcerative colitis (57% female) were identified; mean observation time was 31.8 months for Crohn's disease and 31.0 months for ulcerative colitis patients. Of all patients with IBD, 27.1% were prescribed iron (21.1% in males; 31.1% in females). Patients treated with steroids, immunomodulators, and/or anti-tumor necrosis factor drugs were more frequently treated with iron supplements when compared with those not treated with any medications (35.0% versus 20.9%, odds ratio, 1.94; P < 0.001). The frequency of IV iron prescriptions increased significantly from 2006 to 2009 for both genders (males: from 2.6% to 10.1%, odds ratio = 3.84, P < 0.001; females: from 5.3% to 12.1%, odds ratio = 2.26, P = 0.002), whereas the percentage of PO iron prescriptions did not change. Twenty-seven percent of patients with IBD were treated with iron supplements. Iron supplements administered IV were prescribed more frequently over time. These prescription habits are consistent with the implementation of guidelines on the management of iron deficiency in IBD.

P435 Management of iron deficiency in inflammatory bowel disease: results from a RAND/UCLA appropriateness study

P435 Management of iron deficiency in inflammatory bowel disease: results from a RAND/UCLA appropriateness study

Implication of intestinal VDR deficiency in inflammatory bowel disease

BackgroundTo investigate the function of the intestinal Vdr gene in inflammatory bowel disease (IBD), in conjunction with the discovery of possible metabolic markers for IBD using intestine-specific Vdr knockout mice. MethodsVdrΔIEpC mice were generated, phenotyped and treated with a time-course of 3% dextran sulfate sodium (DSS) to induce colitis. Colitis was diagnosed by evaluating clinical symptoms and intestinal histopathology. Gene expression analysis was carried out. In addition, metabolic markers of IBD were explored by metabolomics. ResultsVdrΔIEpC mice showed abnormal body size, colon structures and feces color. Calcium, collagen, and intestinal proliferation-related gene expression were all decreased, and serum alkaline phosphatase was highly increased. In the acute model which was treated with 3% DSS for six days, VdrΔIEpC mice showed a high score of IBD symptoms; enlarged mucosal layer and damaged muscularis layer. In the recovery experiment model, where mice were treated with 3% DSS for four days and water for three days, VdrΔIEpC mice showed a high score of IBD symptoms; severe damage of mucosal layer and increased expression of genes encoding proinflammatory cytokines. Feces metabolomics revealed decreased concentrations of taurine, taurocholic acid, taurodeoxycholic acid and cholic acid in VdrΔIEpC mice. ConclusionsDisruption of the intestinal Vdr gene showed phenotypical changes that may exacerbate IBD. These results suggest that VDR may play an important role in IBD.General significanceVDR function has been implicated in IBD. This is of value for understanding the etiology of IBD and for development of diagnostic biomarkers for IBD.

Mo1730 Risk Factors for Vitamin D Deficiency and Impact of Repletion in a Tertiary Care Inflammatory Bowel Disease Population

Introduction Many patients with inflammatory bowel disease (IBD) are vitamin D deficient. The purpose of our study was to identify risk factors for vitamin D deficiency in IBD and to assess the impact of vitamin D repletion on disease activity and quality of life (QOL).

Micronutrient deficiencies in inflammatory bowel disease: From A to zinc

Inflammatory bowel disease (IBD) has classically been associated with malnutrition and weight loss, although this has become less common with advances in treatment and greater proportions of patients attaining clinical remission. However, micronutrient deficiencies are still relatively common, particularly in CD patients with active small bowel disease and/or multiple resections. This is an updated literature review of the prevalence of major micronutrient deficiencies in IBD patients, focusing on those associated with important extraintestinal complications, including anemia (iron, folate, vitamin B12) bone disease (calcium, vitamin D, and possibly vitamin K), hypercoagulability (folate, vitamins B6, and B12), wound healing (zinc, vitamins A and C), and colorectal cancer risk (folate and possibly vitamin D and calcium).

Apoptosis of regulatory T lymphocytes is increased in chronic inflammatory bowel disease and reversed by anti-TNFα treatment

Background and aimsInappropriate immune responses contribute to the continuous stimulation of the intestinal immune system in chronic inflammatory bowel disease (IBD). Among several pathogenic factors, a numerical deficiency of regulatory...

Vitamin D deficiency in inflammatory bowel disease.

Vitamin D deficiency in inflammatory bowel disease.

Safety and Efficacy of Total-Dose Infusion of Low Molecular Weight Iron Dextran for Iron Deficiency Anemia in Patients with Inflammatory Bowel Disease

Intravenous iron has been suggested as a safe and effective treatment of anemia complicating inflammatory bowel disease (IBD). Low molecular weight (LMW) iron dextran has the ability to administer the patient's total iron requirement in a single infusion. The aim of this study was to assess the safety and efficacy of the total dose of LMW iron dextran infusion for the treatment of iron deficiency in IBD. Fifty IBD patients (27 female, 35 Crohn's disease, 15 ulcerative colitis) were included in the study. Mean +/- standard deviation (SD) hemoglobin and ferritin levels before the infusion were 9.88 +/- 1.42 g/dl and 13.9 +/- 10.9 ng/ml, respectively. A 25-mg test dose was followed by infusion of the total dose of LMW iron dextran based on the iron deficit. Several clinical and laboratory parameters were measured before and on week 4 after infusion. Four patients (8%) developed adverse reactions during the test infusion and did not receive the total-dose infusion. Only one patient developed an allergic reaction during the total-dose infusion. In the remaining 45 patients, the mean +/- SD iron dose that was given was 1,075 +/- 269 mg. The mean +/- SD elevation of hematocrit and hemoglobin on week 4 was 4.9 +/- 1.9% and 1.7 +/- 0.8 g/dl, respectively. Hematopoietic response was observed in 23 of 45 patients (51.1%). Total parenteral iron replacement with LMW iron dextran is an easy, safe, and effective alternative method for treating iron deficiency anemia in IBD. Harmless adverse reactions may develop in a minority of patients.

Zinc deficiency in inflammatory bowel disease.

Zinc deficiency in inflammatory bowel disease.

Use of agents stimulating erythropoiesis in digestive diseases

Anemia is the most common complication of inflammatory bowel disease (IBD). Control and inadequate treatment leads to a worse quality of life and increased morbidity and hospitalization. Blood loss, and to a lesser extent, malabsorption of iron are the main causes of iron deficiency in IBD. There is also a variable component of anemia related to chronic inflammation. The anemia of chronic renal failure has been treated for many years with recombinant human erythropoietin (rHuEPO), which significantly improves quality of life and survival. Subsequently, rHuEPO has been used progressively in other conditions that occur with anemia of chronic processes such as cancer, rheumatoid arthritis or IBD, and anemia associated with the treatment of hepatitis C virus. Erythropoietic agents complete the range of available therapeutic options for treatment of anemia associated with IBD, which begins by treating the basis of the inflammatory disease, along with intravenous iron therapy as first choice. In cases of resistance to treatment with iron, combined therapy with erythropoietic agents aims to achieve near-normal levels of hemoglobin/hematocrit (11-12 g/dL). New formulations of intravenous iron (iron carboxymaltose) and the new generation of erythropoietic agents (darbepoetin and continuous erythropoietin receptor activator) will allow better dosing with the same efficacy and safety.

Common Misconceptions in the Diagnosis and Management of Anemia in Inflammatory Bowel Disease

Anemia is the most common systemic complication of inflammatory bowel disease (IBD); so common that it is almost invariably not investigated and rarely treated. Several misconceptions are the reason for these clinical errors, and our goal will be to review them. The most common misconceptions are: anemia is uncommon in IBD; iron deficiency is also uncommon; just by treating the intestinal disease, anemia will be corrected; iron deficiency is the only cause for anemia in IBD; ferritin is an accurate parameter for the diagnosis of iron deficiency in IBD; the impact of anemia on the quality of life of IBD patients is limited; iron supplementation is rarely needed in IBD; high-dose oral iron solves the problem of iron malabsorption in IBD; intravenous (IV) iron is dangerous and of no proven benefit in IBD; IV iron is useful only for severe anemia; and erythropoietin has no role in the treatment of IBD anemia. These misconceptions are not evidence-based. On the contrary, there is enough evidence to support the following statements: (a) anemia is very common in IBD, (b) anemia should be investigated with care because many factors can be responsible, (c) treatment of anemia results in clear improvement in the objective parameters of well-being, especially in the quality of life, (d) IV iron is safe and effective in the treatment of iron deficiency anemia in IBD patients, and (e) erythropoietin is useful in a subset of patients with refractory anemia. Anemia diagnosis and treatment must not be neglected in IBD patients, and several misconceptions should be promptly abandoned.

Vascular and Cellular Stress in Inflammatory Bowel Disease: Revisiting the Role of Homocysteine

Moderate hyperhomocysteinemia is a complex trait commonly associated with inflammatory bowel disease (IBD). Nutritional deficiencies and genetic determinants have been identified as risk factors for moderate hyperhomocysteinemia, such as folate and vitamin B(12) deprivation and polymorphisms in the 5,10 methylenetetrahydrofolate reductase (MTHFR) encoding gene, respectively. Homocysteine has a crucial role in cellular stress, epigenetic events, inflammatory processes, and host-microbial interactions. Hyperhomocysteinemia might therefore influence the clinical history of IBD, including disease severity, susceptibility to particular enteric infections, and the risk for the development of colorectal cancer. In contrast, homocysteine metabolism does not seem to contribute to the greater risk of thrombosis in IBD subjects. Herein, we review the evidence linking homocysteine metabolism to the pathophysiology of IBD. Furthermore, we discuss the relevance of screening and treating folate and vitamin B(12) deficiencies in IBD subjects. Given the peculiar frequency of such deficiencies in IBD, normalizing vitamin levels should be an integral part of the management of these patients, especially those with active disease, history of intestinal resection, and/or treated with methotrexate.

Dietary Iron Affects Inflammatory Status in a Rat Model of Colitis

Iron deficiency anemia is a common feature in inflammatory bowel disease, and oral supplementation is one of the mainstay therapies. However, there is some concern that oral iron supplementation may lead to oxidative stress and exacerbation of inflammation. Our objective was to study the effect of severely deficient, moderately deficient, normal and high iron status on oxidative stress and the course of inflammation in a rat model of colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). The rats were randomly assigned to receive the low-iron diet for 3 (moderately iron-deficient group, n = 16) or 5 (severely iron-deficient group, n = 16) wk, the normal iron diet for 2 wk (normal iron group, n = 16) or the high-iron diet for 2 wk (high-iron group, n = 16). Malondialdehyde concentration, electroparamagnetic resonance measurement, myeloperoxidase activity, and histological analysis were used to evaluate oxidative stress. Noncolitic rats in the high-iron group had higher oxidative stress parameters than those in the other groups. The induction of colitis resulted in severe inflammatory changes in the high-iron and severely iron-deficient groups, and produced higher histological scores in the colon of the normal and high-iron groups. Iron overload, oxidative stress, and inflammation were lower in the moderately iron-deficient group compared with the other 3 groups. In conclusion, we suggest that low rather than normal or high iron supplementation should be considered for the treatment of iron deficiency in inflammatory bowel disease.

Impairment of intestinal glutathione synthesis in patients with inflammatory bowel disease

Background—Reactive oxygen species contribute to tissue injury in inflammatory bowel disease (IBD). The tripeptide glutathione (GSH) is the most important intracellular antioxidant.Aims—To investigate constituent amino acid plasma levels and the...

Consensus in clinical nutrition

List of contributors Preface 1. Measurement of body composition in clinical practice S. A. Jebb and M. Ella 2. Assessment of energy requirements J. H. Green 3. Amino acid requirements in health and disease P. J. Garlick, M. A. McNurlan and M. F. Fuller 4. Mineral and vitamin metabolism A. Shenkin 5. Nutritional immunology A. Animashaun and R. V. Heatley 6. Physiology of nutrient absorption: a decade of advance in formulation of enteral diets G. K. Grimble 7. Enteral and parenteral nutrition C. R. Pennington 8. Is nutritional support worthwhile? R. L. Koretz 9. Enteral feeding and food intolerance in paediatrics A. MacDonald 10. Neonatal intravenous feeding I. W. Booth 11. Nutrition and the surgical patient N. Everitt and M. McMahon 12. Perioperative feeding M. M. Meguid and A. C. L. Campos 13. How I feed the starving patient S. P. Allison 14. Intensive care management I. T. Campbell and R. A. Little 15. The role of the liver in nutrition M. S. Losowsky and P. N. Bramley 16. Nutritional deficiencies in inflammatory bowel disease P. Duane and R. V. Heatley 17. Short bowel syndrome J. E. Lennard-Jones 18. Nutrition in cystic fibrosis J. M. Littlewood and S. P. Wolfe 19. Diet, lipids and lipoproteins J. P. Miller and A. Naylor 20. Diet and book pressure J. D. Swales 21. Obesity J. Garrow 22. Eating disorders L. F. Pieri and A. C. P. Sims Index.

Iron deficiency in inflammatory bowel disease. Diagnostic efficacy of serum ferritin.

The prevalence of iron-deficiency anemia was defined in 105 patients with inflammatory bowel disease and an appraisal made of the diagnostic value of serum ferritin for the assessment of iron stores. Iron deficiency, defined by the absence of bone-marrow hemosiderin was found with anemia in 36% of 41 patients with ulcerative colitis (UC) and 22% of 64 patients with Crohn's disease (CD). Iron deficiency without impaired erythropoiesis was detected in an additional 32% of patients with UC and 2% with CD. Anemia with plentiful bone-marrow iron was present in 33 (51%) of patients with CD, only one of whom had vitamin B12 deficiency. Red blood cell morphology, RBC indices, serum iron, and percent transferrin saturation correlated poorly with stainable marrow iron. Serum ferritin, assayed in samples from 45 patients, was 55 ng/ml were invariably associated with the presence of marrow hemosiderin. Based on a lower normal limit of 18 ng/ml, the serum ferritin had an excellent predictive value (100%) but a high predictive error (32%) in the diagnosis of iron deficiency in inflammatory bowel disease. Serum ferritin >55 ng/ml ruled out iron deficiency as the basis for anemia.