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      Anemia, iron deficiency, and cobalamin deficiency in cats with chronic gastrointestinal disease

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          Abstract

          Background

          Iron deficiency and cobalamin deficiency, as sequelae to chronic gastrointestinal (GI) disease, could result in anemia and increased morbidity in cats with chronic enteropathies.

          Objective

          To evaluate iron deficiency in cats with chronic GI disease and its relationship with hypocobalaminemia, anemia, and disease severity.

          Animals

          Twenty client‐owned cats with primary GI disease.

          Methods

          Prospective, cross‐sectional study. Cats were enrolled at the time of evaluation for chronic GI disease, after exclusion of comorbidities. CBC with reticulocyte indices, iron metabolism (serum iron and ferritin concentrations, total iron binding capacity [TIBC]), serum methylmalonic acid (MMA), cobalamin, and folate concentrations, pancreatic lipase and trypsin‐like immunoreactivity, and disease severity were evaluated.

          Results

          Anemia (hematocrit <30%), iron deficiency, and cobalamin deficiency were diagnosed in 4/20, 7/20, and 8/20 cats, respectively. Hematocrit ( r s = −.45; P < .05) and body condition score ( r s = −.60; P < .01) negatively correlated with MMA. Median TIBC was lower in cats with increased vs normal MMA (218 μg/mL; range, 120‐466 μg/mL vs 288 μg/mL; range, 195‐369 μg/mL; P = .02). Hematocrit ( r s = .51; P = .02), reticulocyte MCV ( r s = .52; P = .02), reticulocyte hemoglobin content ( r s = .71; P < .001), and percent transferrin saturation ( r s = .79; P < .0001) positively correlated with serum iron concentration.

          Conclusions and Clinical Importance

          Functional iron deficiency was common in cats with chronic GI disease. Associations between hypocobalaminemia, iron parameters, and hematologic parameters warrant further investigation on the impact of iron deficiency on chronic GI disease morbidity in cats.

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          Most cited references34

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          Correlation Coefficients

          Correlation in the broadest sense is a measure of an association between variables. In correlated data, the change in the magnitude of 1 variable is associated with a change in the magnitude of another variable, either in the same (positive correlation) or in the opposite (negative correlation) direction. Most often, the term correlation is used in the context of a linear relationship between 2 continuous variables and expressed as Pearson product-moment correlation. The Pearson correlation coefficient is typically used for jointly normally distributed data (data that follow a bivariate normal distribution). For nonnormally distributed continuous data, for ordinal data, or for data with relevant outliers, a Spearman rank correlation can be used as a measure of a monotonic association. Both correlation coefficients are scaled such that they range from -1 to +1, where 0 indicates that there is no linear or monotonic association, and the relationship gets stronger and ultimately approaches a straight line (Pearson correlation) or a constantly increasing or decreasing curve (Spearman correlation) as the coefficient approaches an absolute value of 1. Hypothesis tests and confidence intervals can be used to address the statistical significance of the results and to estimate the strength of the relationship in the population from which the data were sampled. The aim of this tutorial is to guide researchers and clinicians in the appropriate use and interpretation of correlation coefficients.
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            Iron homeostasis and the inflammatory response.

            Iron and its homeostasis are intimately tied to the inflammatory response. The adaptation to iron deficiency, which confers resistance to infection and improves the inflammatory condition, underlies what is probably the most obvious link: the anemia of inflammation or chronic disease. A large number of stimulatory inputs must be integrated to tightly control iron homeostasis during the inflammatory response. In order to understand the pathways of iron trafficking and how they are regulated, this article presents a brief overview of iron homeostasis. A major focus is on the regulation of the peptide hormone hepcidin during the inflammatory response and how its function contributes to the process of iron withdrawal. The review also summarizes new and emerging information about other iron metabolic regulators and effectors that contribute to the inflammatory response. Potential benefits of treatment to ameliorate the hypoferremic condition promoted by inflammation are also considered.
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              Death in the intestinal epithelium-basic biology and implications for inflammatory bowel disease.

              Every 4-5 days, intestinal epithelial cells (IEC) are terminated as they reach the end of their life. This process ensures that the epithelium is comprised of the fittest cells that maintain an impermeable barrier to luminal contents and the gut microbiota, as well as the most metabolically able cells that conduct functions in nutrient absorption, digestion, and secretion of antimicrobial peptides. IEC are terminated by apical extrusion-or shedding-from the intestinal epithelial monolayer into the gut lumen. Whether death by apoptosis signals extrusion or death follows expulsion by younger IEC has been a matter of debate. Seemingly a minor detail, IEC death before or after apical extrusion bears weight on the potential contribution of apoptotic IEC to intestinal homeostasis as a consequence of their recognition by intestinal lamina propria phagocytes. In inflammatory bowel disease (IBD), excessive death is observed in the ileal and colonic epithelium. The precise mode of IEC death in IBD is not defined. A highly inflammatory milieu within the intestinal lamina propria, rich in the proinflammatory cytokine, TNF-α, increases IEC shedding and compromises barrier integrity fueling more inflammation. A milestone in the treatment of IBD, anti-TNF-α therapy, may promote mucosal healing by reversing increased and inflammation-associated IEC death. Understanding the biology and consequences of cell death in the intestinal epithelium is critical to the design of new avenues for IBD therapy.
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                Author and article information

                Contributors
                mjugan@vet.k-state.edu
                Journal
                J Vet Intern Med
                J Vet Intern Med
                10.1111/(ISSN)1939-1676
                JVIM
                Journal of Veterinary Internal Medicine
                John Wiley & Sons, Inc. (Hoboken, USA )
                0891-6640
                1939-1676
                23 November 2020
                Jan-Feb 2021
                : 35
                : 1 ( doiID: 10.1111/jvim.v35.1 )
                : 172-178
                Affiliations
                [ 1 ] Department of Clinical Sciences College of Veterinary Medicine, The University of Tennessee Knoxville Tennessee USA
                [ 2 ] Department of Clinical Sciences College of Veterinary Medicine, Kansas State University Manhattan Kansas USA
                Author notes
                [*] [* ] Correspondence

                Maria C. Jugan, Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, 1800 Denison Avenue, Manhattan, KS 66506.

                Email: mjugan@ 123456vet.k-state.edu

                Author information
                https://orcid.org/0000-0002-6963-7646
                Article
                JVIM15962
                10.1111/jvim.15962
                7848310
                33226151
                94b9defc-f132-4d70-90fb-d3660382c0e3
                © 2020 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 07 August 2020
                : 29 October 2020
                : 29 October 2020
                Page count
                Figures: 0, Tables: 2, Pages: 7, Words: 5533
                Funding
                Funded by: Comparative Gastrointestinal Society Royal Canin USA Research Grant
                Categories
                Standard Article
                SMALL ANIMAL
                Standard Articles
                Gastroenterology
                Custom metadata
                2.0
                January/February 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.9.7 mode:remove_FC converted:01.02.2021

                Veterinary medicine
                chronic enteropathy,feline,ferritin,functional iron deficiency,methylmalonic acid

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