Multifactorial Etiology of Anemia in Celiac Disease and Effect of Gluten-Free Diet: A Comprehensive Review.

Rafael Martín-Masot, Maria Teresa Nestares, Javier Diaz-Castro, Inmaculada López-Aliaga, Maria Jose Muñoz Alférez, Jorge Moreno-Fernandez, José Maldonado

Journal: Nutrients 2020;11(11):2557

PMID: 31652803

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Plain Language Summary

Anaemia is a common clinical expression of Celiac Disease (CD) alongside vitamin B12, iron and folate deficiencies. This review looks at the latest evidence and effects of a gluten free diet, the mainstay of treatment for CD. Typically, symptoms subside whilst adhering to a GF diet however in 20% of people anaemia and nutrient deficiencies can persist. Some of this is attributed to lack of adherence to the diet, oftentimes accidental given the wide range of foods containing gluten. This in turn leads to further damage of the intestine and can be difficult to detect and monitor effectively. Inflammation of the gastrointestinal tract, and malabsorption, are the main reasons for nutrient deficiencies leading to anaemia in CD. Iron is a critical nutrient which can easily be affected by damage to the intestinal villi, common in CD, and over time lead to iron deficiency anaemia as the body is unable to absorb dietary iron and the body’s iron stores are depleted. Likewise, absorption of vitamins B12 and B9 (folate) are also impaired by damaged villi and vitamin B12 is further affected by small intestine injuries including decreased gastric acid production, bacterial overgrowth and reduced intrinsic factor efficiency. Deficiencies of these two nutrients can lead to macrocytic anaemia with low blood cell volumes. Overall a gluten free diet is shown to reduce symptoms of CD in a matter of weeks. The more patients adhere to the diet, the more the risk of nutrient deficiencies and anaemia reduces.

Abstract

Celiac disease (CD) is a multisystemic disorder with different clinical expressions, from malabsorption with diarrhea, anemia, and nutritional compromise to extraintestinal manifestations. Anemia might be the only clinical expression of the disease, and iron deficiency anemia is considered one of the most frequent extraintestinal clinical manifestations of CD. Therefore, CD should be suspected in the presence of anemia without a known etiology. Assessment of tissue anti-transglutaminase and anti-endomysial antibodies are indicated in these cases and, if positive, digestive endoscopy and intestinal biopsy should be performed. Anemia in CD has a multifactorial pathogenesis and, although it is frequently a consequence of iron deficiency, it can be caused by deficiencies of folate or vitamin B, or by blood loss or by its association with inflammatory bowel disease (IBD) or other associated diseases. The association between CD and IBD should be considered during anemia treatment in patients with IBD, because the similarity of symptoms could delay the diagnosis. Vitamin B deficiency is common in CD and may be responsible for anemia and peripheral myeloneuropathy. Folate deficiency is a well-known cause of anemia in adults, but there is little information in children with CD; it is still unknown if anemia is a symptom of the most typical CD in adult patients either by predisposition due to the fact of age or because biochemical and clinical manifestations take longer to appear.

Address: Pediatric Clinical Management Unit, Málaga Regional University Hospital, 29010 Málaga, Spain. [email protected].; Department of Physiology and Institute of Nutrition and Food Technology "José MataixVerdú", University of Granada, 18071 Granada, Spain. [email protected].; Department of Physiology and Institute of Nutrition and Food Technology "José MataixVerdú", University of Granada, 18071 Granada, Spain. [email protected].; Department of Physiology and Institute of Nutrition and Food Technology "José MataixVerdú", University of Granada, 18071 Granada, Spain. [email protected].; Department of Physiology and Institute of Nutrition and Food Technology "José MataixVerdú", University of Granada, 18071 Granada, Spain. [email protected].; Department of Physiology and Institute of Nutrition and Food Technology "José MataixVerdú", University of Granada, 18071 Granada, Spain. [email protected].; Department of Pediatrics, University of Granada, 18071 Granada, Spain. [email protected].; Biosanitary Research Institute, 18012 Granada, Spain. [email protected].; Maternal and Child Health Network, Institute Carlos III, 28020 Madrid, Spain. [email protected].; Pediatric Clinical Management Unit. Virgen de las Nieves University Hospital, 18014 Granada, Spain. [email protected].

DOI: 10.3390/nu11112557