Editor’s note: In this case report of infants with severe malabsorption from celiac disease, the treating physicians found copper deficiencies based on blood studies that showed severe low copper levels and white blood cell count. Treatment required copper supplementation in addition to the gluten-free diet. Normally, in the last few months of gestation, an infant stores a large amount of copper in their liver. This storage must last about 6 months because infants must derive their nourishment from copper-poor milk. This case report shows dramatically the terrible effect of malabsorption coupled with a naturally occurring huge demand for copper that could not be satisfied through digestion.
Low stomach acid production is a common disorder in celiac disease and dermatitis herpetiformis that is characterized by lack of sufficient hydrochloric acid needed 1) to properly digest food, which results in malnutrition and subsequent nutritional deficiencies, and 2) to destroy swallowed bacteria and other microbes, which may allow infections to develop.
It is also common in the general population, as well, affecting 50% of people age 60 years and about 80% by age 85 years. Nevertheless, low stomach acid is not generally looked for as a cause of acute and chronic disorders that rob health with far-reaching effects.
Understanding Stomach Acid Production and Function
The stomach digests incoming food into a liquid state, thereby releasing nutrients so they can be absorbed by the small intestine. Powerful stomach muscles churn food and mix it with gastric juice, dissolving and breaking it down.
Gastric juice is produced by gastric glands located in the stomach lining. These numerous, microscopic glands produce about 3 liters of juice a day. Gastric juice is composed of a high concentration of
Iron deficiency anemia is a blood cell disorder that is characterized by formation of small, pale red blood cells, causing tissue hypoxia. Hypoxia is the inability to meet the demands of the body for oxygen.
Q: Why do small, pale red blood cells cause tissue hypoxia?
A: Small, pale red blood cells (erythrocytes) cause tissue hypoxia because they are not able, as do normal erythrocytes, to pick up adequate oxygen from the lungs and carry it to cells that use oxygen.
Red blood cell production and function are dependent on a sufficient level of iron in the body and also the ability to use available iron to make hemoglobin in red blood cells.
Hemoglobin is a protein that binds oxygen in red blood cells to be carried by the bloodstream to cells throughout the body. In iron deficiency anemia, hemoglobin in females is below 12.5g/dl (normal range is 12.5 to 16g/dl) and in males it is below 13.5g/dl (normal range is 13.5 to 17.5g/dl).
Iron must be obtained from the diet, since the body cannot make it, but there are various factors that can interfere with absorption and use in the body, causing anemia. Iron absorption from the gut first requires ionization, or gaining a positive electrical charge, in the strongly acidic environment of stomach juice. Ionized iron, only, can be absorbed in the duodenum, which receives the acidic contents of the stomach before it is neutralized further along.
Dietary iron can be heme or non-heme depending on the food source. Heme iron obtained only from animal food sources is absorbed into the bloodstream by active transport across the brush border (microvilli) which cover the multitudinous villi of the small intestinal lining.
Non-heme iron obtained from plants must bind with apoprotein after entering the enterocyte (surface cell of small intestinal lining) to be ferried to the underlying basolateral membrane and exited by active transport into the bloodstream.
Frequently, chronic anemia due to iron deficiency is accompanied by increased platelets, and this thrombocytosis resolves with iron repletion (normal iron level). Conversely, in severe iron deficiency anemia, patients may have thrombocytopenia (low platelets), which also resolves with iron therapy.1
What Is Iron Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?
Sources:
Koury M and Rhodes M. How to approach chronic anemia. Hematology Am Soc Hematol Educ Program. 2012;2012:183-90. doi: 10.1182/asheducation-2012.1.183. [↩]
Copper is an essential trace element that is required for a number of enzymes which are necessary for normal metabolic function.
In the body almost all the copper is present as a component of copper proteins which are produced and controlled by the liver.
Q: How does the liver control copper?
A: The liver maintains proper copper balance by binding free copper to proteins and by excreting excess copper as part of bile that is then emptied into the intestinal tract and excreted in stool.
Metabolic balance studies have demonstrated that daily copper losses are approximately 1.3 mg/day.1
Among its specific functions listed below, copper is essential for energy production, blood and nerve functions, blood components, immunity, and collagen tissue. The copper enzyme, lysyl oxidase, is involved in the cross-linking of collagen in forming the framework for depositing calcium and other minerals to build and repair bone.
Animal studies suggest that adequate copper levels during pregnancy are critical to development of higher brain function in the offspring.2
What Is Copper Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Williams DM. Copper deficiency in humans. Semin Hematol. 1983 Apr; 20(2):118-28. [↩]
Fisgin T, Yarali N, Duru F, Usta B, Kara A. Hematologic manifestation of childhood celiac disease. Acta Haematol. 2004;111(4):211-4. [↩]
Microscopic View of Gastric Biopsy Showing a Collagen Band Stained Pink Under the Surface Mucosal Cells. Courtesy Gastrolab.com
What Is Collagenous Gastritis?
C ollagenous gastritis is a rarely reported stomach disorder characterized by the deposition of a subepithelial collagen band and accompanying inflammatory infiltrate in the stomach wall.
A subepithelial collagen band means that collagen, a tough fibrous protein, has abnormally accumulated under the surface layer of epithelial cells which form the mucosa lining the stomach.
The surface mucosa may remain intact and not show lymphocytosis and/or gastritis on endoscopic examination or it may become stripped off and bleed from entrapped capillaries. Biopsy is necessary to diagnose collagenous gastritis.1
Q: Why does collagen become deposited under the surface lining of the stomach?
A: It is thought that collagen deposition is preceded by inflammation and tissue damage. However, the natural history and pathogenesis of collagenous gastritis remain unclear.2
What Is Collagenous Gastritis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Jain R, Chetty R. Collagenous gastritis. Int J Surg Pathol. 2010 Dec;18(6):534-6. doi: 10.1177/1066896908329588. Epub 2008 Dec 22. [↩]
Leung ST, Chandan VS, Murray JA, Wu TT. Collagenous gastritis: histopathologic features and association with other gastrointestinal diseases. Am J Surg Pathol. 2009 May;33(5):788-98. doi: 10.1097/PAS.0b013e318196a67f. [↩]
Paleness and Tendon Problem: Symptoms of Hypocupremia.
What Is Hypocupremia?
Hypocupremia, or low plasma copper, means the level of copper is too low to meet metabolic needs of the body for copper and is characterized by these many features:
Impaired energy production causing weakness.
Impaired ability as part of an enzyme to oxidize vitamin C which is required to breakdown histamine.
Faulty blood cell formation and instability of blood cell membranes causing anemia, shortened life span of neutrophils causing susceptibility to infection, faulty platelet formation causing impaired blood clotting.
A blood disorder characterized by presence of an abnormally low number of neutrophils resulting from deficiencies of copper and folate that is marked by profound weakness and predisposition to infection. Click for full description.
A metabolic bone disorder characterized by diminished bone mass (density) with retention of normal cell appearance, but fragile strength, and high bone turnover caused by deficiency of calcium and vitamin D in particular and other…
In this study, researchers investigating the absorption of copper in untreated patients who had damage to their duodenum found anemia in 3 out of 10 of these patients that was due to copper deficiency. They gave all the study subjects a solution of copper to drink that was equal to a daily dose then tested their blood level.
Copper usually receives little coverage, but this unpretentious nutrient deserves center stage. It is time for a serious role review.
Here are two reasons: First, deficiency of this trace mineral can debilitate and threaten our lives, and second, deficiency develops with increased frequency in those of us with celiac disease, unlike the general population.
Copper plays a critical role in the formation of a variety of proteins and enzymes involved in functions that keep us alive. Consequently, many disorders caused by copper deficiency stem from failure to adequately produce or release copper proteins and enzymes.
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Editor’s note: In this case report of infants with severe malabsorption from celiac disease, the treating physicians found copper deficiencies based on blood studies that showed severe low copper levels and white blood cell count. Treatment required copper supplementation in addition to the gluten-free diet. Normally, in the last few months of gestation, an infant stores a large amount of copper in their liver. This storage must last about 6 months because infants must derive their nourishment from copper-poor milk. This case report shows dramatically the terrible effect of malabsorption coupled with a naturally occurring huge demand for copper that could not be satisfied through digestion.
