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Anemia, Iron Deficiency

Red Blood Cell Comparison. Courtesy medindia.com
Red Blood Cell Comparison. Courtesy medindia.com

What Is Iron Deficiency Anemia?

[dropcap]I[/dropcap]ron 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:
  1. 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. []

Anemia, Folic Acid Deficiency  

Folic acid deficiency anemia gluten celiac disease symptom
Red Blood Cells.

What Is Folic Acid Or Folate Deficiency Anemia?

[dropcap]F[/dropcap]olic acid deficiency anemia, also called folate deficiency anemia, is a macrocytic anemia characterized by defective DNA synthesis of red blood cells that results from a lack of folate in the body.

Q: How does folate deficiency cause anemia?

A: Folates are a family of B vitamins and folic acid is an active form.

Folate is required for the formation of both red and white blood cells in the bone marrow and for their maturation.

Also, folate serves as a carrier in the formation of heme, which contains iron, and is the non-protein part of the hemoglobin molecule.1

Red blood cells provide oxygen to body tissues. When there are not enough red blood cells or when they cannot properly carry oxygen, the condition is called anemia. In folic acid deficiency anemia, the red blood cells are abnormally large. Such cells are called macrocytes (macro size cells). They are also called megaloblasts (mega size cells) as seen in the bone marrow where they are produced. This is why this macrocytic anemia is also called megaloblastic anemia.2

Tests that may be done to determine folate adequacy are complete blood count (CBC), red blood cell folate level, methylmalonic acid level, and homocysteine level. Folic acid deficiency anemia shows a decrease in red blood cell folate and/or serum folate levels and normal plasma methylmalonic acid level with elevated homocysteine blood level. These levels distinguish folic acid deficiency anemia from vitamin B12 deficiency anemia.3

What Is Folate Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Kathleen Mahan and Sylvia Escott-Stump, ed. Krause’s Food, Nutrition & Diet Therapy, 10th Edition. Philadelphia, PA. USA: W.B. Saunders Company, 2000. []
  2. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001578/ []
  3. Mark Beers and Robert Berkow. The Merck Manual, 17th Edition. Whitehouse Station, N.J. USA: Merck Research Laboratories, 1999. []

Juvenile Autoimmune Thyroid Disease

Goiter in Grave's disease. Courtesy Wikimedia.
Goiter in Grave’s disease. Courtesy Wikimedia.

What Is Juvenile Autoimmune Thyroid Disease?

Juvenile autoimmune thyroid disease is an autoimmune disorder occurring in childhood that targets and damages the thyroid gland, often causing goiter. It is characterized by abnormal circulating thyroid hormone levels in the bloodstream.

Recent evidence suggests that thyroid autoimmunity originates from an interaction of genetic, endogenous and environmental factors which end up activating thyroid-specific autoreactive T-lymphocyte cells in susceptible children.1

Q: What is the thyroid gland?

Thyroxine molecule, chemical structure. Thyroid gland hormone that plays a role in energy metabolism regulation. It is a iodine containing derivative of thyrosine. Atoms are represented as spheres with conventional color coding: hydrogen (white), carbon (grey), oxygen (red), nitrogen (blue), iodine (purple).
Thyroxine molecule. Atoms are represented as spheres with conventional color coding: hydrogen (white), carbon (grey), oxygen (red), nitrogen (blue), iodine (purple).

A: The thyroid is an endocrine (hormone secreting) gland that produces thyroid hormones in response to the action of thyroid stimulating hormone (TSH) produced by the pituitary gland, and releases them into the bloodstream to be quickly carried to their site of action.

The three thyroid hormones are thyroxine, called T4, triiodothyronine, called T3, and calcitonin. T4 and T3 hormones control the rate of metabolism, meaning 1) the rate of food usage for energy production, 2) the rate of protein production and breakdown in most tissues, 3) the heart rate and force of heart muscle contraction, 4) body temperature, and 5) the rate of growth and development in children.

Dietary iodine and selenium are required for T3 production. Specifically, selenium is part of the enzyme that converts T4 to the active form, T3. Calcitonin hormone is needed to build and maintain dense bones and regulate calcium blood level. The thyroid gland is located in the front of the neck at the top of the trachea (windpipe).

Who Is Affected in the General Population? Autoimmune thyroid disease is the most common etiology of acquired thyroid dysfunction in pediatrics. It is more common in females and usually occurs in early to mid-puberty. Presentation is rare under the age of 3 years, but cases have been described even in infancy.2 

What Is Juvenile Autoimmune Thyroid Disease In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Gopalakrishnan S, Marwaha RK. Juvenile autoimmune thyroiditis. J Pediatr Endocrinol Metab. 2007 Sep;20(9):961-70. []
  2. Cappa M, Bizzarri C, and Crea F. Autoimmune Thyroid Diseases in Children. Journal of Thyroid Research. Volume 2011 (2011), Article ID 675703, 13 pages. http://dx.doi.org/10.4061/2011/675703 []