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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. [↩]

Iron Deficiency

ferritinWhat Is Iron?

[dropcap]I[/dropcap]ron is an essential mineral that is required for normal body function.

Almost two-thirds of iron in the body is found in hemoglobin, the protein in red blood cells that carries oxygen to tissues. Smaller amounts of iron are found in myoglobin, a protein that helps supply oxygen to muscle, and in enzymes that assist biochemical reactions.

Iron is also found in proteins that store iron for future needs and that transport iron in blood.

Q: How are iron stores regulated?

A:Iron stores are regulated by intestinal iron absorption.1That is, whenever iron is needed, more iron is absorbed than when iron is sufficient. This mechanism prevents excess iron in the body which is harmful.

In the brain, iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxid. ase), and for the synthesis of neurotransmitters and myelin.

Iron concentrations in the umbilical artery are critical during the development of the fetus, and in relation with the IQ in the child.2

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

Sources:
  1. http://ods.od.nih.gov/factsheets/Iron-HealthProfessional accessed 12/11/12 [↩]
  2. Bourre JM. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. 2006 Sep-Oct; 10(5):377-85. [↩]

Coronary Artery Disease

Image on left shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.
Figure on right shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.

What Is Coronary Artery Disease (CAD)?

[dropcap]C[/dropcap]oronary artery disease (CAD), also called ischemic heart disease, is a gradual narrowing of medium and large arteries of the heart by fatty buildups, called atherosclerotic plaques.

It is characterized by slowly developing interference with blood flow to heart tissue itself, resulting in oppressive chest pain called angina and, ultimately, thrombosis (clot) causing heart attack.  

The heart is a muscular organ that is working all the time, so it needs a constant supply of oxygen. Oxygen is brought to the working heart tissue by the coronary arteries with each beat of the heart. When heart muscle has to work harder, it needs more oxygen delivered to itself. Lack of oxygen causes pain.

In fact, failure of diseased coronary arteries to deliver adequate oxygen to heart tissue is the most common cause of angina pectoris – substernal pain (under breastbone) or pressure brought on by exertion and relieved by rest. 

Thrombosis, or clot formation, occurs when blood cells within a narrowed artery can no longer get through. Trapped, blood cells pile up and block the artery thus triggering a cascade of events called heart attack. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery.1

Q: How does coronary artery disease develop?

A: Coronary artery disease slowly develops from this combination of events:

  • Dysfunction of epithelial cells that line the inside of arteries cause the vessels to stiffen, and subsequently

  • Accumulation of lipid (fat) in smooth muscle cells beneath the inside lining of arteries and in foam cells cause buildup of fatty deposits on the inside walls progressing to fibrous plaque formation.

Oxidized low-density lipoprotein (oxLDL), so-called bad cholesterol, and oxysterols play important roles in the development of  atherosclerosis. OxLDL triggers the immune system to produce autoantibodies against oxLDL that are detectable in serum. These antibodies are called anti-oxLDL. Anti-oxLDL antibody and oxysterol concentrations are associated with coronary artery stenosis. Oxidative stress may be greatly increased in unstable angina.2 and Chronic inflammation in the general population is a major risk factor for ischemic heart disease.

The pathophysiology of atherosclerosis is, clearly, different in women when compared to the men. The women have a higher risk of blood coagulability making them at high risk for the blood clot formation. In a large number of women endothelial dysfunction, small vessel size and diffuse atherosclerosis have been identified as causes of ischemia without evidence of blockade in the coronary arteries.3

Also, atherosclerotic plaque in women is less fibrotic and contains more lipid filled foam cells, implying greater potential for reversibility but also potentially greater vulnerability for plaque rupture and thrombosis.4

Who is Affected in the General Population?

  • Coronary artery disease remains the leading cause of death in developed countries despite significant progress in primary prevention and treatment strategies.

  • It is the leading cause of death in women, as well as an important cause of disability.

  • Older patients are at particularly high risk of poor outcomes following acute coronary syndrome.5

What Is Coronary Artery Disease In Celiac Disease and/or Gluten Sensitivity?

Ischemic heart disease is the leading cause of death in the United States, making cardiovascular risk assessments and potential interventions or treatments imperative for patients with celiac disease.6

Sources:
  1. http://www.heart.org/HEARTORG/Conditions/HeartAttack/SymptomsDiagnosisofHeartAttack/Unstable-Angina_UCM_437513_Article.jsp# [↩]
  2. Yasunobu Y, Hayashi K, Shingu T, Yamagata T, Kajiyama G, Kambe M. Coronary atherosclerosis and oxidative stress as reflected by autoantibodies against oxidized low-density lipoprotein and oxysterosis. Atherosclerosis. Apr 2001;155(2):445-53. [↩]
  3. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
  4. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
  5. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. [↩]
  6. Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]

Macrocytosis

Comparison of normoblast and megaloblastWhat Is Macrocytosis?

[dropcap]M[/dropcap]acrocytosis is a blood cell disorder characterized by altered blood cell formation that results in abnormally large erythrocytes (red blood cells) circulating in the bloodstream.

The mean corpuscular volume (MCV), which is a measure of the size of red blood cells in the bloodstream, is greater than 100 fL as shown in a complete blood count (CBC) laboratory analysis report.

Macrocytosis produces macrocytic anemias that are classified as megaloblastic or non-megaloblastic:

  1. Megaloblastic anemias result from disorders of DNA synthesis of red blood cell precursors (megaloblasts) in bone marrow due to B vitamin deficiency demonstrated by macro-ovalocytes and hypersegmented neutrophils.1
  2. Non-megaloblastic anemias are or those caused primarily by alcoholism, liver disease and hypothyroidism.2

What Is Macrocytosis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Kaferle J, Strzoda CE.Evaluation of macrocytosis. Am Fam Physician. 2009 Feb 1;79(3):203-8. [↩]
  2. Davenport J. Macrocytic anemia. Am Fam Physician. 1996 Jan;53(1):155-62. [↩]