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Inflammation

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inflammation-post-4What Is Inflammation?

[dropcap]I[/dropcap]nflammation is our body’s necessary self-defense response and repair mechanism for these assaults:

1) injuries such as cuts, scrapes, sprains, broken bones, burns, insect bites, toxins; 2) invading organisms such as bacteria; and 3) allergens and food sensitivities such as gluten.

Inflammation can be immediate (acute) or persistent (chronic).

Acute inflammation is marked by increased blood flow, migration of white blood cells, and release of defensive proteins and chemicals to the site of injured tissue. Among these chemicals are free radicals in the immune response to injury that are beneficial yet require the activity of anti-oxidants such as vitamin E and vitamin C to control.

Free radicals are chemical particles containing one or more unpaired electrons, which may be part of the molecule. They cause the molecule to become highly reactive.1

The majority of this response takes place in the first 12 to 24 hours after the assault. The inflammatory process continues until all the damaged tissue or invading germs are removed (usually about 5 days).2

Chronic inflammation is marked by persistence weeks to months or longer after tissue damage. Note: high concentrations of free radicals generated in chronic inflammation may be important causes of damage to cell structures. The defensive activity of anti-oxidants such as vitamin E and vitamin C are required to remove free radicals.

Chronic inflammation increases the risk for systemic diseases such as type II diabetes, obesity, heart disease, high blood pressure, arthritis, osteoporosis, chronic fatigue, migraine, autoimmune disease, and vasculitis which may cause stroke, heart attack or deep vein thrombosis (DVT).

Importantly, chronic inflammation is a risk factor for the onset of cancer.3

Q: Are there blood tests available for detecting inflammation?

A: Yes. Your medical health practitioner can order either or both of the following blood tests that measure the amount of inflammation present although not the source of inflammation. Abnormal is an elevation in blood levels.

  1. C-reactive protein (CRP). This test measure C-reactive proteins that are released into the bloodstream within a few hours of tissue injury or infection. CRPs are cytokines called ‘acute phase reactants,’ meaning first on the scene. The CRP test is also useful to monitor treatment response and flare-ups of chronic inflammatory disease such as vasculitis, systemic lupus, and inflammatory bowel disease.
  2. Erythrocyte sedimentation rate (ESR or sed rate). This test measures the rate of fall of blood cells in a sample tube of blood. An increase in the rate of fall shows inflammation due to an increase of C-reactive proteins in the blood specimen. Alone or with the CRP test, the ESR is especially useful for monitoring inflammation of veins and arteries.

In regards to celiac disease, disappearance of blood antibody levels of tissue transglutaminase IgA (tTG-IgA) indicate that inflammation has also subsided. These antibodies should be checked at 3 months, 6 months if indicated, and one year after diagnosis to monitor healing. On the other hand, raised antibodies indicate that there is definitely ongoing inflammation in the small intestine.

In regards to non-celiac gluten sensitivity, disappearance of blood antibody levels of anti-gliadin IgA and IgG at 3 months, 6 months if indicated, and one year after diagnosis indicate that inflammation has also subsided. On the other hand, raised antibodies indicate that there is definitely ongoing inflammation caused by gluten within the body.

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

Sources:
  1. Ruttkay-Nedecky B, Nejdl L , Gumulec J. The Role of Metallothionein in Oxidative Stress. Int. J. Mol. Sci. 2013, 14(3), 6044-6066; doi:10.3390/ijms14036044. [↩]
  2. Taber’s Cyclopedic Medical Dictionary. 19th ed. F A Davis Company. Philadelphia, PA. [↩]
  3. Brighenti E, Giannone FA, Fornari F, Onofrillo C, Govoni M, Montanaro L, Treré D, Derenzini M. Therapeutic dosages of aspirin counteract the IL-6 induced pro-tumorigenic effects by slowing-down the ribosome biogenesis rate. Oncotarget. 2016 Aug 20. doi: 10.18632/oncotarget.11441. [↩]

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. [↩]

Angina Pectoris

What Is Angina Pectoris?Coronary Artery Lesion

[dropcap]A[/dropcap]ngina pectoris, or simply angina, is a coronary syndrome characterized by an oppressive substernal pain (pain under breastbone) or pressure brought on by exertion and relieved by rest that results from failure of coronary arteries to deliver adequate oxygen to heart tissue due to ischemic heart disease.

Q: Why do coronary arteries fail to deliver adequate oxygen to heart tissue?

A: Coronary arteries are the blood vessels that serve the heart. In angina, these vessels fail to deliver adequate oxygen to heart tissue because they are narrowed or blocked by fatty buildups, called atherosclerotic plaques or by a blood clot which impair their ability to carry adequate blood that carries the oxygen. Diseased coronary arteries cannot deliver adequate oxygenated blood pumped by the heart to its own muscle cells.

The heart is a muscular organ that is working all the time without rest, so it needs a constant supply of oxygen. When heart muscle has to work harder, it needs more oxygen. Lack of oxygen causes pain which makes the affected person stop activity and rest.

Angina can be stable or unstable. Unstable angina is much more serious and can be life-threatening.

  • Stable angina produces predictable pain and responds to rest and/or medication. It is less serious than unstable angina but can be very painful or uncomfortable. Anything that makes the heart muscle need more oxygen can cause an angina attack in someone with heart disease, including: smoking, cold weather, exercise, emotional stress, obesity, and large meals. Other causes of angina include: abnormal heart rhythms (usually ones that cause the heart to beat quickly), anemia, coronary artery spasm, heart failure, heart valve disease, and hyperthyroidism (overactive thyroid).1
  • Unstable angina produces unpredictable pain that may occur at rest, lasting more than 20 minutes. It is more severe than stable angina and less responsive to medication. Atherosclerosis is by far the most common cause of unstable angina. Oxidized low-density lipoprotein, so-called bad cholesterol, and oxysterols play an important role in atherogenesis, the development of atherosclerosis. 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. People with unstable angina are at increased risk of having a heart attack.2

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

Sources:

  1. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001247/ [↩]
  2. http://www.heart.org/HEARTORG/Conditions/HeartAttack/SymptomsDiagnosisofHeartAttack/Unstable-Angina_UCM_437513_Article.jsp# [↩]

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. [↩]

Atherosclerosis

ahterosclerosis celiac disease complication symtpomWhat Is Atherosclerosis?

[dropcap]A[/dropcap]therosclerosis is a disease of arteries involving the buildup of fatty material called plaque along the walls of medium and large arteries characterized by patchy subintimal thickening, hardening, and loss of elasticity of blood vessels.

The intima is the innermost layer of an artery, having contact with blood. The subintima is beneath it.

Q: What happens when arteries become narrowed and less flexible?

A: Narrowing of the inside diameter of blood vessels and hardening of their walls reduce or obstruct blood flow through them which impairs their ability to supply tissues of the body with oxygen and nourishment.

When tissues are deprived of oxygen, pain and dysfunction results such as angina pectoris involving heart muscle because the heart continually needs oxygen never being able to rest.

It is thought that atherosclerosis develops from 1) epithelial cell dysfunction of the intima, and 2) lipid (fat) accumulation in smooth muscle cells and in foam cells, causing buildup of fatty deposits on the inside walls progressing to fibrous plaque formation. That is, intimal smooth muscle cells are surrounded by connective tissue and intracellular and extracellular lipids (fat build-up inside and outside of these cells).

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