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Gluten Sensitive Enteropathy (Active Celiac Disease)

canstockphoto17997339What Is Gluten Sensitive Enteropathy?

Gluten sensitive enteropathy is active celiac disease characterized by inflammation of the small intestinal mucosa that results from an inherited immunologic intolerance to ingested gluten.

Q: What does the inflammation do to the mucosa in the small intestine?

A: Inflammation is a cell level immune response to gluten that has these effects on the mucosa:

  • Damages the barely visible villi (multitudinous finger-like structures) by causing atrophy or loss.
  • Likely affects the structural support and microcirculation of the villus, leading to collapse of the villus.
  • Elongates the crypts between villi. The thickening of the crypt is not so much a response to loss of surface enterocytes but represents inflammation of the mucosa.1
  • Increases round cells in the lamina propria and surface epithelial cells leaving few, irregular microvilli (brush border) on the surface of villi.
  • Damage is most intense in the duodenum and decreases toward the large intestine.
  • The extent of the damage to the intestine determines the malabsorptive consequences of the disease. Both gastric and small intestinal permeability are disrupted in patients with celiac disease.2
  • Relationship between active celiac disease and intestinal permeability: There is a clear association between degree of mucosal damage and the intestinal-permeability ratio, and a normal ratio generally implies near-normal small intestinal structure. A raised intestinal permeability of the mucosal lining (leaky gut) could predispose to a high absorption of gluten and exacerbate an existing lesion and hence convert a latent to an overt enteropathy.3
  • Relationship between active celiac disease and tight junction proteins: A study of intestinal permeability showed that the expression of all junction proteins of the small intestinal lining (occludin, claudin 3, zonula occludens 1, and E-cadherin) was already decreased in early stage celiac disease when compared with non-celiac controls, showing leaky gut and confirming the above earlier study by Johnston et al. Junction protein expression correlated positively with mucosal villus structure and negatively with the number of intraepithelial lymphocytes (IELs), the intensity of small-intestinal autoantibody deposits, and serum autoantibodies. The expression of claudin 3 showed a negative correlation with diarrheal score.4
  • Relationship between active celiac disease and inflammation. In celiac disease there is an over production of inflammatory interleukin-15 (IL-15) which inhibits the correct removal of damaged intraepithelial lymphocytes caused by the reaction to gluten. Serum levels of IL-15 are directly correlated with the seriousness of tissue damage.5

  • Relationship between active celiac disease and gut microbiota. Results of a study investigating intestinal microbiota (normal bacterial residents) in patients with celiac disease suggest that with lower levels of the genus bifidobacteria, celiac patients have an imbalance in the intestinal microbiota even while on a gluten-free diet. This fact could favor the pathological process of the disorder. The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (2.5 ± 1.5 x107 CFU/g) when compared to celiac patients (1.5 ± 0.63 x108 CFU/g).6

  • Relationship between active celiac disease and endoscopy technique. The most severe degree of villous atrophy was detected when distal duodenal biopsy specimens were taken in addition to a duodenal bulb biopsy specimen from either the 9- or 12-o’clock position (96.4% sensitivity; 95% CI, 79.7%-100%). The difference between the 12-o’clock position biopsy and the 3-o’clock position biopsy in detecting the most severe villous atrophy was 92% (24/26 patients) versus 65% (17/26 patients).7
  • Relationship between active celiac disease and diet adherence. Patients with consistent gluten free diet adherence experience symptomatic responses to dietary gluten (SRDG) faster and more severe in comparison to their prior gluten exposure possibly demonstrating an adept immunological response. Anxiety and depression also enhance the speed of symptom onset and co-existing visceral hypersensitivity is a risk factor for severe reactions to dietary gluten.8
  • Relationship between active celiac disease and atrial fibrillation: Patients with celiac disease, verified by intestinal biopsy, are at increased risk of atrial fibrillation. This observation is consistent with previous findings that elevation of inflammatory markers predicts atrial fibrillation.9

How Prevalent Is Gluten Sensitive Enteropathy?

Sources:
  1. Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
  2. Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
  3. Johnston SD, Smye M, Watson RGP. Intestinal permeability and morphometric recovery in coeliac disease. Lancet. Jul 28, 2001;358(9278):259, 2p. [↩]
  4. Rauhavirta T, Lindfors K, Koskinen O, Laurila K, Kurppa K, Saavalainen P, Mäki M, Collin P, Kaukinen K. Impaired epithelial integrity in the duodenal mucosa in early stages of celiac disease. Transl Res. 2014 Sep;164(3):223-31. doi: 10.1016/j.trsl.2014.02.006 [↩]
  5. Stazi AV, Trinti B. Selenium status and over-expression of interleukin-15 in celiac disease and autoimmune thyroid diseases. Ann Ist Super Sanita. 2010;46(4):389-99.DOI: 10.4415/ANN_10_04_06. [↩]
  6. Golfetto L, de Senna FD, Hermes J, Beserra BT, França Fda S, Martinello F. Lower bifidobacteria counts in adult patients with celiac disease on a gluten-free diet. Arq Gastroenterol. 2014 Apr-Jun;51(2):139-43. [↩]
  7. Kurien M, Evans KE, Hopper AD, Hale MF, Cross SS, Sanders DS. Duodenal bulb biopsies for diagnosing adult celiac disease: is there an optimal biopsy site? Gastrointest Endosc. 2012 Jun;75(6):1190-6. doi: 10.1016/j.gie.2012.02.025. [↩]
  8. Barratt SM, Leeds JS, Sanders DS. Factors influencing the type, timing and severity of symptomatic responses to dietary gluten in patients with biopsy-proven coeliac disease. J Gastrointestin Liver Dis. 2013 Dec;22(4):391-6. [↩]
  9. Emilsson L, Smith JG, West J, Melander O, Ludvigsson JF. Increased risk of atrial fibrillation in patients with coeliac disease: a nationwide cohort study. Eur Heart J. 2011 Oct;32(19):2430-7. doi: 10.1093/eurheartj/ehr167. [↩]

Gas

intest (2)What Is Obnoxious Gas?

Obnoxious gas, or flatus, is gas that is not only offensive when passed but also lingers in the air longer than ordinary gas does.

Gas is a natural digestive product within the colon that is composed mainly of hydrogen and carbon dioxide gases. These gases are given off in the necessary bacterial breakdown of undigested fermentable food entering the colon from the small intestine.

Q: What makes gas obnoxious?

A: The production of obnoxious gas depends on the type and quantity of undigested food residue that is passed into the colon from the small intestine, dysfunctional motility instead of normal peristalsis, and dysbiosis. Dysbiosis is the condition of  having unhealthy or insufficient populations of microbes responsible for digesting (fermenting) foodstuffs in the lower gut or colon. 

Gases produced by intestinal microbes may modulate intestinal motor function (muscle movement) in individuals with functional bowel disease. Methane, produced by enteric bacteria in the human gut, is associated with slowed intestinal transit and constipation.1

What Is Obnoxious Gas In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Jahng J, Jung IS, Choi EJ, Conklin JL, Park H. The effects of methane and hydrogen gases produced by enteric bacteria on ileal motility and colonic transit time. Neurogastroenterol Motil. 2012 Feb;24(2):185-90, e92. doi: 10.1111/j.1365-2982.2011.01819.x. Epub 2011 Nov 20.

    Methane is produced in the colon by intestinal methanogens (microbes) that metabolize hydrogen, one of the end products of normal anaerobic (meaning without oxygen) bacterial fermentation.  Fermentation of the undigested starchy part of carbohydrates produces hydrogen in the intestine, which is the food for methane production by intestinal methanogens.

    Hydrogen and methane are excreted in the flatus and in breath giving the opportunity to indirectly measure their production using breath testing. ((Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]

Dermatomyositis

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What Is Unexplained Weight Gain?

U nexplained weight gain is characterized by increased body mass due to excess fat accumulation that is not desired by the individual.

A body mass index (BMI) of 25 to 30 signifies being overweight.

What Is Unexplained Weight Gain In Celiac Disease and/or Gluten Sensitivity?

Low Plasma Proteins

Image of a protein molecule.
Image of a protein molecule.

What Are Low Plasma Proteins?

Low plasma proteins found in blood indicates an abnormal blood level.

Plasma proteins are any of the proteins that constitute about 6% to 7% of the blood plasma in the body. They include albumin, fibrinogen, prothrombin, and the gamma globulins. All plasma proteins except the gamma globulins are produced in the liver.1

Q: Which protein is most abundant in blood?

A: Of the dozens of plasma proteins, albumin makes up more than half. Albumin level is the most frequently tested in the presence of weight loss and other signs of poor nutrition. Albumin helps maintain water balance that affects osmotic pressure, increase blood viscosity, and helps maintain blood pressure.1

Other commonly tested blood proteins are globulins which make up about a third of plasma proteins. Lab reports show the ratio between albumin and globulin, as well as, their individual values. Fibrinogen, essential for clot formation, makes 7% of plasma proteins while regulatory proteins, which include enzymes and hormones, make up 1%.

What Are Low Plasma Proteins In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Mosby’s Medical Dictionary, 8th edition. © 2009, Elsevier. [↩] [↩]

Iron Deficiency

ferritinWhat Is Iron?

Iron 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. [↩]

Hypertension, Reversible

Grade_1_hypertension[1]What Is Reversible Hypertension?

Reversible hypertension is a pressure disorder of arteries associated with increased systemic (body wide) blood vessel resistance to blood flow due to endothelial (cell) dysfunction of arterial blood vessels that can improve with nutritional treatment.

Hypertension itself is defined as a systolic blood pressure (SBP) of 140 mm Hg (mercury) or greater and/or diastolic blood pressure (DBP) of 90 mm Hg or greater.

Q: What is blood vessel (vascular) resistance to blood flow?

A: Vascular resistance to blood flow means the arteries carrying blood away from the heart cannot relax or dilate when needed to lower blood pressure but stay constricted, which in turn, keeps the pressure high.

Here’s an analogy: if you replace your garden hose having a one inch inside diameter with one that has a smaller half inch diameter and open the water valve as usual, the result would be water shooting out with more force.

What Is Reversible Hypertension In Celiac Disease and/or Gluten Sensitivity?

Homocysteine, Elevated Blood Level (Hyperhomocysteinemia)

A 3-D model of homocysteine.
A 3-D model of homocysteine.

What Is Elevated Homocysteine?

Elevated homocysteine in blood, called hyperhomocysteinemia, indicates an abnormal blood level of this transient amino acid.

Q: How does the level of homocysteine become abnormal?

A: In metabolism, homocysteine is briefly formed in the breakdown of the amino acid methionine. It is normally converted to cystathione and then to the amino acid cysteine by means of an enzyme that requires vitamin B6.

In the reverse, conversion of homocysteine to methionine requires an enzyme dependent on adequate folic acid and vitamin B12 levels.

Insufficient methionine levels and/or inefficiency in this process results in elevated homocysteine plasma levels that are toxic to blood vessels.

Folic acid, vitamin B12 and vitamin B6 are involved in the metabolic removal of homocysteine, but folic acid deficit occurs the most often.1

What Is Elevated Homocysteine In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Lim PO, Tzemos N, Farquharson CA, et al. Reversible hypertension following coeliac disease treatment: the role of moderate hyperhomocysteinaemia and vascular endothelial dysfunction. Journal of Human Hypertension. Jun 2002;16(6):411-5. [↩]

FoxP3+ T cells: definition

FoxP3+ T cells represent a major subset of regulatory T cells. They can be produced as natural or induced cells. FoxP3+ T cells are made in the thymus gland as natural FoxP3+ T cells and… 

T Lymphocytes or T Cells

Comparison of normoblast and megaloblastWhat Is Macrocytosis?

M 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. [↩]