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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. [↩]

Muscle Weakness 

Muscle fiber anatomy. Courtesy NIH.
Muscle Fiber Anatomy. Courtesy NIH.

What Is Muscle Weakness?

[dropcap]M[/dropcap]uscle weakness is the impaired status of muscle function characterized by decreased or low muscle strength and inability to perform normal work such as lifting a pot off the stove.

Q: How do muscles work?

A: Muscles do their work by contracting or shortening. For example, to move the foot up and down at the ankle, muscles attached to the foot by tendons must contract to shorten or relax to return to their resting length. Calf muscles contract to point the foot down (flexion) while the shin muscles relax (extension).  For the foot to point up, calf muscles relax while the opposing shin muscles contract.

Each muscle is made up of individual muscle fibers. A muscle fiber is a long cylindrical cell that contains many nuclei, mitochondria, and sarcomeres. Each muscle fiber is surrounded by a thin layer of connective tissue called the endomysium.

Approximately 20–80 of these muscle fibers are grouped together in a parallel arrangement called a muscle fascicle or fiber bundle that is encapsulated by a perimysium. A distinct muscle is formed by enveloping a large number of muscle fascicles in a thick collagenous external sheath extending from the tendons called the epimysium.1

Muscles fall into three types:

  • Voluntary muscles.  These muscles, also called skeletal, we can control by will. Voluntary muscles function by contracting their fibers to draw one part of the body toward another in flexion while opposing muscles that extend or pull a body part away from another. They move our bones to perform activities such as walking to get somewhere, chewing to eat food, lifting to do work, and moving the eyeball to look at something.
  • Involuntary muscles. These muscles work independently of our conscious control. They are needed for internal organs, sphincters, and other parts to do their work, such as peristalsis in the gut that must function at all times to digest and move food, the squirting of bile juice into the duodenum by the Sphincter of Odi in the presence of fat eaten, and action of the pupil to see.
  • Cardiac muscles. These muscles are specialized to keep the heart functioning at all times.

  Muscle weakness can involve all types of muscles.

What Is Muscle Weakness In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://www.ncbi.nlm.nih.gov/books/NBK57140/ [↩]

Short Duration of Breast Feeding 

canstockphoto5875896What Is Short Duration Of Breast Feeding?

[dropcap]S[/dropcap]hort duration of breast feeding, or lactation, is characterized by inadequate milk production by a mother who has just given birth.

Normally, lactation begins with the production and release of colostrum from the mammary glands during the first few days after birth until the milk comes in. Colostrum is a yellow colored, nutrient rich fluid, high in calories and containing immunoglobulins to protect the baby from infection.

Lactation depends on adequate secretion of prolactin hormone by the pituitary gland which begins after the rapid decrease of estrogen and progesterone from the ovaries that occurs with childbirth. Prolactin secretion is afterward stimulated by sucking of the infant and continues as long as the infant nurses.

Milk production to meet the needs of the infant depends on adequate nutrition on the part of the mother.

What Is Short Duration Of Breast Feeding In Celiac Disease and/or Gluten Sensitivity?