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Vitamin B1 (Thiamin) Deficiency

thiamin deficiency What Is Thiamin?

Thiamin, also called vitamin B1, is an essential vitamin that is required to convert foodstuffs into energy and for the health and proper functioning of the nervous, muscular and cardiovascular systems.

In the bloodstream, 90% of active thiamin (TPP) is carried by red blood cells while 10% is transported in the bloodstream as free thiamin and thiamin monophosphate bound mostly to the protein albumin.

In the diet, animal food sources provide active thiamin while plant food sources provide free thiamin.1

Urinary excretion of thiamin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, thiamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.2

In patients who have thiamin deficiency, the most common conditions that bring them to a clinician include neuropathies, depression, myalgia, cardiomyopathies or takes diuretics and/or eat a high carbohydrate diet.3

What Is Thiamin Deficiency 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. Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. [↩]
  3. Spectracell Labs, Inc. [↩]

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. [↩]

Phosphorus Deficiency

burger_21119511What Is Phosphorus?

Phosphorus is an essential mineral present in every cell of the body mostly in the form of phosphate.

About 85% of phosphorus is present in bone making up a major component of bone formation. As a component of calcium phosphate, phosphorus constitutes 45% of skeletal bone weight while calcium constitutes 40% to support the body.1.

Phosphorus is required for normal tooth development. Inadequate phosphorus in early childhood development makes for defective tooth enamel in permanent teeth.

Phosphorus is crucial for the production of ATP (adenosine triphosphate), a molecule within cells that the body uses to store energy, and is required for production of phosphocreatine to power muscles.  Functions are more fully described below.

One gram of protein in food provides approximately 15 mg of phosphorus. In an adult, the body content of phosphorus ia about 700 grams.

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

Sources:
  1. http://www.nlm.nih.gov/medlineplus/ency/article/002424.htm [↩]

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Vitamin B12 Deficiency

Clams Are Chock Full of Vitamin B12.
Lovely Clams For Vitamin B12.

What Is Vitamin B12?

Vitamin B12, also called cobalamin, is a highly complex vitamin that functions in two coenzyme forms: adenosylcobalamin and methylcobalamin.

These forms of the vitamin play important roles in the physical and chemical processes by which amino acids become proprionate, proprionate that becomes acetate,  and single carbons.

Q: Why are these steps important?

A: These steps are essential for normal function in the workings of all cells, especially for those of the digestive tract, bone marrow and nervous tissue.

Vitamin B12 is mainly excreted through bile into the duodenum (first part of the small intestine) for excretion in stool.1 However, if vitamin B12 is needed, it is reabsorbed in the ileum (end of the small intestine) while excess is excreted in stool and very little in urine.2

The blood level of vitamin B12 in healthy people ranges between 140 and 750 pg/ml.

What Is Vitamin B12 Deficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. [↩]
  2. Shinton N K. Vitamin B 12 and folate metabolism. Br Med J. Feb 26, 1972; 1(5799): 556–559. [↩]

Sarcoidosis

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Lymphoma, Enteropathy-Associated T-Cell (EATL) 

A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.
A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.

What Is Cancer Of The Esophagus?

C ancer of the esophagus is a malignancy arising in the stratified squamous cell lining of any part of the esophagus and having a poor prognosis.

This tumor first invades the deeper layers of the esophagus which includes the layer beneath the mucosa (submucosa) and muscle before it may invade structures close to it including the aorta and trachea. Later, it may spread to organs further away such as the liver, lungs and bones.

Q: What is the stratified squamous cell lining of the esophagus?

A: Stratified squamous cells are flat epithelial cells that are composed of several layers, called the epithelium. This type of epithelium forms the surface mucosa that lines the inside of the esophagus.

The esophagus itself is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx in the throat and ends at the lower esophageal sphincter (LES).

The LES is a circular muscle surrounding the junction of the esophagus and stomach. The LES opens to allow swallowed food and liquids to enter the stomach and closes to prevent their travelling back into the esophagus.

Who is Affected in the General Population?

Esophageal cancer is the fifth leading cause of death in men from cancer worldwide.1

What Is Cancer Of The Esophagus In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Feldman M, Friedman LS, Brandt LJ. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease. ed 9. Philadelphia: Saunders; 2010. pp. 745–767. [↩]

Adenocarcinoma Of Small Intestine (Cancer)

Section of small bowel surgically removed for adenocarcinoma that grew through the wall. By: CDC/ Dr. Edwin P. Ewing, Jr.
Section of small bowel surgically removed for adenocarcinoma that grew through the wall. By: CDC/ Dr. Edwin P. Ewing, Jr.

What Is Adenocarcinoma Of Small Intestine?

Adenocarcinomas are malignant tumors, or cancer, of the small bowel arising out of glandular tissue. They fall in the category of rare neoplasm, comprising only 3% of all gastrointestinal malignancies.

Primary adenocarcinoma is the most common histological (cell) subtype constituting 35–50% of cases.1 

Q: What does adenocarcinoma look like?

A: Adenocarcinoma may manifest as strictures, nodules, excavating masses, or annular lesions.2

What Is Adenocarcinoma Of Small Intestine In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Benhammane H, El M’rabet FZ, Serhouchni KI, El yousfi M, Charif I, Toughray I, et al. Small Bowel Adenocarcinoma Complicating Coeliac Disease: A Report of Three Cases and the Literature Review. Case Rep Oncol Med. 2012; 2012: 935183. Published online 2012 December 1. doi: 10.1155/2012/935183 [↩]
  2. Ramachandran I, Sinha R, Rajesh A, Verma R. Multidetector row CT of small bowel tumors.  Clinical Radiology. 2007; 62:607-614. [↩]

Tuberculosis – Non-Response to Treatment 

Underarm showing skin darkening, which is a feature of Addison's Disease
Underarm showing skin darkening, which is a feature of Addison’s Disease

What Is Primary Addison’s Disease?

A ddison’s disease is an autoimmune destruction of the adrenal glands by autoantibodies that target the adrenal cortex, or outer part of these glands, and is characterized by a slow progressive failure of the adrenal glands to adequately produce its steroid hormones.

Symptoms of adrenal fatigue or failure may not develop until the majority of adrenal tissue is destroyed. When untreated, progression leads to coma, called Addisonian crisis, which is a medical emergency.

There are two adrenal glands each located on top of a kidney and enclosed in a connective tissue capsule. Each is a small, triangular shape that is made of two parts: the outer region and the inner region.

The inner region, called the adrenal medulla, produces epinephrine and norepinephrine chemicals that are needed to deal with stress.

The outer region, called the adrenal cortex, produces adrenocortical (steroid) hormones and releases them into the bloodstream in response to pituitary stimulating hormone from the brain.

Q: What is the function of steroid hormones produced by the adrenal glands?

A: Functions of the three steroid hormones produced by the adrenal glands are:

  1. Glucocorticoids restrain inflammation and metabolism of carbohydrates, fats and proteins to maintain a normal glucose blood level. The major glucocorticoid is hydrocortisone.
  2. Mineralocorticoids regulate the retention and excretion of fluids and electrolytes by the kidneys. The most important mineralocorticoid is aldosterone.
  3. Androgen (testosterone) is a male sex hormone.

Secondary adrenal insufficiency may develop from other causes that are not immune related such as chronic infections, tumor, and medications.

What Is Addison’s Disease In Celiac Disease and/or Gluten Sensitivity?