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Food Allergy – IgE and Non IgE

Baby with Allergic Reaction to Peanuts. GFW
Baby with Allergic Reaction to Peanuts. GFW photo.

What Is Food Allergy?

[dropcap]F[/dropcap]ood allergy is an abnormal immune response to food proteins that may damage the small intestinal  lining and produce malabsorption of food. The reaction is usually delayed which makes it difficult to identify the offending food that is causing symptoms.

Q: How does food allergy develop?

A: The gastrointestinal tract serves not only to digest and absorb foodstuffs but also to protect the body from unwanted substances. When allergic food substances are eaten, the immune response that is triggered in the gut produces inflammation with symptoms such as pain, vomiting and loose bowels.

Inflammation causes swelling of the gut lining that can interfere with the passage of nutrients through it to the body which results in malabsorption. Malabsorption deprives the body of nutrients needed for normal function.

Symptoms other than digestive may involve skin rashes, hives, and respiratory difficulties that can be distressing and life-threatening.

What Is Food Allergy In Celiac Disease and/or Gluten Sensitivity?

Schizophrenia

Collagenous Colitis.
Microscopic Image Showing a Pink Collagen Band in Collagenous Colitis.

What Is Collagenous Colitis?

[dropcap]C ollagenous colitis is a disease of the large intestine (colon) that is characterized by microscopic inflammation of the surface mucosal lining and an abnormally thickened collagen band of tissue that develops wthin the lining of the colon.

The thicker than normal layer of collagen of at least 10 µm (reference value: 2–7 µm) can vary in different locations. Inflammation occurs with increased numbers of lymphocytes (white blood cells) and plasma cells and epithelial (surface cell) damage. These changes can only be seen under microscopic examination of multiple biopsied tissue samples taken during a colonoscopy procedure.

Q: What is collagen?

A: Collagen is a strong, fibrous protein found in connective tissue of the colon and many other tissues such as tendons. The normal basement membrane in the bowel consists mainly of collagen type IV, laminin, and fibronectin. The increased collagen band observed in collagenous colitis consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin to some irritant or drug.1

The biopsies should preferably be taken from the ascending colon, since the pathological hallmarks may be absent in the descending colon, and in the normally occurring thicker collagen layer in the rectosigmoid region.1 Inflammation of the ileum (last segment of the small intestine next to colon) is common.2

Endoscopy and radiological (x-ray) examinations are usually normal.3

Autoimmune disorders are frequently seen in adult patients with collagenous colitis.4 In the study below by Koskela et al. concomittent autoimmune diseases were present in 53% of patients with collagenous colitis.5

Importantly, the finding of collagenous colitis in patients with autoimmune diseases may reflect the treatment with NSAIDs (non-steroidal anti-inflammatory drugs), such as Ibuprofin and aspirin, PPIs (proton pump inhibitors), and other drugs. However, if secondary forms of collagenous colitis are not taken into consideration, underlying, treatable diseases may be overlooked, while only the gastrointestinal symptoms are treated symptomatically or with budesonide (a steroid).6

Treatment with budesonide steroid is efficacious irrespective of bile acid malabsorption.7

Budesonide at a mean dose of 4.5 mg/day maintained clinical remission for at least 1 year in the majority of patients with collagenous colitis and preserved health-related quality of life without safety concerns. Treatment extension with low-dose budesonide beyond 1 year may be beneficial given the high relapse rate after budesonide discontinuation.8

See below for nutritional deficiency problems caused by steroid usage and steps to be taken for correction.

What Is Collagenous Colitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩] [↩]
  2. Bjørnbak C, Engel PJ, Nielsen PL, Munck LK. Microscopic colitis: clinical findings, topography and persistence of histopathological subgroups. Aliment Pharmacol Ther. 2011 Nov;34(10):1225-34. doi: 10.1111/j.1365-2036.2011.04865.x. [↩]
  3. Abdo AA, Urbanski SJ, Beck PL. Lymphotcytic and collagenous colitis: the emerging entity of microscopic colitis. An update on pathophysiology, diagnosis and management. Canadian Journal of Gastroenterology. Jul 2003;17(7):425-32. [↩]
  4. Leung ST, Chandan VS, Murray JA, Wu TT. Collagenous gastritis: histopathologic features and association with other gastrointestinal diseases. Am J Surg Pathol. 2009 May;33(5):788-98. doi: 10.1097/PAS.0b013e318196a67f. [↩]
  5. Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. [↩]
  6. Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩]
  7. Bjørnbak C, Engel PJ, Nielsen PL, Munck LK. Microscopic colitis: clinical findings, topography and persistence of histopathological subgroups. Aliment Pharmacol Ther. 2011 Nov;34(10):1225-34. doi: 10.1111/j.1365-2036.2011.04865.x. [↩]
  8. Münch A, Bohr J, Miehlke S, et al. Low-dose budesonide for maintenance of clinical remission in collagenous colitis: a randomised, placebo-controlled, 12-month trial. Gut. 2014 Nov 25. pii: gutjnl-2014-308363. doi: 10.1136/gutjnl-2014-308363. [↩]

Scleroderma (Systemic Sclerosis)

Geographic Tongue Due to Riboflavin Deficiency.
Geographic Tongue Due to Riboflavin Deficiency.

 What Is Geographic Tongue?

[dropcap]G eographic tongue is a painful alteration in tongue tissue that is characteristic of riboflavin (vitamin B2) deficiency.1

Q: How does the tongue surface appear?

A: Areas of inflamed tissue with flattened papillae develop among areas of normal tissue, giving a map-like appearance to the tongue surface. There are often swollen papillae that hurt or sting, such as is seen in the photo to the left.

A diet that does not provide adequate amounts of riboflavin and any condition that 1) interferes with riboflavin absorption from the gut, 2) depletes the vitamin from the body, 3) overuses the vitamin in the body, or 4) adversely affects its use in the body will result in riboflavin deficiency causing geographic tongue.

Riboflavin is essential for converting foodstuffs into energy, maintaining the normal lifespan of red blood cells and maintaining healthy skin, eyes, hair, and nervous system. Riboflavin is converted into its active forms, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). These enzymes are primarily involved as co-factors in oxidation reduction reactions that are essential for cellular energy production and respiration.

Riboflavin is required for the conversion of pyridoxine (vitamin B6) to its functional form and the production of niacin (vitamin B3) from the amino acid tryptophan. Riboflavin has a role in antioxidant status by activating glutathione reductase, which regenerates used glutathione, a powerful antioxidant.

Respiratory infection, exercise, certain diseases, drugs and hormones can adversely influence riboflavin status.2 Stress is a major depleter of riboflavin.

What Is Geographic Tongue In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Krause’s Food, Nutrition, & Diet Therapy. 10th Edition. Kathleen Mahan, Sylvia Escott-Stump. 2000. W.B. Saunders Company. [↩]
  2. Lakshmi AV. Riboflavin metabolism–relevance to human nutrition. Indian J Med Res. 1998 Nov;108:182-90. [↩]

Prolonged Prothrombin Time

bloodvialWhat Is Prolonged Prothrombin Time?

[dropcap]P[/dropcap]rolonged prothrombin time (PT) is a laboratory blood test result showing that blood clots too slowly which makes the patient subject to abnormal bleeding.

Q: What does the prothrombin time (PT) test measure?

A: The prothrombin test measures the clotting ability of blood protein factors I, II (prothrombin), V, VII, and X. If any of these factors are too low, it takes longer than normal for the blood to clot. Prothrombin is a vitamin K dependent factor meaning a deficiency of vitamin K will cause low prothrombin.

Blood is drawn into a blood collection tube with a light blue stopper which has a buffering additive. Tubes must be completely filled.

What Is Prolonged Prothrombin Time In Celiac Disease and/or Gluten Sensitivity?

Prurigo Nodularis (Hyde’s Prurigo)

Canker Sore Inside Mouth. Notice The White Spot on This Person's Nail Showing Zinc Deficiency.
Inflammation/Sore Inside Mouth. Notice White Spot on Fingernail Nail Showing Zinc Deficiency.

What Are Chronic Oral Mucosal Lesions?

Chronic lesions of the oral mucosa are disorders of the mouth that are characterized by soreness and sores of the soft mucosal lining of the mouth.

What Are Chronic Oral Mucosal Lesions In Celiac Disease and/or Gluten Sensitivity?

Progressive Multifocal Leukoencephalopathy

jejunitis
Copyright © 2014 Sigman et al.; licensee BioMed Central Ltd.1

What Is Chronic Ulcerative Jejunitis?

[dropcap]C hronic ulcerative jejunitis is a disease of the small intestine that is characterized by inflammation and ulceration of the mucosal lining of the jejunum.

Q: How do inflammation and ulceration affect digestion in the jejunum?

A: Inflammation swells the lining and this impairs absorption of nutrients. Together with ulceration the inflamed and swollen jejunum hampers peristalsis, or the rhythmic movement of food by intestinal muscles.

Impaired peristalsis promotes constipation and/or diarrhea. Bacterial overgrowth may develop. Ulcerations may bleed which could cause the development of iron deficiency anemia.

What Is Chronic Ulcerative Jejunitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Sigman T, Nguyen VH, Costea F, Sant’Anna A, Seidman EG. Ulcerative jejunitis in a child with celiac disease. BMC Gastroenterol. 2014 Feb 13;14:29. doi: 10.1186/1471-230X-14-29. [↩]

Anti-Endomysium Antibodies (EMA) Present In Blood

Smooth muscle. Courtesy pathguy.com
Smooth Muscle. Courtesy pathguy.com

What Are Anti-Endomysium Antibodies?

[dropcap]A[/dropcap]nti-endomysium antibodies (EmA) are connective tissue autoantibodies produced in persons who have inherited the genes for celiac disease, an autoimmune disease, and are reacting to gluten in their diet.

Autoantibodies are abnormal in that they attack the body’s own tissue.

Q: What is endomysium?

A: Endomysium is the delicate connective tissue that surrounds individual muscle fibers. The autoantigen, or target, that stimulates the autoimmune response is the naturally occuring enzyme in endomysium called tissue transglutaminase (tTG), or more specifically tranglutaminase-2 (TG2). Anti-tissue transglutaminase antibodies recognize the same antigen as EmA, from which they differ in terms of detection method.

Anti-endomysium antibodies (EmA) are tested by the indirect immunofluorescence method and directed against “reticulin-like” fibres in connective tissue around smooth muscle fibres in the esophagus, liver, stomach, and bladder of monkeys, in the sections of the jejunum and kidneys of rats and in sections of the human umbilical cord. In comparison, for the determination of anti-tissue transglutaminase IgA and IgG antibodies, ELISA with human extractive or recombinant transglutaminase is recommended.1

EmA‐binding patterns in serum samples from patients with celiac disease have proved to be exclusively TG2‐targeted and the correlation between EmA and TG2 antibodies is therefore good. Evidence shows that celiac autoantibodies are produced in the small‐bowel mucosa.2

What Are Anti-Endomysium Antibodies In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Trigoni E, Tsirogianni A, Pipi E, Mantzaris G, Papasteriades C. Celiac disease in adult patients: specific autoantibodies in the diagnosis, monitoring, and screening. Autoimmune Dis. 2014;2014:623514. doi: 10.1155/2014/623514. [↩]
  2. Salmi TT, Collin P, Korponay-Szabó IR, Laurila K, Partanen J, Huhtala H, Király R, Lorand L, Reunala T, Mäki M, Kaukinen K. Endomysial antibody‐negative coeliac disease: clinical characteristics and intestinal autoantibody deposits.Gut. 2006 Dec;55(12):1746-53. [↩]

Progressive Myoclonic Ataxia 

biliary system primary biliary cirrhosisWhat Is Primary Biliary Cirrhosis?

[dropcap]P rimary biliary cirrhosis (PBC) is a biliary tract disease characterized by chronic cholestasis (build-up of bile) and gradual destruction of bile ducts within the liver, called intrahepatic bile ducts, caused by chronic inflammation.

Primary biliary cirrhosis comes under the umbrella term autoimune liver disease in which the end result is immune-mediated hepatocellular (liver cell) or hepatobiliary (bile duct) injury.1

Q: What is the end result of destruction of bile ducts?

A: The end result of destruction of bile ducts is liver damage.

Injured liver tissue from chronic inflammation and the buildup of bile leads to cirrhosis, a condition in which the liver slowly deteriorates and malfunctions.

Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. Scarring also impairs the liver’s normal ability to control infections, remove bacteria and toxins from the blood, process nutrients, hormones, and drugs, make proteins that regulate blood clotting, produce bile, and effectively replace its own cells when they become damaged.2

The liver is the largest organ within the body. It lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells (epithelial) form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts.

Bile ducts carry bile, a greenish brown liquid made by the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat and fat-soluble vitamins A, D, E, and K from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components which can then be absorbed into the body.

Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. Bile is continually made by the liver from phospholipids, bile acids, cholesterol, and aging blood cells it removes from circulation. As such, bile must continually flow out of the liver to prevent build-up in the liver.

There is no cure for primary biliary cirrhosis.

What Is Primary Biliary Cirrhosis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Trivedi PJ, Adams DH. Mucosal immunity in liver autoimmunity: a comprehensive review. J Autoimmun. 2013 Oct;46:97-111. doi: 10.1016/j.jaut.2013.06.013. [↩]
  2. http://digestive.niddk.nih.gov/ddiseases/pubs/primarybiliarycirrhosis/ [↩]

Anti-Gliadin Antibodies Present

This is a model of Immunoglobulin-G Antibody (IgG)
This is a model of Immunoglobulin-G Antibody (IgG)

What Are Anti-Gliadin Antibodies?

[dropcap]A[/dropcap]nti-gliadin antibodies (AGA) are produced by the body as an immune response against partially digested gliadin peptides (fragments) that have abnormally entered the body from the intestinal tract. Gliadin is a protein in wheat grain.

Anti-gliadin antibodies circulating in blood are measured by laboratory testing on blood that is drawn. The antibodies are both immunoglobulin A (IgA) and immunoglobulin G (IgG) types, which are termed AGA-IgA and AGA-IgG.

The presence of anti-gliadin antibodies in blood is an abnormal laboratory finding. That is, when the intestinal lining is healthy and able to keep out undigested matter from the body, there are no molecules of gliadin present to trigger the immune system for defense.

Q: Who produces anti-gliadin antibodies?

A: Persons, with or without celiac disease, can produce anti-gliadin antibodies if and when leaky gut (increased intestinal permeability) develops that then allow gliadin peptides to get into the bloodstream.

Gliadin itself causes leaky gut, but there are other causes such as various foods, intestinal infections, medications, and other diseases of the gastrointestinal tract. Whatever the cause of leaky gut, if poorly digested gliadin is present, it can slip through the leaky lining and enter the bloodstream where it can trigger an antibody response by anti-gliadin antibodies.

What Are Anti-Gliadin Antibodies In Celiac Disease and/or Gluten Sensitivity Or Non-Celiac Gluten Sensitivity?

Secondary Hyperparathyroidism

Hepatitis-C-Healthy-Liver-and-Inflammation-of-Liver

What Are Elevated Liver Enzymes?

[dropcap]H ypertransaminasemia is a chronic condition of elevated blood liver transaminase enzymes, commonly called “liver enzymes,” that signifies hepatocellular (liver) injury.

Q: What are serum transaminases?

A: Transaminases are the liver enzymes ALT and AST. ALT is the abbreviation for alanine aminotransferase enzyme and AST is the abbreviation for aspartate aminotransferase enzyme.

Transaminases are commonly measured in routine blood tests to determine liver function. Elevated ALT and AST transaminases  indicate inflammation of the liver. Other specific tests must follow to determine the cause of inflammation.

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