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Osteonecrosis

Each antibody binds to a specific antigen; an interaction similar to a lock and key. Courtesy Wikipedia.
Each antibody binds to a specific antigen; an interaction similar to a lock and key. Courtesy Wikipedia.

What Are Autoimmune Disorders?

A utoimmune disorders refer to those conditions that involve an abnormal immune attack on the body’s own tissues perpetuated by the production of autoantibodies directed against the body, or “self.” Auto means self.

Q: Why does the immune system attack the body?

A: The exact answer is not yet known why the immune system turns against body tissue or “self.” 

Normally, the immune system protects the body from harmful substances and pathogens and produces antibodies against the offending foreign substances, called antigens, to get rid of them. The immune system (humoral) thereafter remembers all antigens and is ready for the next encounter should it happen.

Production of autoimmune antibodies is catastrophic because there is no turning off the readiness to attack a remembered threat (antigen) which is unfortunately “self.” 

Yes, steroids and anti-inflammatory drugs can control symptoms, but nothing can undo the memory programmed into the immune system to produce autoantibodies. There is an enormous research effort ongoing for the answer. 

Autoimmune disorders cover a wide range of diseases that may target only a particular organ, such as autoimmune hepatitis (liver), while others are systemic because the autoantibodies target a particular tissue that is part of more than one organ, such as scleroderma (connective tissue).

Autoimmune diseases as a group affect approximately 8.5% of people worldwide.

What Are Autoimmune Disorders In Celiac Disease and/or Gluten Sensitivity?

Hypocalciuria (Low Urine Calcium)

IgA Molecule.
Depiction of the IgA Molecule

What Is IgA Deficiency?

I gA deficiency (IgAD) is an immunodeficiency disease characterized by lack of immunoglobulin A type antibody production, called IgA antibody, with no detectable levels in blood or secretions.

Q: What is an IgA antibody?

A: IgA is an antibody of the immune system that is secreted by plasma cells (specialized white blood cells) through epithelial cell linings of mucosal surfaces into mucosa secretions to protect the lining from microbe invasion.

In fact, immunoglobulin class A is the main protein of the mucosal immune system. This includes mucosa of the eye surface, digestive tract, respiratory tract, urinary tract, and genital tract.

Both major histocompatibility complex (MHC) and non-MHC genes contribute to susceptibility to the disease. The former genes appear to be located in different parts of the MHC region depending on the HLA haplotype. The latter show a marked overlap with genes associated with a variety of autoimmune disorders including Graves’ disease, systemic lupus erythematosus, type 1 diabetes and celiac disease, suggesting common pathophysiological mechanisms. The involvement of genes associated with autoimmunity may suggest that IgAD in itself is an autoimmune disease.1

IgA deficiency may progress into a common variable immunodeficiency (CVID).2

What Is IgA Deficiency (IgAD) In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Wang N, Hammarström L. IgA deficiency: what is new? Curr Opin Allergy Clin Immunol. 2012 Dec;12(6):602-8. doi: 10.1097/ACI.0b013e3283594219. [↩]
  2. Binek A, Jarosz-Chobot P.Selective immunoglobulin A deficiency. Pediatr Endocrinol Diabetes Metab. 2012;18(2):76-8. [↩]

PMS (Premenstrual Syndrome) 

DSCN4758aWhat Are Brittle Nails?

B rittle nails are abnormalities of the nail plate that are characterized by poor nail structure affecting all fingernails and toenails seen as thin, dry nails that easily chip, split, and are difficult to maintain a clean edge. Usually longitudinal ridging occurs from the nail base to the tips.

Q: What is the nail plate?

A: The nail plate is the hard keratin cover protecting the finger tip and toe tip. The nail plate (non-living tissue) is produced by the nail matrix (living tissue) at the base of the nail plate under the lunula (moon), which is the site of brittle nail development.

Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org
Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org

Poor nail structure affecting all nails may be a feature of nutritional deficiency in poor diet or malabsorption such as occurs in celiac disease.

Some other causes are: idiopathic (unknown cause), the result of aging, the effects of certain drugs, or an association with systemic autoimmune disorders such as vitiligo, alopecia areata (with pitting), psoriasis (with pitting), and lichen planus. 

External (non-nutritional or disease) causes of dry, brittle nails, such as detergents and cleaners, would only affect fingernails but not toenails.

Note: It has been shown that working with your hands in water or soaking them through activities like swimming does not cause dry, brittle nails but will worsen them.

What Are Brittle Nails In Celiac Disease and/or Gluten Sensitivity?

Impotence

This White Spot Is A Feature of Zinc Deficiency.
This White Spot Is A Feature of Zinc Deficiency.

What Are White Spots And White Bands In Nails?

W hite spots in the nails is a feature of zinc deficiency and white bands signify protein deficiency characterized by abnormal appearance anywhere in one or more nails.

White spots and bands can appear separately or together in nails. There may be just one mark or many marks depending on the level of deficiency.

Q: What part of the nail is affected by zinc and/or protein deficiency?

A: Zinc and protein deficiencies affect the nail plate.

The nail plate is the hard keratin cover of the finger tip and toe tip, simply called “the nail.” The nail plate is produced by the living nail tissue at its base. Here is an illustration of the parts that make up a fingernail:

Nail Anatomy. Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org.

A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.

What Are White Spots And White Bands In Nails In Celiac Disease and/or Gluten Sensitivity?

Irritability

Small Bowel Volvulus, Courtesy African Journal of Pediatric Surgery.
Small Bowel Volvulus Caused the  Enlarged Dark Loops. Courtesy African Journal of Pediatric Surgery.

What Is Volvulus?

V olvulus is twisting of a loop(s) of bowel onto itself which effectively closes it thus preventing digested matter from passing and causing engorgement of the closed loop with gas and fluid.

Q: How does the bowel get untwisted?

A: This condition usually necessitates surgical correction although some do return to their proper position.

The danger is that there may develop necrosis of the twisted loop(s) in which case, if left untreated, death will ensue.

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

Hypoparathyroidism, Idiopathic

hypocalcemia celiac disease gluten symptomWhat Is Hypocalcemia?

H ypocalcemia, or low plasma calcium, means the level of calcium in blood is too low to meet metabolic needs of the body for calcium.

Low blood calcium is characterized by bone and tooth demineralization (loss of calcium causing weak teeth and fragile bones), and these impaired functions: nerve conduction, muscle contraction, blood clotting, blood pressure regulation, glycogen to glucose conversion, many hormone actions, many enzyme activities, and acetylcholine production.

Q: Where is calcium found in the body?

A: Calcium is the most abundant mineral in the body, with 99% residing in bones and teeth where it constitutes 40% of skeletal bone weight along with 45% phosphorus. As a component of bone (hard tissue), calcium fulfills a structural role to maintain body size and act as attachments for musculoskeletal tissues. The remaining 1% of calcium is present in blood and soft tissues.

Calcium levels in the blood are maintained within very strict limits by dietary intake, hormonal regulation by the parathyroid gland and a rapidly exchangeable pool in bone tissue.

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

Epilepsy (Convulsions)

chronic diarrhea gluten celiac disease symptomWhat Is Chronic Diarrhea?

C hronic diarrhea is an intestinal motility disorder characterized by 1) alteration in stool formation causing loose to fluid movements and quantity of movements with or without abdominal pain and 2) interference with normal carbohydrate salvage by the intestinal microbe population.

The severity of diarrhea is determined by the frequency and quantity of fluid lost.

Q: What is carbohydrate salvage by microbes in the colon?

A: Carbohydrate salvage in the colon is the necessary process whereby billions of microbes normally present in the colon work to breakdown undigestible carbohydrate foodstuffs such as fiber that continually arrive from the small intestine.

The microbial action releases energy to the body that would otherwise be lost with defecation, generates short-chain fatty acids, and stimulates sodium and fluid absorption. In this important process, butyrate and proprionate are produced which nourish the colonocytes (cells that line the colon), and acetate is produced for the liver.

While diarrhea may be a common symptom of small bowel mucosal disease, the consequent malabsorption can lead to substantial malnutrition and nutrient deficiencies. The small intestine, unlike the colon, has been relatively inaccessible, and systematic evaluation is often necessary to identify and treat small intestinal mucosal diseases that lead to diarrhea. All patients with severe diarrhea or diarrhea associated with features suggestive of malabsorption may have a disease of the small intestinal mucosa that requires careful evaluation and targeted management.1

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

Sources:
  1. Murray JA1, Rubio-Tapia A. Diarrhoea due to small bowel diseases. Best Pract Res Clin Gastroenterol. 2012 Oct;26(5):581-600. doi: 10.1016/j.bpg.2012.11.013. [↩]