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Secondary Amenorrhea

Hives. Courtesy wikimedia.
Hives. Courtesy wikimedia.

What Is Chronic Urticaria?

U rticaria is an immune based skin disorder characterized by multiple eruptions of well-demarcated edematous, intensely pruritic (itchy) plaques that may be small or reach the diameter of many centimeters with surrounding erythema (redness) each lasting less than 24 hours.1

Q: What is the immune reaction in hives?

A: Hives form when, in response to histamine, blood plasma leaks out of small blood vessels in the skin. Histamine is a chemical released from specialized cells along the skin’s blood vessels. Allergic reactions, chemicals in certain foods, insect stings, sunlight exposure, or medications can all cause histamine release.2

In many patients, in spite of extensive investigations, the cause remains elusive. The term idiopathic is often used to denote this category. Now it is known that autoimmunity is the cause of chronic urticaria in 50% of cases.

Treatment is generally started with nonsedating antihistamine in the daytime and sedating antihistamine in the night.3

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

Sources:
  1. Scala E, Giani M, Pirrotta L, Guerra EC, DePita O, Puddu P. Urticaria and adult celiac disease. Allergy. 1999;54:1008-9. [↩]
  2. www.webmd.com [↩]
  3. Godse KV. Chronic urticaria and treatment options. Indian J Dermatol. 2009 Oct-Dec; 54(4): 310–312. [↩]

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. [↩]

Dental Enamel Defects (Defective Tooth Enamel)

Enamel_celiac[1]What Are Dental Enamel Defects?

Dental enamel defects (DED) comprise a variety of abnormalities in the dental enamel of the second or permanent teeth and of primary or baby teeth.

Teeth may appear with pits, thin or missing enamel, non-white enamel (yellow, orange, or gray colored teeth), and demarcated opacities (very white spots) even if teeth are white.

Q: What is enamel?

A: Dental enamel is the shiny, hard, white, dense, inorganic substance covering the crowns of the teeth. The crown is the tooth portion above the gum. Under the enamel is hard dentin which surround the living pulp. In teeth with missing enamel, the areas with exposed dentin appear dull and tan colored.

What Are Dental Enamel Defects In Celiac Disease and/or Gluten Sensitivity?

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. [↩]

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. [↩] [↩]

Vitamin B3 (Niacin) Deficiency

SumptuousTuna For Niacin.
Sumptuous Tuna For Niacin.

What Is Vitamin B3 (Niacin)?

Niacin is an essential water-soluble B vitamin that is required by all cells of the body.

During digestion of food containing it, niacin (the form in food) is changed in the small intestines to the active form niacinamide (niacin plus an amide group), which is then absorbed into the bloodstream. 

Niacinamide is converted by the body into co-enzymes which are present in all cells. These are niacinimide adenine dinucleotide (NAD) and NADP. NADP is formed when the body adds a phosphate to NAD.

Q: How do these enzymes work?

A: These enzymes function in oxidation-reduction reactions essential for release of energy from carbohydrates, fats, and proteins and are needed as components for more than 200 enzymes involved in metabolism.

In addition to producing energy, niacinamide is essential for healthy skin and the mucosal lining of the digestive tract, normal functioning of the brain and nervous system, and production of steroid hormones in adrenal glands and hormones in sex glands.  Functions are more fully described below.

Urinary excretion of niacin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, the vitamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.1

What Is Niacin 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. eCollection 2014. [↩]

Copper Deficiency

mmm...copper is in chocolate!
mmm…copper is in chocolate and nuts!

What Is Copper Deficiency?

Copper is an essential trace element that is required for a number of enzymes which are necessary for normal metabolic function.

In the body almost all the copper is present as a component of copper proteins which are produced and controlled by the liver.

Q: How does the liver control copper?

A: The liver maintains proper copper balance by binding free copper to proteins and by excreting excess copper as part of bile that is then emptied into the intestinal tract and excreted in stool.

Metabolic balance studies have demonstrated that daily copper losses are approximately 1.3 mg/day.1

Among its specific functions listed below, copper is essential for energy production, blood and nerve functions, blood components, immunity, and collagen tissue. The copper enzyme, lysyl oxidase, is involved in the cross-linking of collagen in forming the framework for depositing calcium and other minerals to build and repair bone.

Animal studies suggest that adequate copper levels during pregnancy are critical to development of higher brain function in the offspring.2

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

Sources:
  1. Williams DM. Copper deficiency in humans. Semin Hematol. 1983 Apr; 20(2):118-28. [↩]
  2. Fisgin T, Yarali N, Duru F, Usta B, Kara A. Hematologic manifestation of childhood celiac disease. Acta Haematol. 2004;111(4):211-4. [↩]

Chromium Deficiency

Broccoli is a Good Source of Natural Chromium.
Broccoli is a Good Source of Natural Chromium.

What Is Chromium?

Chromium is a mineral that the body absolutely requires in trace amounts for normal metabolism, meaning the physical and chemical processes by which energy is produced and used.

Chromium is especially involved in the use of glucose sugar and lipids such as cholesterol and the effectiveness of insulin hormone.

Q: How is chromium involved in the use of glucose?

A: Very small amounts of chromium are required to enable insulin to move glucose from the bloodstream into cells for use as energy.

Insulin is a hormone that controls the use and storage of glucose in two ways: 1) lowers a rise of glucose in blood after meals by moving it out of the bloodstream into body cells, especially muscle cells and 2) limits the release of glucose from the liver between meals. Insulin is produced by beta cells on the surface of the pancreas.

To date, the molecular mechanism by which chromium affects glucose and lipid metabolism is still unclear.1

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

Sources:
  1. Lewicki S, Zdanowski R, Krzyżowska M, Lewicka A, Dębski B, Niemcewicz M, Goniewicz M. The role of Chromium III in the organism and its possible use in diabetes and obesity treatment. Ann Agric Environ Med. 2014 Jun 10;21(2):331-335. [↩]

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. [↩]

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 [↩]