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Obstetrical Complications
What Is Eczema?
E czema, or atopic dermatitis, is a chronic recurring inflammatory skin disorder characterized by itching, eczematous plaques and a defective epidermal barrier (surface layer of skin cells) that fails to hold moisture, with affected areas becoming dry then inflamed.
Q: Why does eczema develop?
A: Patients with atopic dermatitis have genetically determined risk factors that affect the barrier function of the skin and immune responses that interact with environmental factors.1
Atopic eczema is associated both with an abnormal skin matrix and impaired systemic immune response. Therefore, isolated topical treatment may have suboptimal effect.2
Atopic eczema is a common presentation of immune response towards food proteins in infancy.3
Global evidences reflect a marked increase in prevalence, which has tripled since 1960. In the United States, the current prevalence rates range from 10% to 20% in children and 1 to 3% in adults.4
What Is Eczema In Celiac Disease and/or Gluten Sensitivity?
Sources:- Mesquita Kde C, Igreja AC, Costa IM. Atopic dermatitis and vitamin D: facts and controversies. An Bras Dermatol. 2013 Nov-Dec;88(6):945-53. doi: 10.1590/abd1806-4841.20132660. [↩]
- Caffarelli C, Santamaria F, Vottero A, Bernasconi S. Progress in Pediatrics in 2012: choices in allergy, endocrinology, gastroenterology, hematology, infectious diseases, neurology, nutrition and respiratory tract illnesses. Ital J Pediatr. 2013 May 8;39(1):26. [↩]
- Ho MH, Wong WH, Chang C. Clinical Spectrum of Food Allergies: a Comprehensive Review. Clin Rev Allergy Immunol. 2012 Nov 16. [↩]
- Mesquita Kde C, Igreja AC, Costa IM. Atopic dermatitis and vitamin D: facts and controversies. An Bras Dermatol. 2013 Nov-Dec;88(6):945-53. doi: 10.1590/abd1806-4841.20132660. [↩]
Muscle Spasm And Muscle Cramps
What Is A Gastric Ulcer?
G astric ulcer is a painful stomach disorder characterized by an open sore involving the mucosa lining and deeper muscle layer of the stomach.
Gastric ulcer is associated with lymphocytic gastritis which is inflammation of the mucosal lining of the stomach. The thick mucosal lining normally protects the stomach from the erosive action of stomach acid.
Q: How do ulcers develop?
A: Ulcers develop if hydrochloric acid secreted by the gastric glands of the stomach for the purpose of digesting food damages the normally resistant mucosal walls of the stomach. In the reverse, ulcers may be accompanied by achlorhydria (insufficient acid production).
Damage occurs when there is a predisposing factor that alters the health of the mucosal lining. The most common cause is infection with a bacteria called h. pylori bacter, stress and chronic use of the pain relievers aspirin and non-steroidal drugs like ibuprofen.
Smoking tocacco and consuming alcohol aggravate an ulcer but do not cause it to develop.
The most common location for ulcer formation is along the stomach antrum which is the area of the stomach before the pylorus, the lower region that empties liquid stomach contents into the small intestine.
What Is A Gastric Ulcer In Celiac Disease and/or Gluten Sensitivity?
Chronic Fatigue / Lassitude / Tiredness
What Are Erosions In The Second Part Of The Duodenum?
E rosions in the second part of the duodenum typically are superficial excoriations (sores) in the mucosal lining that do not penetrate into the muscle layer as does an ulcer.
Of note, most erosions develop in the first part of the duodenum rather than the second part.
Q: Are duodenal erosions serious?
A: Yes duodenal erosions are serious and can be life-threatening for the following reasons:
- Duodenal erosions may occur together with gastric erosions, therefore they can jointly induce massive bleeding.
- Duodenal erosions may be associated with duodenal ulcer but hemorrhage originates from the erosion and the ulcer itself does not bleed.
- Duodenal erosion in itself might induce bleeding. The intensity of bleeding, if there is no hemorrhage from other places, is not so severe, as the one originating from gastric erosions.1
What Are Erosions In The Second Part Of The Duodenum In Celiac Disease and/or Gluten Sensitivity?
Sources:- Preisich P, Farkas I, Konyár EJ. The role of duodenal erosions in the occurrence of upper gastrointestinal haemorrhage. Scand J Gastroenterol Suppl. 1989;167:36-8. [↩]
Nails, Dry And Brittle (Chip, Peel, Crack, Break Easily)
What Is Atherosclerosis?
A therosclerosis is a disease of arteries involving the buildup of fatty material called plaque along the walls of medium and large arteries characterized by patchy subintimal thickening, hardening, and loss of elasticity of blood vessels.
The intima is the innermost layer of an artery, having contact with blood. The subintima is beneath it.
Q: What happens when arteries become narrowed and less flexible?
A: Narrowing of the inside diameter of blood vessels and hardening of their walls reduce or obstruct blood flow through them which impairs their ability to supply tissues of the body with oxygen and nourishment.
When tissues are deprived of oxygen, pain and dysfunction results such as angina pectoris involving heart muscle because the heart continually needs oxygen never being able to rest.
It is thought that atherosclerosis develops from 1) epithelial cell dysfunction of the intima, and 2) lipid (fat) accumulation in smooth muscle cells and in foam cells, causing buildup of fatty deposits on the inside walls progressing to fibrous plaque formation. That is, intimal smooth muscle cells are surrounded by connective tissue and intracellular and extracellular lipids (fat build-up inside and outside of these cells).
What Is Atherosclerosis In Celiac Disease and/or Gluten Sensitivity?
Dermatitis Herpetiformis or Duhring’s Disease
What Is Obesity?
O besity is an inflammatory metabolic disorder that is characterized by body mass index greater than 30% resulting from excessive body fat stored in adipose tissue.
Q: What is body fat?
A: Body fat is part of the body that functions as a reserve of stored energy. It is composed of fat cells, called adipocytes, having thin membranes between these cells. Adipocytes expand to store fat and shrink as fat is released as needed into the bloodstream for other body cells to use for metabolizing energy.
Each adipocyte contains a drop of triglyceride which is a type of lipid (fat). Triglycerides are a normal component in the bloodstream and, as such, are transported wherever needed as a form of energy. Excess triglycerides are the form of fat that is stored.
Initially, fat that is eaten in the diet is changed by digestive enzymes into the triglyceride form which is a molecule composed of three fatty acids and glycerol. Triglycerides are then absorbed through the small intestinal wall to be delivered to the liver. Of note, the liver can make triglycerides from excess protein and carbohydrates eaten in a meal, especially sugar and alcohol. The liver on the other hand makes cholesterol from triglycerides.
Triglyceride levels in the blood generally increase as weight increases. It is thought that an elevated blood triglyceride level hampers the body’s ability to feel full or satisfied with food that is eaten. Elevated triglyceride levels also increase the risk of clot formation because they cause the blood to become thicker. A normal triglyceride blood level is 150 mg/dL.
The causes of obesity are complex and varied. Those related to gluten sensitivity are discussed below.
What Is Obesity In Celiac Disease and/or Gluten Sensitivity?
Muscle Wasting
What Are Multiple Gastric Ulcerations?
M ultiple gastric ulcerations denote a stomach disorder that involves damage to the superficial mucosa characterized by many sores of the stomach antrum that are marked by inflammation, necrosis (death of the affected cells) and sloughing of destroyed tissue.
Q: Where is the stomach antrum?
A: The antrum is the lower region of the stomach before the pylorus which is nearest the duodenum (first part of the small intestine). The stomach and duodenum are separated by the powerful pyloric sphincter.
The stomach antrum propels food in the stomach against the pylorus which resists passage of food until it is turned into chyme. Chyme is highly acidic liquified food that has been thoroughly mixed with stomach juices.
Gastric ulcerations are typically associated with widespread gastritis (inflammation), inflammatory involvement of acid producing cells, and atrophy of acid and pepsin producing cells.1
The primary causes of gastric ulcerations are H. pylori infection, use of Aspirin and non-steroidal drugs (NSAIDS), and stress.1
What Are Multiple Gastric Ulcerations In Celiac Disease and/or Gluten Sensitivity?
Sources:Anemia, Iron Deficiency
What Is Iron Deficiency Anemia?
Iron deficiency anemia is a blood cell disorder that is characterized by formation of small, pale red blood cells, causing tissue hypoxia. Hypoxia is the inability to meet the demands of the body for oxygen.
Q: Why do small, pale red blood cells cause tissue hypoxia?
A: Small, pale red blood cells (erythrocytes) cause tissue hypoxia because they are not able, as do normal erythrocytes, to pick up adequate oxygen from the lungs and carry it to cells that use oxygen.
Red blood cell production and function are dependent on a sufficient level of iron in the body and also the ability to use available iron to make hemoglobin in red blood cells.
Hemoglobin is a protein that binds oxygen in red blood cells to be carried by the bloodstream to cells throughout the body. In iron deficiency anemia, hemoglobin in females is below 12.5g/dl (normal range is 12.5 to 16g/dl) and in males it is below 13.5g/dl (normal range is 13.5 to 17.5g/dl).
Iron must be obtained from the diet, since the body cannot make it, but there are various factors that can interfere with absorption and use in the body, causing anemia. Iron absorption from the gut first requires ionization, or gaining a positive electrical charge, in the strongly acidic environment of stomach juice. Ionized iron, only, can be absorbed in the duodenum, which receives the acidic contents of the stomach before it is neutralized further along.
Dietary iron can be heme or non-heme depending on the food source. Heme iron obtained only from animal food sources is absorbed into the bloodstream by active transport across the brush border (microvilli) which cover the multitudinous villi of the small intestinal lining.
Non-heme iron obtained from plants must bind with apoprotein after entering the enterocyte (surface cell of small intestinal lining) to be ferried to the underlying basolateral membrane and exited by active transport into the bloodstream.
Frequently, chronic anemia due to iron deficiency is accompanied by increased platelets, and this thrombocytosis resolves with iron repletion (normal iron level). Conversely, in severe iron deficiency anemia, patients may have thrombocytopenia (low platelets), which also resolves with iron therapy.1
What Is Iron Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?
Sources:- Koury M and Rhodes M. How to approach chronic anemia. Hematology Am Soc Hematol Educ Program. 2012;2012:183-90. doi: 10.1182/asheducation-2012.1.183. [↩]
Zincemia (Low Zinc Blood Level)
What Is Zincemia?
Zincemia means the zinc level in blood plasma is too low to meet metabolic needs of the body for this mineral.
Q: How important is a normal blood level of zinc?
A: A low blood level of zinc is characterized by widespread alterations in energy metabolism, growth, hemoglobin, carbon dioxide transport, hormone activity, insulin storage, many enzyme activities, prostaglandin function, collagen production, male fertility, protein synthesis, and vitamin A metabolism.
What Is Zincemia In Celiac Disease and/or Gluten Sensitivity?
Gluten Sensitive Enteropathy (Active Celiac Disease)
What 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
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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:- Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
- Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
- Johnston SD, Smye M, Watson RGP. Intestinal permeability and morphometric recovery in coeliac disease. Lancet. Jul 28, 2001;358(9278):259, 2p. [↩]
- 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 [↩]
- 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. [↩]
- 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. [↩]
- 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. [↩]
- 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. [↩]
- 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. [↩]