F ollicular hyperkeratosis is an abnormal skin condition characterized by disordered overgrowth of the horny layer of the epidermis with horny plugs filling the openings of hair follicles. The plugs look like bumps in hair follicles.
Follicular hyperkeratosis with corkscrew hairs (coiled hairs in the follicles) appears in scurvy, which is advanced vitamin C deficiency.1
Typical hyperkeratotic papules first appear on the extensor surfaces of the extremities (e.g. the back of upper arms), shoulders, and buttocks.
Phrynoderma is a distinctive form of follicular hyperkeratosis with papule formation in dilated hair follicles believed to be a manifestation of severe malnutrition.
Q: Why does hyperkeratosis develop?
A: Follicular hyperkeratosis develops from lack of necessary nutrients to support healthy skin. Although originally thought to represent only vitamin A deficiency or vitamin C in the case of scurvy, several studies have demonstrated deficiencies of B vitamins and vitamin E. General malnutrition seems to be the strongest association. The clinical picture typically improves with enhanced nutritional status.2
What Is Follicular Hyperkeratosis In Celiac Disease and/or Gluten Sensitivity?
Maronn M, Allen DM, Esterly NB. Phrynoderma: a manifestation of vitamin A deficiency?… The rest of the story. Pediatr Dermatol. 2005 Jan-Feb;22(1):60-3. [↩]
S eborrhea dermatitis is a recurring inflammatory disorder of sebaceous glands characterized by scaly patches of skin, often with bumps.
Seborrhea dermatitis results from the body’s inflammatory reaction to invasion by pityrosporum yeast that naturally inhabits the scalp and skin.1 Inflammation is the normal response to tissue injury and germ invasion.
Pityrosporum is a yeast that is commonly present worldwide. Its development depends on various factors that predispose to pityriasis versicolor, a chronic and mild superficial yeast infection. These infections usually are asymptomatic without itching or pain and without cellular and/or antibody responses.2
Q: Why are the sebaceous glands particularly affected by this yeast?
A: Pityrosporum yeast is an organism that needs oil produced by sebaceous glands to grow. If conditions permit, this yeast invades the superficial layer of skin and hair shafts to reproduce, causing infection. Such conditions include weakened skin due to nutritional deficiencies, excessive build-up of oil on skin, and altered immunity due to systemic disease such as psoriasis.
In adults, areas of skin that are the most affected have the greatest number of sebaceous glands especially the scalp, back, underarms, and the face including the eyelids, eyebrows and side folds of the nose.
All ages are subject to seborrhea dermatitis, and males have a higher occurence than females.
What Is Seborrhea In Celiac Disease and/or Gluten Sensitivity?
Zarei-Mahmoudabadi A, Zarrin. M, Mehdinezhad F. Seborrheic dermatitis due to Malassezia species in Ahvaz, Iran. Iran J Microbiol. 2013 Sep;5(3):268-71. [↩]
This 21 year-old woman (right) appears as old as her 70 year-old grandmother (left). Courtesy Prof Dr Chua Chung Nen
What Is Acquired Cutis Laxa?
A cquired cutis laxa is an uncommon skin disorder characterized by abnormal reduction and degeneration of elastic fibers of the skin that can appear simply as thick, saggy skin with loose folds to severe involvement showing a premature aged appearance.
Q: What are elastic fibers of the skin?
A: Elastic fibers of the skin are connective tissue found in the dermis, which is the layer of skin under the epidermis, or surface layer. They hold the shape of skin and are important for wound healing in the development of scars.
What Is Cutis Laxa In Celiac Disease and/or Gluten Sensitivity?
Parathyroid Glands in the Neck. Courtesy Wikipedia.com
What Is Secondary Hyperparathyroidism?
S econdary hyperparathyroidism is a parathyroid disorder resulting from hypocalcemia (low blood calcium level) that is characterized by excessive production of parathyroid hormone in the attempt to normalize the low blood calcium by releasing calcium from bone.
Parathyroid hormone is produced by the four pea sized parathyroid glands that are located on the thyroid gland in the front of the neck. In part, because the thyroid and parathyroid glands share the same anatomic place in the body and because they have similar names, they are often confused although they have completely different actions.
Parathyroid hormone regulates calcium and the opposing mineral phosphorus in the blood. In secondary hyperparathyroidism, calcium blood levels are low to normal while phosphorus levels are increased which stimulates the outpouring of parathyroid hormone.
Q: How does secondary hyperparathyroidism differ from primary hyperparathyroidism?
A: In primary hyperparathyroidism blood calcium is high and phosphorus is low, which is the opposite of secondary hyperparathyroidism.
The most common cause of secondary hyperparathyroidism is kidney disease causing failure to reabsorb calcium followed by vitamin D deficiency and malabsorption.
What Is Secondary Hyperparathyroidism In Celiac Disease and/or Gluten Sensitivity?
Arachidonic acid is a major essential (must have/can’t make) omega-6 fatty acid.
Structurally, arachidonic acid is a key component of nerve membranes, together with docosahexaenoic acid (DHA), a major opposing omega-3 fatty acid, making up 15-20% of the brain’s dry mass and more than 30% of the retina.
In healthy human volunteers, positron emission tomography (PET) has shown that the normal human brain consumes 17.8 mg/day of arachidonic acid.1
Arachidonic acid is particularly concentrated in highly active membranes such as nerve synapses (junctions) and in photoreceptors in the eye retina.2
Arachidonic acid is an important building substance for the eicosanoids.
Q: What function do the eicosanoids have that are derived from arachidonic acid?
A: Eicosanoids are a large group of highly bioactive hormone-like substances including prostaglandins, leukotrienes, and thromboxanes that are involved in blood clotting, inflammation, and vasoconstriction. Eicosanoids derived from arachidonic acid are pro-inflammatory, pro-blood clotting, and constrict blood vessels in opposition to those derived from the omega-3 fatty acids which do the opposite in order to keep a balance in the body.
What Is Arachidonic Acid Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Rapoport SI. Brain arachidonic and docosahexaenoic acid cascades are selectively altered by drugs, diet and disease. Prostaglandins Leukot Essent Fatty Acids. 2008 Sep-Nov;79(3-5):153-6. Epub 2008 Oct 29. [↩]
Richardson AJ. The importance of omega-3 fatty acids for behavior, cognition, and mood. Scandinavian Journal of Nutrition. 2003;47(2):92-8. [↩]
Swollen Tongue Causing Tooth Indentations. Notice the Accompanying Denuded Area Due to Riboflavin Deficiency and Mild Candida Overgrowth. GFW
What Is A Pale, Smooth, Burning Tongue?
A pale, smooth, burning tongue is an alteration in tongue tissue characteristic of iron deficiency. The tongue is also swollen.1
Additionally, the sore tongue surface may be invaded by candida yeast which takes advantage of the sore tissue.
Iron deficiency itself increases susceptibility to infection.
Q: What is iron deficiency?
A: Iron deficiency results when the level within cells is too low to meet metabolic needs of the body for this mineral.
Deficiency is characterized by impaired red blood cell formation, free-radical disposal, oxygenation of cells, immune response to infection, enzyme activity, cognitive performance, digestion, nail structure, and fetal health.2
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. Iron stores are regulated by intestinal iron absorption.3
What Is A Pale, Smooth, Burning Tongue In Celiac Disease and/or Gluten Sensitivity?
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?
Microscopic Image Showing a Pink Collagen Band in Collagenous Colitis.
What Is Collagenous Colitis?
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:
Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩] [↩]
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. [↩]
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. [↩]
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. [↩]
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. [↩]
Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩]
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. [↩]
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. [↩]
Baby with Allergic Reaction to Peanuts. GFW photo.
What Is Food Allergy?
Food 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?
Riboflavin, also called vitamin B2, is fundamentally required for the breakdown of carbohydrates, amino acids, and fats in metabolism, enables oxygen to be used by cells, and acts as a component of more than a dozen enzymes involved in energy production and use.
Some enzymes needing riboflavin also require magnesium to properly function.
In other activities, riboflavin is required for healthy cardiovascular and nervous systems, eye health, and supports antioxidant protection. Functions are more fully described below.
Urinary excretion of riboflavin 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
There is no specific name for riboflavin deficiency disease.
What Is Riboflavin Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
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. [↩]
