P ruritic skin is a symptom of a primary disease that may involve only the skin or a systemic disorder with other features and is characterized by chronic itching.
Q: What part of skin is affected by itchiness?
A: Itching may arise from any layer of skin, depending on the cause.
In the image to the right, the outermost protective surface layer, or stratum cornem, is shown as a thin tan line. It is the top dead layer of the epidermis that normally sloughs off as new cells move up to replace it. The epidermis is shown as a dark pink layer. It is composed of five layers of keratinocytes that flatten as they move upward.
The pink layer under the epidermis is the dermis, or true skin, which is composed of collagen and elastin tissue. It contains oil glands that lubricate skin, sweat glands, blood vessels, nerve endings, lymphatics, and hair follicles. Under the dermis is subcutaneous tissue containing fat cells here colored yellow on the bottom of the image.
What Is Pruritic Skin In Celiac Disease and/or Gluten Sensitivity?
Beefy, red, smooth, burning tongue is an inflammatory alteration in tongue tissue characteristic of vitamin B12 deficiency.
Inflammation makes the tongue red and sore which, when untreated, progresses to atrophied papillae (shrunken taste buds) that makes the tongue smooth.
Q: Why does vitamin B12 alter the tongue?
A: Vitamin B12 is essential for the metabolism of all cells, especially for those of the digestive tract of which the tongue is an organ.1
These easily seen changes to tongue tissue are an important diagnostic feature of deficient vitamin B12, which causes other devastating unseen damage, because the discomfort generally causes the individual to seek medical care.
What Is Beefy Red, Smooth, Burning Tongue In Celiac Disease and/or Gluten Sensitivity?
Mucosa in refractory celiac disease immunostained sequentially for CD3 (alkaline phosphatase-blue) and CD8 (peroxidase-brown). Most intraepithelial lymphocytes are CD3+, CD8-. Courtesy pubcan.org
What Is Refractory Celiac Disease?
R efractory celiac disease, formerly called refractory sprue, is a severe complication characterized by persistence of symptoms and intestinal inflammation despite gluten free diet after 12 months.1
Refractory celiac disease appears in two forms, ulcerative jejunitis (RCD I) and cryptic intestinal T-cell lymphoma (RCD II).
Patients with RCD I seem to profit from immunosuppressive treatment, but positive response to corticosteroid treatment does not exclude underlying enteropathy–associated T-cell lymphoma (EATL).
Patients with RCD II have a high percentage of abberant T-cells and is usually resistant to medical therapies. The presence of an aberrant clonal intraepithelial T-cell population has led to the designation of refractory celiac disease with this population as a cryptic intestinal T-cell lymphoma, characterized by frequent dissemination to the blood and the entire gastrointestinal lining.2
Refractory sprue may occur after an initial response to gluten free diet or without any evidence of preexisting celiac disease. All other causes of malabsorption must be excluded, such as collagenous colitis.
In a subgroup of patients with enteropathy-associated T-cell lymphoma (EATL) there is progressive deterioration of a refractory form of celiac disease. The prognosis is poor, although some patients respond to corticosteroids and immunosuppressive agents.3
A nationwide Finnish study showed that patients of male gender, older age, severe symptoms or seronegativity (negative antibody result) at the diagnosis of celiac disease are at risk of future refractory coeliac disease and should be followed up carefully.4
Chorea has been described as a paraneoplastic phenomenon in patients with non-Hodgkin’s lymphoma and has been described as associated with lymphoma arising from a background of refractory celiac disease. The finding of chorea in association with celiac disease should prompt a search for possible underlying intestinal T-cell lymphoma.5
How Prevalent Is Refractory Celiac Disease?
Sources:
Murray JA, The widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999;69 (3):354-365. [↩]
Culliford AN, Green PH. Refractory sprue. Current Gastroenterology Reports. Oct 2003;5(5):373-8. [↩]
Culliford AN, Green PH. Refractory sprue. Current Gastroenterology Reports. Oct 2003;5(5):373-8. [↩]
Ilus T, Kaukinen K, Virta LJ, Huhtala H, Mäki M, Kurppa K, Heikkinen M, Heikura M, Hirsi E, Jantunen K, Moilanen V, Nielsen C, Puhto M, Pölkki H, Vihriälä I, Collin P. Refractory coeliac disease in a country with a high prevalence of clinically-diagnosed coeliac disease. Aliment Pharmacol Ther. 2014 Feb;39(4):418-25. doi: 10.1111/apt.12606. [↩]
Kitiyakara T, Jackson M, Gorard DA. Refractory coeliac disease, small-bowel lymphoma and chorea. J R Soc Med. 2002 Mar;95(3):133-4. [↩]
A fiery red, smooth, burning tongue is an alteration in tongue tissue that is characteristic of advanced niacin deficiency.1
Q: How does niacin deficiency cause the tongue to be red and sore?
A: Niacin is an essential B vitamin that is required for a healthy tongue and by all body cells as well. Deficiency first shows in tissues with rapid cellular turnover, such as mucosal cells of the tongue.
When absorbed from the small intestines, niacin (the form in food) becomes the active form niacinamide. Niacinamide is converted by the body into co-enzymes which are present in all cells. 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 from adrenal glands and hormones from sex glands.
What Is A Fiery Red, Smooth, Burning Tongue 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?
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?
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. [↩]
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. [↩]
What Is Vitamin B12 Deficiency Anemia? Vitamin B12 deficiency anemia is a megaloblastic anemia that is characterized by defective DNA synthesis of red blood cells due to a lack of vitamin B12. Vitamin B12 is essential…
