K oilonychia is a feature of an iron deficiency state characterized by abnormally shaped nails, called spoon shaped nails, meaning that the normal downward curve is reversed.
Depending on the inadequacy of iron, nails may simply remain flat or with a slight dip without progressing to a reversed curve.
These nails develop vertical ridges from the base to the nail tip that can become deep, called washboard nails.
Q: Are all nails affected?
A: All nails are affected in varying degrees. The small finger shows the least effect while the thumb shows the greatest change which begins as flattening before scooping upward.
Nail Anatomy. .
A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.
What Is Koilonychia In Celiac Disease and/or Gluten Sensitivity?
S ubungual (under the nail) splinter hemorrhage is characterized by fragility of the underlying capillaries resulting in bleeding under the nail . Bleeding that results looks like a brown streak or splinter.1
Because the streak of blood is not in the nail but under the nail, it does not grow out with the nail. It can be a feature of vitamin C deficiency which resolves with adequate nutrition.
Nail Anatomy. .
A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.
Splinter hemorrhage can be seen in a diet poor in vitamin C, disorders of food absorption, systemic disease such as psoriasis, nail lichen planus, an aggressive disease that may destroy the nail plate, and endocarditis. Some drugs, such as oral contraceptives, cause vitamin C deficiency.
Who is Affected in the General Population? Both sexes are commonly affected, though it occurs significantly more frequently in males. Where present in females, they were confined to a single digit.2
What Are Splinter Hemorrhages In Nails In Celiac Disease and/or Gluten Sensitivity?
Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikimedia.org
What Are Rounded Nails With Curved Ends?
R ounded, curved, dark and dry nails are a well known feature of vitamin B12 deficiency.
Q: How does vitamin B12 deficiency cause the nails to grow this way?
A: Vitamin B12 deficiency affects 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 matrix at its base.
What Are Rounded Nails With Curved Ends In Celiac Disease and/or Gluten Sensitivity?
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. .
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?
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?
Cutaneous vasculitis is a vascular disease of small blood vessels serving the skin that is characterized by segmental (spotty) inflammation of affected vessel walls resulting in their necrosis (destruction). Scarring is seen in the affected skin that lies over the destroyed blood vessels.
Skin appearance varies from small flat, purplish spots to raised purplish areas over damaged vessels.
In most cases, cutaneous vasculitis results from deposits of toxic immune complexes in the affected vessel walls that is caused by autoimmune activity targeting small blood vessels.1
Cutaneous vasculitis can also result from infection, drug reactions, or malignancies.
Who is Affected in the general Population? Cutaneous vasculitis affects all ages.
The overall annual incidence of cutaneous vasculitis was 38.6 persons per million in 1998.2
What Is Cutaneous Vasculitis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Abenavoli L, Proietti I, Leggio L, Ferrulli A, Vonghia L, Capizzi R, Rotoli M, Amerio PL, Gasbarrini G, Addolorato G. Cutaneous manifestations in celiac disease. World J Gastroenterol. 2006 Feb 14;12(6):843-52. [↩]
Watts RA, Jolliffe VA, Grattan CE, Elliott J, Lockwood M, Scott DG. Cutaneous vasculitis in a defined population–clinical and epidemiological associations. J Rheumatol. 1998 May;25(5):920-4. [↩]
Microscopic view of pancreatic islet cells. Courtesy Dr. José Sánchez Gonzales
What Is Type I Diabetes Mellitus?
T ype 1 diabetes mellitus (T1DM), also termed type 1A, is an inherited autoimmune disorder in which anti-islet autoantibodies destroy the islet cells of the pancreas that secrete insulin hormone. Type 1 diabetes mellitus was formerly called juvenile diabetes because it usually afflicts persons under the age of 25 years.
Loss of insulin production results in failure to metabolize glucose. Glucose is a simple sugar that is a required source of energy for the body, especially the brain and muscles.
Type 1 diabetes mellitus is characterized by sustained fasting blood glucose levels above 126 mg/dL (hyperglycemia) with subsequent loss of glucose from the body by removal through the urine (glucosuria) as the body attempts to lower blood glucose, and cell starvation that follows.
That is, while glucose accumulates in blood, the body cannot access it. Without insulin treatment, this disorder quickly produces coma and ultimately results in death. In fact, it is 5th leading cause of death in the United States.
Q: How does insulin work?
A: Insulin moves glucose from the bloodstream into body cells where it is used or reformulated for high energy storage. For example, muscles can use glucose for immediate work or store it in the form of glygogen for later work, depending on need. Healthy insulin production keeps an 8 hour fasting blood glucose level to less than 100 mg/dL. Upon eating carbohydrate food, glucose is digested and absorbed from the small intestine into the bloodstream which then raises blood glucose levels. The elevated level is controlled by prompt action of insulin to lower it to below 140 mg/dL within 2 hours of eating.
Insulin does not work alone. The islets of Langerhans manage glucose in the body. The islets are specialized formations located on the outer surface of the pancreas. The islets are composed of two different types of cells known as alpha and beta cells. These cells make the competing hormones that keep blood glucose within a healthy range.
Alpha cells secrete glucagon to raise blood glucose levels by triggering the body to release stored energy in the form of glycogen. In the opposite, beta cells secrete insulin to lower blood glucose by opening body cells so that glucose in blood can enter. Without insulin, glucose cannot enter cells but remains in the bloodstream where it accumulates.
Insulin is also needed to move magnesium into cells from the bloodstream. On the other side, magnesium is needed to produce insulin. Insulin has other functions such as building muscle and helping regulate cholesterol which directly impacts the sex hormones, estrogen, progesterone, and testosterone.
Onset of symptoms usually occurs over a period of days or weeks, although beta cell destruction can begin years earlier. The SEARCH for Diabetes in Youth multicenter study, funded by the Centers for Disease Control and Prevention (CDC) and the National Institutes of Health (NIH), has determined that based on data from 2002 to 2003, a total of 15,000 youth in the United States were newly diagnosed with type 1 diabetes each year. Non-Hispanic white youth had the highest rate of new cases of type 1 diabetes according to NIH.
Type 1A diabetes mellitus has become one of the most intensively studied autoimmune disorders. It is now possible to predict its development, beginning with HLA-encoded genetic susceptibility, followed by the development of a series of anti-islet autoantibodies.1
What Is Type I Diabetes Mellitus In Celiac Disease and/or Gluten Sensitivity?
Sources:
Liu E, Eisenbarth GS. Type 1A diabetes mellitus-associated autoimmunity. Endocrinology and Metabolism Clinics of North America. Jun 2002;31(2):391-410, vii-viii. [↩]
Image of Pancreas From Gray’s Anatomy. Courtesy Wikipedia.org
What Is Pancreatic Insufficiency?
P ancreatic insufficiency is a disorder characterized by insufficient exocrine production of pancreatic enzymes for normal digestion of fats, proteins, and carbohydrates that results in maldigestion of these foodstuffs.
Pancreatic insufficiency also causes malabsorption of the fat-soluble vitamins: vitamin A, vitamin D, vitamin E, and vitamin K.
Q: What are the exocrine enzymes produced by the pancreas?
A: Exocrine enzymes produced by the pancreas include amylase for the digestion of carbohydrates, lipase for the digestion of fats, and protease for the digestion of proteins.
While lipases and amylase are secreted in the active form, proteases are secreted as pro-enzymes (need to be activated). Trypsinogen is converted to its active form trypsin in the duodenum by enterokinase, a protease secreted by the enterocytes (surface cells that line the duodenum), and trypsin in turn activates the other pancreatic proteases.1
Pancreatic enzymes are released by the pancreas into the internal pancreatic duct that empties into the common bile duct from which they are pumped through the Sphincter of Odi directly into the duodenum as needed. Tthe Sphincter of Odi is a strong circular muscle that controls the entrance of pancreatic enzymes into the duodenum.
After a meal, enzyme secretion into the duodenum increases quickly reaching peak output within the first 20 to 60 minutes, then decreasing to a stable level before reaching an interdigestive level at the end of the digestive period, that is, about 4 hours after meal intake.2
Medical treatment is with medication that contains enzymes to break down carbohydrates, fats, and protein in food at mealtime. This treatment is safe, effective, and has few side effects.
What Is Pancreatic Insufficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Fieker A, Philpott J, Armand M. Enzyme replacement therapy for pancreatic insufficiency: present and future. Clin Exp Gastroenterol. 2011;4:55-73. doi: 10.2147/CEG.S17634. [↩]
Fieker A, Philpott J, Armand M. Enzyme replacement therapy for pancreatic insufficiency: present and future. Clin Exp Gastroenterol. 2011;4:55-73. doi: 10.2147/CEG.S17634. [↩]
S teatorrhea is a condition of abnormal stool composition and consistency that is due to high fat content because fat from food is not digested and absorbed into the body but rather passes out with stool.1
Q: How does fatty stool look?
A: The stool in steatorrhea appears pale, bulky and may float in the toilet. If stool is loose, it varies from a pudding consistency to whipped cream. If it is solid, it can vary from thin sqiggles to big turds that smear the sides of the toilet bowl. All types have a foul smell.
Fat of any kind must be digested, or broken down, by enzymes into fatty acids and glycerol and then these parts only are absorbed through the small intestinal lining into the body. The failure to digest or absorb fats deprives the body of these foodstuffs needed for many functions such as blood clotting and vital cell parts such as eye and brain structure.
Fat malabsorption produces malabsorption of vitamins A, D, E, and K because these vitamins can only be absorbed along with fatty acids.
What Is Steatorrhea In Celiac Disease and/or Gluten Sensitivity?
Sources:
Murray JA, The widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999;69 (3):354-365. [↩]
B leeding and/or swollen gums is an inflammatory disorder characterized by changes in gum integrity that may result in tooth loss.
Sponginess of the gum (swelling) indicates inflammation, called gingivitis.
Q: What causes gingivitis?
A: Gingivitis that is caused by inadequate dental hygiene shows as pockets of swollen gum between or along the base of teeth where sticky plaque was allowed to build up. Plaque holds bacteria that inflames the gums where it occurs.
Gingivitis that is caused by vitamin C deficiency, pregnancy, certain drugs such as the anti-epileptic drug phenytoin, and leukemia affects the whole gum irrespective of mouth care.
What Are Bleeding / Swollen Gums In Celiac Disease and/or Gluten Sensitivity?
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