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. [↩]
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?
Tissue Changes in Hyperparathyroidism Causing Brown Tumor. Courtesy Quizlet.com
P rimary hyperparathyroidism is a parathyroid disorder characterized by excessive secretion of parathyroid hormone by one or more parathyroid glands for more than 6 months.
In primary hyperparathyroidism, blood calcium levels are high while phosphorus levels are decreased due to the action of parathyroid hormone.
Parathyroid hormone is produced by the four pea sized parathyroid glands that are located on the thyroid gland in the front of the neck. Partly because the thyroid and parathyroid glands share the same anatomic place in the body and partly because they have similar names, they are often confused although they have completely different actions.
Parathyroid hormone normally keeps calcium and the opposing mineral phosphorus levels in balance by drawing calcium as needed from bones to increase it in blood and releasing excess phosphorus through the kidneys to decrease blood levels.
Primary hyperparathyroidism is commonly caused by an adenoma (tumor) in a parathyroid gland (80%) or 15% due to hyperplasia of gland tissue (overgrowth). It is seldom associated with autoimmune disorders. However, cancer is a possibility.
Q: What is a parathyroid adenoma?
A: A parathyroid adenoma is usually a solitary, well circumscribed, soft, tan reddish-brown nodule with a capsule. Gland tissues outside of the adenoma are normal or slightly shrunken (not needed anymore).1
Untreated, primary hyperparathyroidism results in cyst formations in bone marrow (osteitis fibrosa cystica) and brown tumors in bone tissue. Cysts contain large amounts of fibrous tissue with areas of hemorrhage. Brown tumors contain aggregates of osteoclasts (bone cells), hemorrhage and giant cells resembling neoplasms.2
Here is the symptomatolgy: “Painful Bones, Renal Stones, Abdominal Groans, and Mental Moans.”
What Is Primary Hyperparathyroidism 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?
Jaundice, or yellowing of the skin and sclera of eyes, is a symptom of autoimmune hepatitis.
What Is Autoimmune Hepatitis?
Autoimmune hepatitis is an autoimmune attack against liver cells that is characterized by inflammation and results in chronic liver disease which includes low blood albumin and cirrhosis.
Autoimmune hepatitis is diagnosed by detection of autoantibodies in blood and liver biopsy.
Q: What is cirrhosis?
A: Cirrhosis is a degenerative process of the liver that can be fatal. Normal lobular liver structure is distorted and replaced with nodules of regenerating liver cells separated by bands of fibrous tissue that cannot properly carry out liver function and block the necessary flow of blood through the liver, ending in liver failure.
The liver is the largest organ within the body and lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts.
Bile ducts carry bile, a greenish brown liquid made by the liver, to the gall bladder for storage until needed to aid in the digestion and absorption of fat from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lipase can break it down into its fatty acid and glycerol components.
The liver is a very busy organ, carrying out over 500 metabolic processes! Nutritionally, it is the first to receive all the blood carrying nutrients freshly absorbed from the digestive tract. Hepatocytes then convert the nutrients to provide the body with energy, a host of amino acids as building blocks for numerous cell activities, and proteins such as albumin and fibrinogen. In fact, hepatocytes build the structural proteins for the liver itself. Imagine the array of nutrients the liver uses and keeps at its disposal for its metabolic functions. Included in liver storage are vital vitamins and minerals such as vitamin A and vitamin B12.
As a detoxifier, Kupffer cells located in the sinusoids act like amoebas to engulf and digest unwanted matter. As a blood cleanser, the liver removes waste products produced by normal metabolism and toxic substances and rids it by preparing these substances for elimination in urine, such as ammonia converted to urea, and/or excreting them in bile for eventual elimination in stool. Bile is continually made by the liver from phospholipids salt, cholesterol, aging blood cells it removes from circulation.
Autoimmune hepatitis is classified into several types. Type 1 autoimmune hepatitis is the most common form in North America. Type 1 can occur at any age; however, it most often starts in adolescence or young adulthood. People with type 1 autoimmune hepatitis commonly have other autoimmune disorders (see listed below).
Type 2 autoimmune hepatitis is less common and occurs more often in children than adults. People with type 2 can also have any of the autoimmune disorders (see listed below).
Both types of autoimmune hepatitis are treated with prednisone, a corticosteroid hormone to control inflammation and reduce the body’s immune activity against the liver.1
What Is Autoimmune Hepatitis In Celiac Disease and/or Gluten Sensitivity?
Sources:
National Digestive Diseases Information Clearinghouse [↩]
Enlarged heart showing dilated cardiomyopathy at autopsy.
What Is Idiopathic Dilated Cardiomyopathy?
I diopathic dilated cardiomyopathy (IDCM) is a disorder of myocardial (heart muscle) function characterized by dilation or enlargement of the cardiac chambers and reduction in the ability of the ventricles (lower chambers) to contract with the required force needed to pump blood out of the heart to the body.
Idiopathic means the cause is not known.
Q: What is the prognosis for idiopathic dilated cardiomyopathy?
A: This disorder often results in symptomatic heart failure due to the inability of the heart to pump blood as required to supply the body with oxygen and meet metabolic needs.
What Is Idiopathic Dilated Cardiomyopathy In Celiac Disease and/or Gluten Sensitivity?
This photo taken during laparoscopy shows the gall bladder (small white organ in middle) surrounded by yellow fat. Liver (dark red organ) is overlying.
What Is Impaired Gall Bladder Motility?
I mpaired gall bladder motility means the gall bladder is slow to empty or is dysfunctional.
The functional disorder of the gallbladder is caused initially either by metabolic abnormalities or by an alteration in its muscular ability to contract (motility dysfunction).
The diagnostic criteria based on symptoms of motility dysfunction of the gallbladder are episodes of moderate to severe steady pain located in the epigastrium and right upper abdominal quadrant that last at least 30 minutes.
Gallbladder motility disorder is suspected after gallstones and other structural abnormalities have been excluded.1
Q: What does the gallbladder do?
A: The gallbladder is a small pouch-like organ about the size of a pear that receives bile produced by the liver and stores it until needed during digestion. It lies just under the liver.
Bile is a complex fluid containing water, electrolytes and many organic molecules including bile acids, cholesterol, phospholipids and bilirubin. Bile acids are critical for digestion and absorption of fats and fat-soluble vitamins in the small intestine. Many waste products, including bilirubin, are eliminated from the body by secretion into bile and elimination in feces.2
Before a meal, the gallbladder is usually full of bile. In response to fat in the diet, the gallbladder squeezes stored bile into the small intestine through a series of ducts. When emptied after meals, the gallbladder is flat.
What Is Impaired Gall Bladder Motility In Celiac Disease and/or Gluten Sensitivity?
Sources:
Behar J, Corazziari E, Guelrud M, Hogan W, Sherman S, Toouli J. Functional gallbladder and sphincter of oddi disorders. Gastroenterology. 2006 Apr;130(5):1498-509. [↩]
This is a model of Immunoglobulin-G Antibody (IgG)
What Are Anti-Gliadin Antibodies?
A nti-gliadin antibodies (AGA) are produced by the body as an immune response against partially digested gliadin peptides (fragments) that have abnormally entered the body from the intestinal tract. Gliadin is a protein in wheat grain.
Anti-gliadin antibodies circulating in blood are measured by laboratory testing on blood that is drawn. The antibodies are both immunoglobulin A (IgA) and immunoglobulin G (IgG) types, which are termed AGA-IgA and AGA-IgG.
The presence of anti-gliadin antibodies in blood is an abnormal laboratory finding. That is, when the intestinal lining is healthy and able to keep out undigested matter from the body, there are no molecules of gliadin present to trigger the immune system for defense.
Q: Who produces anti-gliadin antibodies?
A: Persons, with or without celiac disease, can produce anti-gliadin antibodies if and when leaky gut (increased intestinal permeability) develops that then allow gliadin peptides to get into the bloodstream.
Gliadin itself causes leaky gut, but there are other causes such as various foods, intestinal infections, medications, and other diseases of the gastrointestinal tract. Whatever the cause of leaky gut, if poorly digested gliadin is present, it can slip through the leaky lining and enter the bloodstream where it can trigger an antibody response by anti-gliadin antibodies.
What Are Anti-Gliadin Antibodies In Celiac Disease and/or Gluten Sensitivity Or Non-Celiac Gluten Sensitivity?
Figure on right shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.
What Is Coronary Artery Disease (CAD)?
C oronary artery disease (CAD), also called ischemic heart disease, is a gradual narrowing of medium and large arteries of the heart by fatty buildups, called atherosclerotic plaques.
It is characterized by slowly developing interference with blood flow to heart tissue itself, resulting in oppressive chest pain called angina and, ultimately, thrombosis (clot) causing heart attack.
The heart is a muscular organ that is working all the time, so it needs a constant supply of oxygen. Oxygen is brought to the working heart tissue by the coronary arteries with each beat of the heart. When heart muscle has to work harder, it needs more oxygen delivered to itself. Lack of oxygen causes pain.
In fact, failure of diseased coronary arteries to deliver adequate oxygen to heart tissue is the most common cause of angina pectoris – substernal pain (under breastbone) or pressure brought on by exertion and relieved by rest.
Thrombosis, or clot formation, occurs when blood cells within a narrowed artery can no longer get through. Trapped, blood cells pile up and block the artery thus triggering a cascade of events called heart attack. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery.1
Q: How does coronary artery disease develop?
A:Coronary artery disease slowly develops from this combination of events:
Dysfunction of epithelial cells that line the inside of arteries cause the vessels to stiffen, and subsequently
Accumulation of lipid (fat) in smooth muscle cells beneath the inside lining of arteries and in foam cells cause buildup of fatty deposits on the inside walls progressing to fibrous plaque formation.
Oxidized low-density lipoprotein (oxLDL), so-called bad cholesterol, and oxysterols play important roles in the development of atherosclerosis. OxLDL triggers the immune system to produce autoantibodies against oxLDL that are detectable in serum. These antibodies are called anti-oxLDL. Anti-oxLDL antibody and oxysterol concentrations are associated with coronary artery stenosis. Oxidative stress may be greatly increased in unstable angina.2 and Chronic inflammation in the general population is a major risk factor for ischemic heart disease.
The pathophysiology of atherosclerosis is, clearly, different in women when compared to the men. The women have a higher risk of blood coagulability making them at high risk for the blood clot formation. In a large number of women endothelial dysfunction, small vessel size and diffuse atherosclerosis have been identified as causes of ischemia without evidence of blockade in the coronary arteries.3
Also, atherosclerotic plaque in women is less fibrotic and contains more lipid filled foam cells, implying greater potential for reversibility but also potentially greater vulnerability for plaque rupture and thrombosis.4
Who is Affected in the General Population?
Coronary artery disease remains the leading cause of death in developed countries despite significant progress in primary prevention and treatment strategies.
It is the leading cause of death in women, as well as an important cause of disability.
Older patients are at particularly high risk of poor outcomes following acute coronary syndrome.5
What Is Coronary Artery Disease In Celiac Disease and/or Gluten Sensitivity?
Ischemic heart disease is the leading cause of death in the United States, making cardiovascular risk assessments and potential interventions or treatments imperative for patients with celiac disease.6
Yasunobu Y, Hayashi K, Shingu T, Yamagata T, Kajiyama G, Kambe M. Coronary atherosclerosis and oxidative stress as reflected by autoantibodies against oxidized low-density lipoprotein and oxysterosis. Atherosclerosis. Apr 2001;155(2):445-53. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. [↩]
Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]
A 3D Image From Magnetic Resonace Cholangiography showing biliary tree. NIHMS
What Is Primary Sclerosing Cholangitis?
P rimary sclerosing cholangitis (PSC) is an uncommon, slowly progressive bile duct disease that results in stagnation or build-up of bile in the liver, called cholestasis.
Primary sclerosing cholangitis is characterized by sclerosis, or scarring inflammation in bile ducts both within the liver (intra-hepatic ducts), and outside the liver (extra-hepatic ducts), causing progressive narrowing and, eventually, obliteration of the bile ducts.
Primary sclerosing cholangitis comes under the umbrella term autoimune liver disease in which the end result is immune-mediated hepatocellular (liver cell) or hepatobiliary (bile duct) injury.1
Q:What happens when scarred bile ducts can no longer transport bile out of the liver?
A:Bile that cannot be removed from the liver by the biliary duct system backs up and damages the liver, causing cirrhosis.
Bile is continually made by the liver from phospholipids salt, cholesterol, and aging blood cells that it removes from circulation to be carried out of the liver. Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. As such, bile must continually flow out of the liver to prevent build-up in the liver.
Bile is a greenish brown liquid made by the liver. Bile ducts carry it out of the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components.
The liver is the largest organ within the body. It lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells (epithelial) form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts.
Build-up of bile in the liver is the end result of the inflammatory process in primary sclerosing cholangitis, that by swelling and scarring of bile ducts impedes and eventually prevents bile flow out of the liver, leading to liver failure. There is no curative treatment available for primary sclerosing cholangitis, besides liver transplantation.2
The appearance of the intrahepatic and extrahepatic biliary ducts can be assessed by use of cholangiography, and magnetic resonance (MR) imaging is the best way to identify patients. See image above.3
MR cholangiography offers a noninvasive method of obtaining images of the biliary system without the use of a contrast agent. There is no radiation exposure. Pulse sequences can be chosen to obtain bright bile or black bile cholangiograms. Image processing algorithms can be selected to obtain a three-dimensional representation of biliary anatomy and pathology, and those images can be rotated in any plane so that ductal anatomy and pathology can be seen to best advantage.4
There is no cure for primary sclerosing cholangitis but there are symptom treatments one of which is supplementation for low levels of vitamins A,D,E, and K. Liver transplant is the only effective option.
What Is Primary Sclerosing Cholangitis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Trivedi PJ, Adams DH. Mucosal immunity in liver autoimmunity: a comprehensive review. J Autoimmun. 2013 Oct;46:97-111. doi: 10.1016/j.jaut.2013.06.013. [↩]
Kummen M, Schrumpf E, Boberg KM. Liver abnormalities in bowel diseases. Best Pract Res Clin Gastroenterol. 2013 Aug;27(4):531-42. doi: 10.1016/j.bpg.2013.06.013. [↩]
Eaton JE, Talwalkar JA, Lazaridis KN, Gores GJ, Lindor KD. Pathogenesis of primary sclerosing cholangitis and advances in diagnosis and management. Gastroenterology. 2013 Sep;145(3):521-36. doi: 10.1053/j.gastro.2013.06.052. Epub 2013 Jul 1. [↩]
Meakem TJ 3rd, Schnall MD. Magnetic resonance cholangiography. Gastroenterol Clin North Am. 1995 Jun;24(2):221-38. [↩]
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