What Is Plummer-Vinson Syndrome Affecting the Esophagus?
[dropcap]P[/dropcap]lummer-Vinson syndrome is a manifestation of severe, long-term, iron deficiency anemia that is characterized by post-cricoid esophageal webs and dysphagia.
Q: What are esophageal webs?
A: Esophageal webs are one or more thin horizontal membranes consisting of squamous epithelium (cells that line the surface of the esophagus) and submucosa. They usually protrude from the anterior (front) wall, extending laterally across the inside esophagus but not to the posterior (rear) wall, which means that they rarely encircle the lumen.1
Dysphagia, or difficulty swallowing, from these webs is commonly painless and intermittent or progressive and may cause obstruction.
Webs can be detected by barium swallow X-ray, but the best way for demonstration is videofluoroscopy and by upper gastrointestinal endoscopy. They appear smooth, thin, and gray with eccentric or central lumen space. The webs typically occur in the upper part of the esophagus and may be missed and accidentally ruptured unless the endoscope is introduced under direct visualization.1
Iron deficiency is believed to decrease the contraction amplitude or force of the esophageal muscle resulting in motility impairment. Slower transit times have been recorded at the proximal and middle parts of the esophagus of Plummer-Vinson syndrome patients compared to healthy volunteers.2 Transit time is how fast ingested food and fluids travel through the esophagus.
Gude et al, report that iron replacement does not necessarily reverse the dysphagia in all the cases of Plummer-Vinson syndrome and that close monitoring of the web is mandated to watch for malignant change. In fact, 3 to 15 per cent of the patients with Plummer-Vinson syndrome, mostly women between 15 and 50 years of age, have been reported to develop esophageal or pharyngeal cancer.2
What Is Plummer-Vinson Syndrome Affecting the Esophagus In Celiac Disease and/or Gluten Sensitivity?
Sources:
Novacek G. Plummer-Vinson syndrome. Orphanet J Rare Dis. 2006; 1: 36. Published online 2006 September 15. doi: 10.1186/1750-1172-1-36. [↩] [↩]
Gude D, Bansal DP, and Malu A. Revisiting Plummer Vinson Syndrome. Annals of Medical and Health Sciences Research. 2013 Jan-Mar;3(1):119-121. [↩] [↩]
[dropcap]A utoimmune disorders refer to those conditions that involve an abnormal attack on the body’s own tissues perpetuated by the production of autoantibodies directed against self.
Q: What happens when autoantibodies attack the body’s own tissues?
A: This abnormal immune activity by autoantibodies causes inflammation and damage to targeted body tissues.
Dermatitis herpetiformis is a skin manifestation of celiac disease characterized by extremely itchy blisters that commonly erupt on forearms and knees but may appear on the face, scalp or buttocks.
Autoimmune diseases as a group affect approximately 8.5% of people worldwide.
What Are Autoimmune Disorders In Dermatitis Herpetiformis?
Bristol Stool Chart Showing Normal and Abnormal Stool.
What Is Chronic Constipation Alternating With Diarrhea?
[dropcap]C hronic constipation alternating with diarrhea is an intestinal motility disorder, or irregularity, characterized by alteration in stool formation, consistency, and evacuation which results in a bowel movement that consists of some hard or balled stool along with some loose stool that can cause leakage.
Q: How do irregular movement patterns develop in the colon?
A: The colon produces irregular movements as a result of problems that originate in the colon (large intestine) itself and/or the small intestine which then affects function of the colon.
Here are listed the many types of problems or diseases that cause these abnormal bowel movements:
Disorders that adversely affect the colon, an organ which must propel stool, remove excess water, absorb electrolytes, ferment undigested food material that passes into it, and produce nutrients from the fermentation process:
Poor diet that does not contain adequate nutrition, fiber, probiotics, prebiotics, and water to form normal stool.
Diet that contains irritating, toxic or allergenic food that cause spasms.
Diseases that inflame the mucosa lining such as collagenous colitis, altering the proper absorption of water and electrolytes.
Diseases that damage and swell the colon walls, such as Crohn’s disease, ulcerative colitis, and diverticulitis.
Diseases that obstruct the lumen or passageway so that stool passes with difficulty.
Diseases that hamper normal peristalsis (muscle action), such as irritable bowel syndrome (IBS), diabetes and thyroid disease.
Disorders that adversely affect the small intestine, an organ which must digest and absorb nutrients needed by the body while passing unabsorbed food material to the colon:
Diet that conatins too much fat, sugar or artifical sweeteners, causing diarrhea.
Disorders that result in malabsorption, such as gluten enteropathy, milk enteropathy, steatorrhea (fat malabsorption), lactose intolerance, sucrose intolerance, maltose intolerance, and bacterial overgrowth, passing abnormal amounts of undigested food material to the colon where it is fermented producing excessive gas, diarrhea and spasm.
Disorders that impair peristalsis, such as active celiac disease, diabetes, scleroderma, and thyroid disease.
Tumors like cancer and lymphoma impair regular passage of material to colon.
Drugs that impair peristalsis, such as iron supplements, aluminum containing antacids, narcotics, some anti-depressants, some anti-seizure, and some diuretics.
What Is Chronic Constipation Alternating With Diarrhea In Celiac Disease and/or 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)?
[dropcap]C[/dropcap]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. [↩]
Arrows Show Abnormal Movement of Gastric Acid in Gastroesophageal Reflux Disease.
What Is Gastroesophageal Reflux Disease (GERD)?
[dropcap]G[/dropcap]ERD is an upper digestive disorder that is characterized by a decrease in lower esophageal sphincter pressure (LES,) which allows the abnormal reflux or backflow of stomach contents into the esophagus. It is also called erosive esophagitis or reflux esophagitis and is the most common disorder of the esophagus.
The esophagus is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx and ends at the lower esophageal sphincter (LES).
The lower esophageal sphincter is located at the junction of the esophagus and the stomach. It functions like a circular band to tighten after food is ingested in order to prevent its going back up the esophagus.
Q: How does reflux damage the esophagus?
A: Damage to the lining of the esophagus is induced by the caustic, chemical action of acid and pepsin in gastric juice and, in severe cases, also bile salts, that back upwards from the stomach through an impaired LES. Gastric acid combined with pepsin or bile salts seems to be more harmful to the esophageal epithelial layers than gastric acid alone.1
Pepsin is normally produced by the stomach to dissolve protein in swallowed food. Unfortunately, when the esophagus is inflamed, pepsin will act on it to break down the protein in its sore wall. These sores are called erosions.
Importantly, refluxate to the esophagus in patients with acid suppression therapy is different from those in patients without. Higher levels of secondary bile acids are detected in patients with acid suppression therapy. Even if acid suppression is successful, weakly acidic reflux with bile acids can damage the esophagus.1
Damage starts at the luminal surface (inside where food passes through) of the squamous epithelium (tough surface cells) and progresses through the underlying layers into the submucosa.
One of the primary functions of the esophageal epithelium is to protect the underlying tissue from mechanical and chemical damage by acting as a barrier. The epithelial layers of the distal esophagus need to withstand reflux from the stomach and its contents. When the epithelium fails to protect the underlying tissue from this damage, it leads to erosions, esophagitis, and may lead to Barrett’s esophagus.1
Barrett’s esophagus and esophageal small cell cancer are severe complications of GERD that can be fatal.
GERD can result from too much, or more commonly, too little stomach acid.
What Is Gastroesophageal Reflux Disease (GERD) In Celiac Disease and/or Gluten Sensitivity?
Sources:
Chen X, Oshima T, Tomita T, Fukui H, Watari J, Matsumoto T, Miwa H. Acidic bile salts modulate the squamous epithelial barrier function by modulating tight junction proteins. Am J Physiol Gastrointest Liver Physiol. 2011 Aug;301(2):G203-9. doi: 10.1152/ajpgi.00096.2011. Epub 2011 May 26. [↩] [↩] [↩]
This is a stained liver biopsy sample showing advanced cellular changes in non-alcoholic fatty liver disease. Blue is fibrosis. White is fat accumulation in degenerated cells. Courtesy of Nephron’s work.
What Is Non-Alcoholic Fatty Liver Disease?
[dropcap]N on-alcoholic fatty liver is a non-inflammatory liver disorder characterized by degenerative changes in the liver caused by excessive accumulation of lipid (fat) in hepatocytes (liver cells) that is called free fatty acid-generated lipotoxicity.
Non-alcoholic fatty liver shows an increase in liver enzymes called transaminases.
Q: What are the enzymes that increase?
A: The transaminases that increase are ALT and AST. ALT is the abbreviation for alanine aminotransferase enzyme and AST is the abbreviation for aspartate aminotransferase enzyme. They are commonly measured in blood tests to determine liver function and when elevated indicate inflammation.
What Is Non-Alcoholic Fatty Liver In Celiac Disease and/or Gluten Sensitivity?
[dropcap]E rythema elevatum diutinum is a rare leucocytoclastic vasculitis thought to be caused by an immune response that is characterized by inflammation, a rash, and scarring of small blood vessels of the skin.
A characteristic poorly defined rash develops symmetically in the skin of extremities where the vessels are inflamed. Nodules and plaques are yellowish red and crust on healing, leaving darkened areas (hyperpigmentation).
Q: What is leucocytoclastic vasculitis?
A: Leucocytoclastic vasculitis is the most common form of vasculitis (inflammation of blood vessels) of the skin and usually results from deposition of immune complexes at the vessel wall. It presents in different forms and in association with different diseases. Diagnosis is made by skin biopsy with immunofluorescence.1
Erythema elevatum diutinum may be caused by inflammatory disease, certain infections such as HIV, immunological disease, malignancy, and drugs.
Corticosteroids are indicated when there are signs of incipient skin necrosis or when the disease is severe. Otherwise, treatment is with Colchicine or Dapsone medications.2
What Is Erythema Elevatum Diutinum In Celiac Disease and/or Gluten Sensitivity?
Sources:
Sunderkötter C, Bonsmann G, Sindrilaru A, Luger T. Management of leukocytoclastic vasculitis. J Dermatolog Treat. 2005;16(4):193-206. [↩]
Sunderkötter C, Bonsmann G, Sindrilaru A, Luger T. Management of leukocytoclastic vasculitis. J Dermatolog Treat. 2005;16(4):193-206. [↩]
[dropcap]E rythema nodosum is an inflammatory disorder involving the deep dermis layer of skin and subcutaneous fat septa that underlies the skin. It is characterized by eruptions of recurrent or persistent multiple painful, red nodules under the skin that leave a bruised appearance when healing and do not scar.
The lower legs are most affected, but sores can appear anywhere there is subcutaneous fat.
Q: How do the nodules develop in erythema nodosum?
A: The edges of nodules are poorly defined, and the nodules vary from 2-6 cm.
During the first week of eruption, nodules become tense, hard, and painful. During the second week, they change color from bright red to bluish or livid and may become soft, but do not ulcerate. As absorption progresses, the color gradually fades to a yellowish hue, resembling a bruise. This disappears in 1 or 2 weeks as the overlying skin sloughs off and is replaced.1
The eruptive phase of erythema nodosum begins with flulike symptoms of fever and generalized aching followed by a painful rash within 1-2 days. Aching legs and swelling ankles may occur and precede the eruption or appear during the eruptive phase and may persist for weeks.2
Currently, the most common cause of erythema nodosum is streptococcal infection in children and streptococcal infection and sarcoidosis in adults.3Most sores in infection-induced erythema nodosum heal within 7 weeks, but active disease may last up to 18 weeks.
In contrast, 30% of idiopathic erythema nodosum cases may last more than 6 months. Idiopathic means that the cause is not known.
What Is Erythema Nodosum In Celiac Disease and/or Gluten Sensitivity?
What Is Intraepithelial Lymphocytosis In Normal Small Bowel Samples? [dropcap]I ntraepithelial lymphocytosis is characterized by an abnormal increase in the numbers of intraepithelial lymphocytes (IELs) that are present in the small intestinal mucosa. Q: What…
[dropcap]H angnail is a broken strip of epidermis (piece of skin) at root or lateral (side) edge of fingernail or toenail that causes sharp pain.
A hangnail develops because the skin around the nail is unhealthy due to inadequate nutrition. Injury from trauma including biting the skin and pushing back the cuticles or exposure to excessive detergents and water that remove protective oils promote the development of hangnail.
All ages and both sexes can be affected.
Q: Can a hangnail become infected?
A: Infection, called paronychia, may develop from invasion of sore skin by any of these pathogens: bacteria, fungus, or yeast (Candida). Infected skin is red, swollen, and painful. Topical ointment is required to treat the infection.1
What Is Hangnail In Celiac Disease and/or Gluten Sensitivity?
What Is Plummer-Vinson Syndrome Affecting the Esophagus?
![Crohnie_sores_4[1]](https://glutenfreeworks.com/health/wp-content/uploads/sites/10/Crohnie_sores_41.jpg)
