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Hypoparathyroidism, Idiopathic

hypocalcemia celiac disease gluten symptomWhat Is Hypocalcemia?

H ypocalcemia, or low plasma calcium, means the level of calcium in blood is too low to meet metabolic needs of the body for calcium.

Low blood calcium is characterized by bone and tooth demineralization (loss of calcium causing weak teeth and fragile bones), and these impaired functions: nerve conduction, muscle contraction, blood clotting, blood pressure regulation, glycogen to glucose conversion, many hormone actions, many enzyme activities, and acetylcholine production.

Q: Where is calcium found in the body?

A: Calcium is the most abundant mineral in the body, with 99% residing in bones and teeth where it constitutes 40% of skeletal bone weight along with 45% phosphorus. As a component of bone (hard tissue), calcium fulfills a structural role to maintain body size and act as attachments for musculoskeletal tissues. The remaining 1% of calcium is present in blood and soft tissues.

Calcium levels in the blood are maintained within very strict limits by dietary intake, hormonal regulation by the parathyroid gland and a rapidly exchangeable pool in bone tissue.

What Is Hypocalcemia In Celiac Disease and/or Gluten Sensitivity?

Lymphomas, Extraintestinal

What Is Dysphagia? D ysphagia is a functional upper digestive disorder characterized by difficulty in swallowing or food getting stuck and swallowing that takes longer than 10 seconds to complete. Q: What determines the symptoms?… 

Hypokalemic Rhabdomyolysis in Celiac Disease and Dermatitis Herpetiformis

mucosal web in plummer-vinson syndromeWhat Is Plummer-Vinson Syndrome Affecting the Esophagus?

P 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:
  1. Novacek G. Plummer-Vinson syndrome. Orphanet J Rare Dis. 2006; 1: 36. Published online 2006 September 15. doi:  10.1186/1750-1172-1-36. [] []
  2. 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. [] []

Hair, Fine With Rough Texture

Inflamed Aorta. Courtesy Quizlet.com
Inflamed Aorta. Courtesy Quizlet.com

What Is Aortic Vasculitis?

A ortic vasculitis is an inflammatory disease of the aorta that causes dilation of the aorta wall with narrowing of the inside passageway and results in widespread impairment of blood flow to tissues served by the aorta.

Q: What is the result of inflammatory disease of the aorta?

A: The aorta is the largest artery in the body. It extends from the left ventricle (lower chamber) of the heart and carries blood out of the heart with each beat to rest of the body. Narrowing of the aorta’s inside diameter due to swelling from inflammation causes elevated blood pressure and enlarged heart because of back pressure of blood unable to be fully pumped out of the heart with each beat. The heart enlarges because the difficulty of pumping blood out makes it work harder than normal.

Vasculitis that causes midaortic syndrome is a variety of aortic coarctation (narrowing) located in the lower thoracic aorta, the abdominal aorta or both, involving the intestinal and renal vessels (kidney). It usually presents with arterial hypertension.1

What Is Aortic Vasculitis  In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Massel D. n-3 polyunsaturated fatty acids reduced mortality and morbidity after recent myocardial infarction. Therapeutics. Jan-Feb 2000:6 []

Ataxia, Gait

Normal Liver Lobule. Courtesy almostadoctor.com
Figure 1: Normal Liver Lobule. Courtesy almostadoctor.com

What Is Autoimmune Cholangitis?

A utoimmune cholangitis is a rare inflammatory self-targeted disease of the biliary tract produced by high levels of immunoglobulin G (IgG) antibodies and antinuclear antibodies (ANA).

Autoimmune cholangitis is characterized by progressive inflammation and scarring that leads to narrowing and destruction of the bile ducts and development of biliary cirrhosis of the liver.

Autoimmune cholangitis is also termed anti-mitochondrial antibody-negative primary biliary cirrhosis because there is no production of anti-mitochondrial antibodies.

Q: What happens when bile ducts can no longer transport bile out of the liver?

A: Bile that cannot be removed from the liver by the biliary tract backs up and damages the liver, causing cirrhosis. In Figure 1, bile back up would directly damage the hepatic (liver) cells seen here as grey “blocks.” 

Bile is a greenish brown liquid continually made by the liver cells (hepatocytes) from phospholipids salt, cholesterol, and aging blood cells that it removes from circulation. 

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 from the hepatic cells drains into small tubes called canniculi and then into larger bile ducts to be carried 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. 

Unfortunately, autoimmune cholangitis is difficult to diagnose because it mimics many other diseases such as primary sclerosing cholangitis, sarcoidosis, cancer and lymphoma.

What Is Autoimmune Cholangitis In Celiac Disease and/or Gluten Sensitivity?

Cutis Laxa, Acquired

Image on left shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.
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

Sources:
  1. http://www.heart.org/HEARTORG/Conditions/HeartAttack/SymptomsDiagnosisofHeartAttack/Unstable-Angina_UCM_437513_Article.jsp# []
  2. 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. []
  3. 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. []
  4. 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. []
  5. 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. []
  6. Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. []

Edema

Cachexia with Wasted Muscles, Weakness, and That Developed over 3 Years Time.
Cachexia with Wasted Muscles, Weakness, Weight Loss, Anemia, Skin Hemorrhages, Anorexia. GFW

What Is Cachexia?

C achexia is a state of ill health involving deteriorating body composition that is characterized by general malnutrition and loss of lean tissue such as muscle.

Q: What are typical findings in cachexia?

A: Arm muscle triceps (the muscles at the back of the upper arm), skin folds, subscapular skin folds, fat area index, and bone mineral content are significantly lower than normal.

Cachexia may develop in protein-losing enteropathy such as celiac disease, chronic or severe infection such as pneumonia, tuberculosis, malaria, or many chronic diseases such as heart failure and cancer.

Cachexia can develop in persons of any age.

What Is Cachexia In Celiac Disease and/or Gluten Sensitivity?

Epilepsy (Convulsions)

chronic diarrhea gluten celiac disease symptomWhat Is Chronic Diarrhea?

C hronic diarrhea is an intestinal motility disorder characterized by 1) alteration in stool formation causing loose to fluid movements and quantity of movements with or without abdominal pain and 2) interference with normal carbohydrate salvage by the intestinal microbe population.

The severity of diarrhea is determined by the frequency and quantity of fluid lost.

Q: What is carbohydrate salvage by microbes in the colon?

A: Carbohydrate salvage in the colon is the necessary process whereby billions of microbes normally present in the colon work to breakdown undigestible carbohydrate foodstuffs such as fiber that continually arrive from the small intestine.

The microbial action releases energy to the body that would otherwise be lost with defecation, generates short-chain fatty acids, and stimulates sodium and fluid absorption. In this important process, butyrate and proprionate are produced which nourish the colonocytes (cells that line the colon), and acetate is produced for the liver.

While diarrhea may be a common symptom of small bowel mucosal disease, the consequent malabsorption can lead to substantial malnutrition and nutrient deficiencies. The small intestine, unlike the colon, has been relatively inaccessible, and systematic evaluation is often necessary to identify and treat small intestinal mucosal diseases that lead to diarrhea. All patients with severe diarrhea or diarrhea associated with features suggestive of malabsorption may have a disease of the small intestinal mucosa that requires careful evaluation and targeted management.1

What Is Chronic Diarrhea In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Murray JA1, Rubio-Tapia A. Diarrhoea due to small bowel diseases. Best Pract Res Clin Gastroenterol. 2012 Oct;26(5):581-600. doi: 10.1016/j.bpg.2012.11.013. []

Constipation Alternating with Diarrhea

Bristol Stool Chart Showing Normal and Abnormal Stool.
Bristol Stool Chart Showing Normal and Abnormal Stool.

What Is Chronic Constipation Alternating With Diarrhea?

Chronic 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?

Ichthyosis, Acquired  

cheilosisWhat Is Cheilosis?

C heilosis is a painful feature of nutritional deficiencies, especially riboflavin and/or pyridoxine deficiency, and less frequently, from vitamin B12, folic acid, and iron. It is characterized by redness of the lips with cracking and weeping in the corner of the mouth.

Q: What is the consequence of weeping at the corners of the mouth?

A: The open sores that develop at the corners of the mouth invite infection by candida albicans, a yeast organism, and less commonly by bacteria normally present on the skin such as staphylococcus aureus.

These sores make opening the mouth very painful and so restrict eating, talking, socializing, and dental care.

What Is Cheilosis In Celiac Disease and/or Gluten Sensitivity?