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Autoimmune Hepatitis

 

Jaundice, or yellowing of the skin and sclera of eyes.
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:
  1. National Digestive Diseases Information Clearinghouse [↩]

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?… 

Pancreatic Insufficiency

Model of coagulation factors found in blood.
Model of coagulation factors found in blood.

What Are Low Coagulation Factors?

C oagulation factors II, VII, IX, X found in blood are essential for normal blood clotting.  Low coagulation factors on blood assay indicate an altered secondary coagulation disorder that is characterized by impaired clot formation.

Each coagulation factor must be present in sufficient quantity in order for normal clotting to occur, but the level required is different for each factor. Results are frequently reported as a percentage with 100% being normal. For example, a factor VIII that is 30% would be considered abnormally low.1

The production of the coagulation factors II, VII, IX, and X requires vitamin K without which the factors will be low.

Q: What happens when coagulation factors II, VII, IX, and X are low?

A: When any of the blood clotting factors are lacking or not working properly, the blood tests prothrombin (PT) and partial thromboplastin time (PTT) will be abnormally prolonged. Prothrombin and partial thromboplastin time measure the time it takes for blood to clot.  When you bleed, the body launches a series of activities that help the blood clot. This is called the coagulation cascade. There are three pathways to this event. These tests looks at coagulation factors, found in two of these pathways.2

What Are Low Coagulation Factors In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://labtestsonline.org/understanding/analytes/coagulation-factors/tab/test [↩]
  2. http://www.nlm.nih.gov/medlineplus/ency/article/003653.htm [↩]

Lymphadenopathy

Beaded Barium Swallow Shows Spasms of Espophagus. Courtesy Quizlet.com
Beaded Barium Swallow Shows Spasms of Espophagus. Courtesy Quizlet.com

What Are Esophageal Motor Abnormalities?

E sophageal motor abnormalities are disorders of the esophagus involving altered muscular motility characterized by impaired esophageal peristalsis, or the progressive wave-like movement that occurs automatically when food or fluids are swallowed.

Q: What is altered motility?

A: Altered motility describes the lack of coordinated muscular movements or weak muscular movement needed to rapidly propel food and fluids through the highly muscular esophagus from the throat to the stomach.

The esophagus is a tube-like organ that begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx and ends at the lower esophageal sphincter (LES).

The LES is a very strong, circular muscle surrounding the junction of the esophagus and stomach. The LES opens to allow swallowed food and liquids to enter the stomach and closes to prevent their travelling back into the esophagus.

Failure of the lower esophageal sphincter to remain tightly closed after swallowing allows stomach contents to reenter the esophagus giving symptoms of heartburn.

On the other hand, failure of the LES to relax traps the contents of the esophagus so that it cannot quickly empty into the stomach as it should. Because the esophagus is not designed to hold food/fluids, the abnormal expansion results in pain, anxiety and possibly vomiting and choking.  If the contents are aspirated into the windpipe upon choking, there will be coughing with attempts to clear it.

What Are Esophageal Motor Abnormalities In Celiac Disease and/or Gluten Sensitivity?

Gastrointestinal Complications Of Type I Diabetes Mellitus

Model of cholesterol molecule.
Model of cholesterol molecule.

What Is Low Cholesterol?

L ow cholesterol found in blood indicates an abnormal blood level of this essential lipid (fat) that is characterized by decreased production of steroid hormones and bile.

Cholesterol is a soft, fat-like substance found in the bloodstream and is an essential structural component in all body cells. It is required for membrane fluidity and permeability of cells. Within the cell membrane, cholesterol also functions in intracellular transport, cell signaling and nerve conduction.

Cholesterol is required for these essential body processes:

  1. Cholesterol is converted to bile by the liver and stored in the gallbladder until needed for digestion of fats in the small intestine.  
  2. Cholesterol is used by the adrenal glands to produce the steroid hormones cortisol and aldosterone.
  3. Cholesterol is used by the sex glands to make progesterone, estrogen, and testosterone and their derivatives.
  4. Cholesterol is needed for the production of vitamin D.

Q: What makes cholesterol bad for you?

A: There are different forms of cholesterol that can be bad or good depending on the level. In blood vessels, low-density lipoprotein (LDL or ‘bad’) cholesterol can abnormally join with fats and other substances to build up in the inner walls of arteries. The arteries can become clogged and narrow, and blood flow is reduced. This is atherosclerosis which can lead to stroke, heart attack and thrombosis.

High-density lipoprotein (HDL or ‘good’) carries harmful cholesterol away from the arteries and helps protect from heart attack and stroke.1

What Is Low Cholesterol In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=hdlldl [↩]

Hyposplenism

Heartburn Due to Acidic Stomach Contents Re-entering the Esophagus. Courtesy kaiserpermanente.org
Heartburn Due to Acidic Stomach Contents Re-entering the Esophagus.

What Is Heartburn?

H eartburn is a functional upper digestive symptom of esophagitis that is characterized by a burning sensation behind the breastbone.

Q: Why does esophagitis cause heartburn?

A: Esophagitis is inflammation of the mucosal lining of the esophagus. The most common cause of esophagitis is the re-entering of stomach contents into the esophagus because the lower esophageal sphincter (LES) does not close tightly after food or fluids enter the stomach from the esophagus and/or the LES does not remain tightly closed.

The LES 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 when powerful stomach muscles churn ingested food.

Damage to the lining of the esophagus (esophagitis) results upon contact with hydrochloric acid and pepsin in gastric juice. Hydrochloric acid, produced by the stomach to dissolve food, inflames the esophagus, which is the opposite, or alkaline. Pepsin, produced by the stomach to dissolve protein in swallowed food, acts on the inflamed esophagus to break down the protein in its sore wall.

Heartburn can be caused by other disorders such as low stomach acid, obesity, and smoking. Relaxation of the LES can also result from dietary items such as chocolate, mint, caffeine, and alcoholic drinks.

Who is Affected in the General Population? Heartburn affects an estimated 42% of the US population.1

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

Sources:
  1. http://informahealthcare.com/doi/abs/10.1185/03007990903553812. [↩]

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. [↩] [↩]

Diabetic Instability 

Vertebrae. Courtesy FreePik.com
Vertebrae. Courtesy FreePik.com

What Is Elevated Bone Alkaline Phosphatase?

E levated bone alkaline phosphatase (BALP) is a laboratory result that indicates an abnormal blood level of this bone enzyme.

A bone alkaline phosphatase blood level is one of the most frequently used biochemical markers of bone formation.

Q: Why is the purpose of  bone alkaline phosphatase?

A: Bone alkaline phosphatase is produced by bone cells called osteoclasts in normal bone maintenance for the purpose of breaking down old or damaged bone so that other bone cells called osteoblasts can fill in the excavated areas with new bone. This process keeps bone stong and healthy.

Elevated bone alkaline phosphatase shows that more bone is being broken down than is being replaced. It can be caused by hyperparathyroidism, bone tumors from cancer, and malnutrition.

What Is Elevated Bone Alkaline Phosphatase (BALP) In Celiac Disease and/or Gluten Sensitivity?

Diabetes Mellitus, Type I

Image depicts tissue transglutaminase (tTg).
Image Depicts Tissue Transglutaminase (tTG).

What Are Anti-tissue Transglutaminase Antibodies?

A nti-tissue transglutaminase antibodies (anti-tTG) are connective tissue autoantibodies and can be detected in blood samples from affected persons who are reacting to gluten in the diet.

Autoantibodies are abnormal because they attack the body’s own tissue, which in the case of these antibodies is tissue transglutaminase 2 (TG2).

Q: What is tissue transglutaminase 2 (TG2)?

A: Tissue transglutaminase 2 (TG2) is an enzyme that appears in many cell locations and is particularly abundant in endothelial cells that line the small intestine. It has been implicated in a variety of cellular processes, such as differentiation, cell death, inflammation, cell migration and wound healing.

The cell appears to adapt the dynamics of this enzyme to meet specific sub-cellular needs or to respond to stress or other stimuli. Substantial evidence indicates that the location of TG2 within cells is critical for the regulation of its various biochemical activities, which subsequently trigger diverse downstream events,1

Although initially studied as an enzyme within cells, TG2 is now known to be secreted also into the extracellular space (between cells) or onto the cell surface.1

Abnormal activation of TG2 or deregulation of its function(s) is involved in a variety of human diseases, such as celiac disease, diabetes, neurodegenerative diseases, multiple sclerosis and rheumatoid arthritis. A role in inflammatory disorders and septic shock has also been shown. Moreover, multiple studies have revealed elevated TG2 expression in many types of cancer cells.1

What Are Anti-tissue Transglutaminase Antibodies In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Piacentini M, D’Eletto M, Farrace MG, Rodolfo C, Del Nonno F, Ippolito G, Falasca L. Characterization of distinct sub-cellular location of transglutaminase type II: changes in intracellular distribution in physiological and pathological states. Cell Tissue Res. 2014 Dec;358(3):793-805. doi: 10.1007/s00441-014-1990-x. [↩] [↩] [↩]

Liver or Hepatic Granulomatous Disease 

This is a model of Immunoglobulin-G Antibody (IgG)
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?