Lipase Enzyme. Courtesy Johnson Matthey Catalysts.
What Is Macrolipasemia?
[dropcap]M acrolipasemia is a rare enzyme disorder characterized by altered molecules of lipase, a pancreatic enzyme needed to digest fats, that are abnormally bound with serum antibody proteins. These antibodies are commonly immunoglobulin G (IgG) and/or less likely immunoglobulin A (IgA).
Q: What happens when lipase is bound to immunoglobulins (IgA and/or IgG)?
A: The resulting molecule is too large to be filtered by the kidneys and excreted in the urine, consequently these abnormal molecules build up in the plasma causing sustained elevation of lipase levels called macrolipasemia.
Macrolipasemia occurs with or without macroamylasemia, which is the binding of immunoglobulin A and/or G to amylase, a pancreatic enzyme needed to digest starches.1
What Is Macrolipasemia In Celiac Disease and/or Gluten Sensitivity?
Sources:
La Villa G, Pantaleo P, Tarquini R, Cirami L, Perfetto F, Mancuso F, Laffi G. Multiple immune disorders in unrecognized celiac disease: a case report. World J Gastroenterol. 2003;9(6):1377-1380, Available at: http://www.wjgnet.com/1007-9327/9/1377.asp. Accessed Jan 3, 2005. [↩]
[dropcap]F[/dropcap]olic acid deficiency anemia, also called folate deficiency anemia, is a macrocytic anemia characterized by defective DNA synthesis of red blood cells that results from a lack of folate in the body.
Q: How does folate deficiency cause anemia?
A: Folates are a family of B vitamins and folic acid is an active form.
Folate is required for the formation of both red and white blood cells in the bone marrow and for their maturation.
Also, folate serves as a carrier in the formation of heme, which contains iron, and is the non-protein part of the hemoglobin molecule.1
Red blood cells provide oxygen to body tissues. When there are not enough red blood cells or when they cannot properly carry oxygen, the condition is called anemia. In folic acid deficiency anemia, the red blood cells are abnormally large. Such cells are called macrocytes (macro size cells). They are also called megaloblasts (mega size cells) as seen in the bone marrow where they are produced. This is why this macrocytic anemia is also called megaloblastic anemia.2
Tests that may be done to determine folate adequacy are complete blood count (CBC), red blood cell folate level, methylmalonic acid level, and homocysteine level. Folic acid deficiency anemia shows a decrease in red blood cell folate and/or serum folate levels and normal plasma methylmalonic acid level with elevated homocysteine blood level. These levels distinguish folic acid deficiency anemia from vitamin B12 deficiency anemia.3
What Is Folate Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?
What Is Milk Intolerance (Bovine Beta Casein Enteropathy)?
[dropcap]B ovine beta casein enteropathy is characterized by raised serum IgA antibodies to bovine beta casein found by blood testing and damage to mucosa of the jejunum found by biopsy.
The jejunum is the second section of the small intestine, between the duodenum and the ileum.
Mucosa damage is similar to damage caused by gluten.
Q: What is bovine beta casein?
A: Bovine beta casein is a protein found in cow’s milk.
An immune reaction to protein in milk is totally different from lactose intolerance. Lactose intolerance develops from deficiency of an intestinal enzyme called lactase which is required to digest lactose, the sugar in milk.
What Is Milk Intolerance In Celiac Disease and/or Gluten Sensitivity?
[dropcap]S mall bowel intussusception is a bowel derangement that is characterized by the slipping of one section of intestine into another, leading to bowel obstruction.
Acute bowel intussusception is a rare manifestation in adults, which mainly involves the small intestine.1
What Is Small Bowel Intussusception In Celiac Disease and/or Gluten Sensitivity?
Sources:
Grados A, Bernard F, Coquet-Reinier B, Rossi P, Bagneres D, Demoux AL, Marciano S, Frances Y, Granel B. Acute bowel intussusception revealing celiac disease a new case and literature review. Rev Med Interne. 2011 Oct;32(10):628-32. doi: 10.1016/j.revmed.2011.03.334 [↩]
Bread is a Major Source of Maltose. Courtesy Johnson Mathey Catalyst
What Is Maltose Intolerance?
[dropcap]M altose intolerance is an enzymopathy (enzyme failure) characterized by inability of the gut to properly break down maltose sugar molecules in food due to low maltase enzyme activity of the small intestinal lining.
Q: What is maltose and maltase?
A: Maltose is a double sugar made up of two molecules of glucose and is derived from starch. Maltase is the enzyme required to digest or release glucose from maltose. Maltase is produced in the microscopic brush border (microvilli) at the base of villi.
Here’s what happens when maltose is not digested:
Undigested maltose cannot be absorbed into the body but remains inside the small intestine where it acts osmotically to draw an unnatural amount of water from the body into the intestine which produces diarrhea.
Additionally, normal gut bacteria ferment the abnormal abundance of unabsorbed maltose, thereby generating an abundance of short-chain fatty acids and hydrogen gas which result in bloating and pain.1
Positive response to a breath hydrogen test (BHT), involving 1 – 3 hours of time post ingestion of maltose test dose, signifies malabsorption in the small intestine and fermentation in the colon. If BHT is positive before 60 minutes, the result implies bacteria is abnormally present in the small intestine, causing fermentation there.
What Is Maltose Intolerance 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?
[dropcap]A utoimmune 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 [↩]
Lost patch of hair at base of scalp due to alopecia areata. Courtesy Wikimedia,
What Is Alopecia Areata?
[dropcap]A lopecia areata is an autoimmune attack on hair follicles characterized by sudden hair loss involving scalp or beard, although any hairy area may be affected.
Areas of hair loss have a patchy pattern with sharply defined edges.
Q: Can all hair be affected?
A: All body hair may be lost, which is called alopecia universalis although this is uncommon.
In alopecia areata, white blood cells of the immune system attack the rapidly growing cells in the hair follicles. The affected hair follicles become small and drastically slow down hair production. Fortunately, the stem cells that continuously supply the follicle with new cells do not seem to be targeted. So the follicle always has the potential to regrow hair but regrowth is unpredictable.1
What Is Alopecia Areata In Celiac Disease and/or Gluten Sensitivity?
Pitting edema. Right photo shows that indent remains from pressing. Courtesy wikimedia.
What Is Edema?
[dropcap]E dema is an abnormal swollen condition of the skin characterized by excess extracellular fluid volume, meaning there is an increase of the fluid that normally surrounds cells. Edema may be hardly noticeable or it can become extensive.
Edema can have various appearances and can develop from various causes.
Q: What are the appearances and causes of edema?
A: Here are the appearances of edema:
Pitting edema. It is called pitting edema if when the skin is pressed with a finger, the indent remains. This edema results from fluid leaking out of the bloodstream into the surrounding tissues. Pitting edema can be a feature of many disorders including heart disease, kidney disease, vascular disease, cancer, and malnutrition.
Myxedema is a firm swelling or thickening of subcutaneous skin that does not pit, as seen in thyroid disease.
Here are causes of edema:
Local edema as a response to trauma or infection.
Lower extremity edema from poor circulation and malnutrition.
Edema in the lungs from right sided heart disease.
Abdominal edema from liver disease, intestinal disease.
Body wide edema from heart disease, kidney disease, thyroid disease.
What Is Edema In Celiac Disease and/or Gluten Sensitivity?
[dropcap]S ucrose intolerance is the inability to digest sucrose, a widely available sugar, while sucrosemia is the abnormal presence of sucrose in the bloodstream.
Q: Why cannot the body digest sucrose?
A: Sucrose, such as cane or beet sugar, is a double molecule sugar which must first be digested before being absorbed from the gut into the bloodstream. That is, sucrose must be split into its component single molecules of fructose and glucose, which are then properly absorbed.
The inability to properly digest sucrose results directly from low production and activity of sucrase in the small intestine. Sucrase is the specific enzyme that splits or digests sucrose.
Undigested sucrose does not remain idle. Its presence acts osmotically to draw water from the body into the intestine, causing watery diarrhea.
Meanwhile, microbiota (normal bacteria) in the colon eagerly ferment the abnormally present sucrose that arrives from the small intestine. Fermentation generates short-chain fatty acids and hydrogen gas, which results in bloating pain.1
In sucrosemia, sucrose molecules abnormaly pass through an unhealthy small intestinal lining and enter the bloodstream where there presence is abnormal. Sucrose in the blood is filtered out by the kidneys and excreted in urine.
Positive response to a breath hydrogen test (BHT), involving 1 – 3 hours of time post ingestion of sucrose test dose, signifies malabsorption in the small intestine and fermentation in the colon. If BHT is positive before 60 minutes, the result implies bacteria is abnormally present in the small intestine, causing fermentation there. Endoscopy is used to measure sucrase activity in tissue samples.
What Is Sucrose Intolerance And Sucrosemia In Celiac Disease and/or Gluten Sensitivity?
Reproduction of a lithograph plate showing inside of the stomach from Gray’s Anatomy. Courtesy Wikipedia Commons.
What Is Delayed Gastric Emptying?
[dropcap]D elayed gastric emptying is a stomach motility or movement disorder characterized by abnormally slow movement of gastric contents from the stomach through the pyloric sphincter into the duodenum, causing dyspepsia.
Q: What determines how fast the stomach empties?
A: How fast the stomach empties depends on the pressure of strong coordinated muscle contractions in the top region of the stomach propelling chyme against resistance at the pylorus (base region of the stomach).
Chyme is food that has been dissolved and thoroughly mixed with stomach secretions.
In the digestion of carbohydrate, protein and fat, protein leaves the stomach first (1 hour), then carbohydrates (1 1/2 to 2 hours), and fat takes longest to digest (2-4 hours). Plain water is able to pass through the pylorus within 5 minutes.
What Is Delayed Gastric Emptying In Celiac Disease and/or Gluten Sensitivity?
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