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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 [↩]

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 [↩]

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?

Hemochromatosis (Iron Overload Disease)

Hemochromatosis
Microscopic View of Hemochromatosis Stained Blue. Courtesy Wikimedia

What Is Hemochromatosis?

Hemochromatosis, also called iron overload liver disease, is a common inherited disease in the Caucasian population that is characterized by increased iron deposition within the tissues (overload) associated with injury to them.

Hemochromatosis is an autosomal recessive disease, meaning a pair of abnormal genes are inherited from each parent. Parents are unaffected because they carry only one gene.

Q: Where is iron deposited?

A: In hemochromatosis, more iron is absorbed from the small intestine than is needed by the body. Subsequently, because the body has no satisfactory means to release iron overload, excess iron is deposited in various organs such as the liver causing cirrhosis, joints causing arthritis, and the pancreas causing diabetes mellitus.1

Consumption of alcoholic drinks with food should be avoided because alcohol increases leaky gut and greatly increases the absorption of iron. On the flip side, eggs and foods containing calcium such as milk and cheese are beneficial for hemochromatosis because they impair the absorption of iron. Another iron inhibitor is food that contains phytic acid which includes the bran and outer layer of grains, seeds, nuts, peas, beans, and lentils.

Iron overloading, as measured by a random (non-fasting) elevated transferrin saturation value, is estimated to occur in 1 to 6 people per 100 in the United States according to the CDC (Center for Disease Control and Prevention). Too much iron increases the risk for metabolic syndrome, type 2 diabetes mellitus, cancer, liver disease, and osteoporosis.

Medical treatment to remove excess iron from the body uses phlebotomy that draws blood through a vein and/or certain injectable drugs (deferoxamine and deferairox) that bind to iron.

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

Sources:
  1. www.irondisorders.org [↩]

Cirrhosis, Primary Biliary

biliary system primary biliary cirrhosisWhat Is Primary Biliary Cirrhosis?

Primary biliary cirrhosis (PBC) is a biliary tract disease characterized by chronic cholestasis (build-up of bile) and gradual destruction of bile ducts within the liver, called intrahepatic bile ducts, caused by chronic inflammation.

Primary biliary cirrhosis 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 is the end result of destruction of bile ducts?

A: The end result of destruction of bile ducts is liver damage.

Injured liver tissue from chronic inflammation and the buildup of bile leads to cirrhosis, a condition in which the liver slowly deteriorates and malfunctions.

Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. Scarring also impairs the liver’s normal ability to control infections, remove bacteria and toxins from the blood, process nutrients, hormones, and drugs, make proteins that regulate blood clotting, produce bile, and effectively replace its own cells when they become damaged.2

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.

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 and fat-soluble vitamins A, D, E, and K 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 which can then be absorbed into the body.

Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. Bile is continually made by the liver from phospholipids, bile acids, cholesterol, and aging blood cells it removes from circulation. As such, bile must continually flow out of the liver to prevent build-up in the liver.

There is no cure for primary biliary cirrhosis.

What Is Primary Biliary Cirrhosis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. 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. [↩]
  2. http://digestive.niddk.nih.gov/ddiseases/pubs/primarybiliarycirrhosis/ [↩]

Immune Thrombocytopenic Purpura

Photo of Skin Rash in ITP Courtesy Wikipedia.
Photo of Skin Rash in ITP Courtesy Wikipedia.

What Is Immune Thrombocytopenic Purpura?

Immune thrombocytopenia purpura (ITP), formerly called idiopathic, is an immune mediated bleeding disorder characterized by destruction of circulating platelets (thrombocytes) by autoantibodies in the presence of normal bone marrow and without other conditions that cause bleeding problems including many medications.

Q: How do autoantibodies destroy platelets?

A: Autoantibodies bind to normal platelet surface antigens (targets) which forms a complex that is cleared from blood by the reticuloendothelial system. Consequently, this condition results in an abnormal decrease in the number of platelets circulating in blood plasma.

Platelets are cells that are needed to stop bleeding. A normal platelet count is in the range of 150,000 to 450,000. With ITP, the platelet count is less than 100,000. By the time significant bleeding occurs, the patient may have a platelet count of less than 10,000. The lower the platelet count, the greater the risk of bleeding. 

Because of inability of blood to properly clot due to lack of sufficient platelets, a distinctive purplish rash develops under the skin from blood leakage and an appearance of many small red spots of varying size can cover the skin. Depending on the number of platelets, there may be minimal to extensive bleeding in various parts of the body.  Bleeding in the brain is the worst complication, causing death in approximately 1% of affected children and 5% of affected adults.

Immune thrombocytopenic purpura is common in childhood, on average 50 cases per 1,000,000 per year with same incidence in boys as girls. It may follow a viral infection or immunization and is caused by an inappropriate response of the immune system to cross react against the body’s platelets.1

The incidence of immune thrombocytopenic purpura in adults is approximately 66 cases per 1,000,000 per year.  Older persons and persons with a previous history of hemorrhage are at increased risk of severe bleeding in adult ITP.  

Spontaneous remission occurs in most children (80%).  Remission in adults usually requires treatment. 

What Is Immune Thrombocytopenic Purpura In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Dogan M, Sal E, Akbayram S, Peker E, Cesur Y, Oner AF. Concurrent celiac disease, idiopathic thrombocytopenic purpura and autoimmune thyroiditis. Clin Appl Thromb Hemost. 2011 Nov-Dec;17(6):E13-6. doi: 10.1177/1076029610378502. Epub 2010 Aug 3. [↩]

Primary Sclerosing Cholangitis 

A 3D Image From Magnetic Resonace Cholangiography. NIHMS
A 3D Image From Magnetic Resonace Cholangiography showing biliary tree. NIHMS

What Is Primary Sclerosing Cholangitis?

Primary 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:
  1. 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. [↩]
  2. 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. [↩]
  3. 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. [↩]
  4. Meakem TJ 3rd, Schnall MD. Magnetic resonance cholangiography. Gastroenterol Clin North Am. 1995 Jun;24(2):221-38. [↩]

Neutropenia 

neutrophilWhat Is Neutropenia?

Neutropenia  is a blood disorder characterized by presence of an abnormally low number of neutrophils.

Neutrophils are white blood cells (leukocytes) that serves as the primary defense against infections by destroying bacteria in the blood. 

Specfically, neutrophils are a type of granulocyte that contain granules filled with potent chemicals to break down the microbes they ingest. Some of these chemicals, such as histamine, also contribute to inflammation and allergy.

The process of eating and digesting microbes is called phagocytosis. Neutrophils are phagocytes.1

Q: How do neutrophils eat microbes?

A: Segmented neutrophils  are the mature phagocytes that migrate through tissues to destroy microbes and respond to inflammatory stimuli. Segmented neutrophils comprise 40-75 % of the peripheral leukocytes. They are usually 9 to 16 µm in diameter. The nuclear lobes, normally numbering from 2 to 5, may be spread out so that the connecting filaments are clearly visible, or the lobes may overlap or twist. The chromatin pattern is coarse and clumped. The cytoplasm is abundant with a few nonspecific granules and a full complement of rose-violet specific granules.1

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

Sources:
  1. http://www.wadsworth.org/chemheme/heme/microscope/seg.htm [↩] [↩]

Erythroblastopenia, Transient

Courtesy of slideshow.net
Courtesy of slideshow.net

What Is Transient Erythroblastopenia?

Transient erythroblastopenia is a rare disorder of red blood cell formation characterized by brief, reversible disappearance of erythroblasts (red blood cell precursors) in the bone marrow of children.

Q: What do the red blood cells look like?

A: Circulating red blood cells appear normal so that the anemia which develops is a normocytic (normal cellular) anemia in contrast to microcytic (small cell) anemia in iron deficiency or macrocytic (large cell) anemia in vitamin B12 or folic acid deficiency.

Because new red blood cells are failing to mature, packed red blood cell transfusions may be necessary in severe anemia.

In adults, this disorder is called pure red blood cell anemia.

What Is Transient Erythroblastopenia In Celiac Disease and/or Gluten Sensitivity?

Milk Intolerance – Bovine Beta Casein Enteropathy

Cows Milk enteropathyWhat Is Milk Intolerance (Bovine Beta Casein Enteropathy)?

Bovine 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?