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Lactose Intolerance

Lactose IntoleranceWhat Is Lactose Intolerance?

Lactose intolerance is a well known symptom of carbohydrate malabsorption characterized by inability to properly digest lactose, the sugar in milk, due to low lactase digesting activity in the small intestine.

Lactase is an enzyme produced by specialized cells in the tips of villi within the brush border of the small intestinal lining that digests lactose.

Lactose is a disaccharide, or double sugar, made up of a molecule of glucose and a molecule of galactose (simple sugars). Lactose cannot be absorbed as is into the body unless it is broken down by lactase into glucose and galactose.

Q: How does lactose cause diarrhea?

A: If lactose is not broken down, undigested lactose moves into the colon where it acts osmotically to draw water from the walls of the colon into the lumen, which causes diarrhea by the unnatural amount of water. How much water? Can be 2 liters! Meanwhile, the normal population of colonic bacteria ferment the undigested lactose, generating short-chain fatty acids and hydrogen gas, resulting in bloating pain and flatulence.

Testing for intolerance is based on the action of lactose to increase intestinal permeability.1 Positive response to a breath hydrogen test (BHT), involving 1 – 3 hours of time post ingestion of lactose 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 activity of lactase in a tissue sample.

Treatment is avoidance of milk and dairy products that contain lactose. Nevertheless, milk treated with lactase enzyme can be safely consumed. Fermented milk products like yogurt or kefir are safe because the lactose has been digested by organisms. If there is also a problem with milk protein, then no milk is acceptable that comes from the cow or animal that is causing the allergy.

What Is Lactose Intolerance In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. [↩]

Cancer, Post-Cricoid

Anatomy of Upper Airway and Throat. Courtesy Wikipedia.org
Anatomy of Upper Airway and Throat. Courtesy Wikipedia.org

What Is Post-Cricoid Carcinoma?

Post-cricoid carcinoma is a rare malignancy arising in the hypopharynx.

Q: What is the hypopharynx?

A: The hypopharynx is the lower portion of the pharynx that opens into the larynx. It is comprised of the postcricoid region, pyriform sinus, and posterior hypopharyngeal wall.

Tumors rarely appear in the posterior pharyngeal wall or postcricoid region without also involving the pyriform sinus. The lack of anatomic barriers between these sites and a propensity for these tumors to develop in the pyriform sinus and spread outward account for this phenomenon.

Overall prognosis for these tumors is poor. Because of the rich organic lymphatic and vascular networks, aggressive growth and early cervical metastases (compared with cancers at other head and neck sites) characterize these cancers.

A study investigating the clinical course of 21 patients with post-cricoid carcinoma found the 5-year cause-specific survival rate was 52%. All the patients who eventually died did so within 3 years of the treatment. Seven patients had distant metastases, representing a higher frequency as compared with that of patients with recurrence of the primary focus and cervical lymph node metastasis. All of these patients who had been treated by surgery died of the cancer.1

Unfortunately, hypopharyngeal cancers are discovered at a later stage than other head and neck cancers. The delay in diagnosis from symptom onset averages 10 months.2

What Is Post-Cricoid Carcinoma In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Asakage T, Nakao K, Ebihara Y, Fujishiro Y, Watanabe K. A clinical study of post-cricoid carcinoma. Acta Otolaryngol Suppl. 2007 Dec;(559):118-22. doi: 10.1080/03655230701599354. [↩]
  2. http://emedicine.medscape.com/article/848359-overview [↩]

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/ [↩]

Maltose Intolerance

Fermentation of Grain by Yeast Releases Carbon Dioxide Which rises the Dough. Courtesy Johnson Mathey Catalyst
Bread is a Major Source of Maltose. Courtesy Johnson Mathey Catalyst

What Is Maltose Intolerance?

Maltose 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?

Sources:
  1. Krause’s Food, Nutrition, & Diet Therapy. 10th Edition. Kathleen Mahan, Sylvia Escott-Stump. 2000. W.B. Saunders Company. [↩]

Cancer Of The Esophagus 

A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.
A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.

What Is Cancer Of The Esophagus?

Cancer of the esophagus is a malignancy arising in the stratified squamous cell lining of any part of the esophagus and having a poor prognosis.

This tumor first invades the deeper layers of the esophagus which includes the layer beneath the mucosa (submucosa) and muscle before it may invade structures close to it including the aorta and trachea. Later, it may spread to organs further away such as the liver, lungs and bones.

Q: What is the stratified squamous cell lining of the esophagus?

A: Stratified squamous cells are flat epithelial cells that are composed of several layers, called the epithelium. This type of epithelium forms the surface mucosa that lines the inside of the esophagus.

The esophagus itself 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 in the throat and ends at the lower esophageal sphincter (LES).

The LES is a 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.

Who is Affected in the General Population?

Esophageal cancer is the fifth leading cause of death in men from cancer worldwide.1

What Is Cancer Of The Esophagus In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Feldman M, Friedman LS, Brandt LJ. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease. ed 9. Philadelphia: Saunders; 2010. pp. 745–767. [↩]

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. [↩]

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?

Dysphagia (Difficulty Swallowing)

What Is Dysphagia? Dysphagia 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? A:… 

Abdominal Distention, Chronic  (Bloating)

chronic abdominal distention celiac disease gluten symptomWhat Is Chronic Abdominal Distention?

Abdominal distention, or bloating, is characterized by enlargement in normal size of abdomen not due to fatty tissue.

Q: Why does the abdomen enlarge?

A: The abdomen enlarges because the bowel is dysfunctional. Loops of bowel usually lack normal peristalsis (rhythmic wave-like muscle movement) trapping gas in stagnant loops of bowel, inflammation swells loops of bowel also trapping gas, and dysbiosis overproduces gas. All these factors distend the abdomen.

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

Ulceration And Stenosis, Postbulbar Duodenal

What Is Postbulbar Duodenal Ulceration/Stenosis?

Postbulbar duodenal ulceration is a chronic inflammatory disorder characterized by thickening of the intestinal lining with excoriation penetrating the muscularis mucosae (muscle layer of the intestine) associated with villous atrophy.

The ulcer is well-defined. Stenosis due to thickening of the area narrows the hollow inside of the duodenum which impairs passage of foodstuffs and may lead to obstruction.

Q: Is postbulbar duodenal ulceration painful?

A: Postbulbar duodenal ulceration may not cause symptoms but usually causes gnawing pain that is relieved by eating food. After eating there develops nausea and bloating.

Complications include obstruction, bleeding, and perforation of the duodenal lining. Ulcers do not usually become malignant.

What Is Postbulbar Duodenal Ulceration/Stenosis In Celiac Disease and/or Gluten Sensitivity?