Low plasma proteins found in blood indicates an abnormal blood level.
Plasma proteins are any of the proteins that constitute about 6% to 7% of the blood plasma in the body. They include albumin, fibrinogen, prothrombin, and the gamma globulins. All plasma proteins except the gamma globulins are produced in the liver.1
Q: Which protein is most abundant in blood?
A: Of the dozens of plasma proteins, albumin makes up more than half. Albumin level is the most frequently tested in the presence of weight loss and other signs of poor nutrition. Albumin helps maintain water balance that affects osmotic pressure, increase blood viscosity, and helps maintain blood pressure.1
Other commonly tested blood proteins are globulins which make up about a third of plasma proteins. Lab reports show the ratio between albumin and globulin, as well as, their individual values. Fibrinogen, essential for clot formation, makes 7% of plasma proteins while regulatory proteins, which include enzymes and hormones, make up 1%.
What Are Low Plasma Proteins In Celiac Disease and/or Gluten Sensitivity?
Microscopic View of a Liver Granuloma. Courtesy pathology.med.umich.edu/greensonlab.
What Is Hepatic Granulomatous Disease?
H epatic granulomatous disease is an infiltrative chronic liver disorder characterized by growth of small granulomas.
Rather than being a final diagnosis, the presence of hepatic granulomas entails the need for further investigations towards identifying the underlying etiology, with a pathologist being at the center of the diagnostic process.1
Q: What are hepatic granulomas?
A: Hepatic granulomas are unique inflammatory formations that require liver biopsy for diagnosis.2
Hepatic granulomas develop through the interactions of T lymphocytes and macrophages, with the integral involvement of T-helper (T(H)) 1 or T(H)2 pathways or both, depending on the specific granulomatous disease.
Hepatic granulomas may be detected clinically by elevated levels of serum alkaline phosphatase and g-glutamyltransferase enzymes, damage to specific structures (e.g., intrahepatic bile ducts in primary biliary cirrhosis), or infrequently, progressive liver disease with portal hypertension and cirrhosis (e.g., sarcoidosis).
Systemic immunologic disorders, infectious diseases, drug hepatotoxicity, and reaction to neoplastic disease are the major causative factors responsible for granulomas in the liver.3
What Is Hepatic Granulomatous Disease In Celiac Disease and/or Gluten Sensitivity?
Sources:
Turhan N, Kurt M, Ozderin YO, Kurt OK. Hepatic granulomas: a clinicopathologic analysis of 86 cases. Pathol Res Pract. 2011 Jun 15;207(6):359-65. doi: 10.1016/j.prp.2011.03.003. Epub 2011 Apr 30. [↩]
D iabetic instability, also called brittle diabetes, is poor control of blood sugar characterized by frequent rise (hyperglycemia) and fall (hypoglycemia). These fluctuations can be life-threatening and cause unnecessary complications.
Q: What are complications in diabetes?
A: Complications of diabetes include any/all of the following:
Peripheral neuropathy that causes burning, numbness, or tingling in the extremities.
Skin infections and ulcers that do not heal and can lead to amputation of toes, feet or legs.
Damage to retina that can progress to blindness.
Cataracts and glaucoma that impair vision and can cause blindness.
Increased susceptibility to serious infections of the genitourinary tract, lung and upper respiratory tract that can become systemic and life-threatening.
Kidney disease that can lead to kidney failure.
Heart disease that can lead to heart failure.
Vascular disease that can lead to stroke.
Impaired motility in digestive tract that can lead to dyspepsia and constipation.
Pregnancy complications.
Shortened life expectancy.
The main causes of brittleness include malabsorption, certain drugs (alcohol, antipsychotics), defective insulin absorption or degradation, defect of hyperglycemic hormones especially glucocorticoid and glucagon, and above all delayed gastric emptying as a result of autonomic neuropathy.1
What Is Diabetic Instability In Celiac Disease and/or Gluten Sensitivity?
Sources:
Vantyghem MC, Press M. Management strategies for brittle diabetes. Ann Endocrinol (Paris). 2006 Sep;67(4):287-96. [↩]
Malignant lymphoma high grade B-cell. Courtesy Wikimedia
What Is B-Cell Non-Hodgkin’s Lymphoma?
B cell non-Hodgkin’s lymphoma is a malignant, monoclonal (arising from a single cell) proliferation of lymphocytes that is preceded by lymphadenopathy and characterized by varying, less predictable spread than Hodgkin’s disease.
Lymphadenopathy is enlargement of lymph nodes greater than 1.5 cm caused by activation and increased production of lymphocytes and phagocytes (type of white blood cell that engulfs pathogens during infection) or invasion by a tumor.
Q: How does this type of lymphoma develop?
A: 80% to 85% of non-Hodgkin’s lymphoma arise from B-lymphocytes (B-cells).
What Is B Cell Non-Hodgkin’s Lymphoma In Celiac Disease and/or Gluten Sensitivity?
EATL of Jejunum with Thickening And Yellowish Ulcers Visible. Courtesy pubcan.org
What Is Enteropathy-Associated T-Cell Lymphoma?
E nteropathy associated T-cell lymphoma (EATL), although rare, is a tumor of intraepithelial lymphocytes. It is the most common primary gastrointestinal T-cell lymphoma and is characterized by its aggressive course and poor prognosis.
Primary means this malignancy starts out in the intestinal wall rather than spreading to it from a tumor somewhere else in the body.
EATL usually affects the jejunum and grossly (visible to the eye) appears as multiple ulcers causing circumferential thickening of affected bowel wall without the formation of definite tumor masses most commonly in the proximal small bowel. As such, patients may present with intestinal perforation, obstruction or hemorrhage.1
Mesenteric lymph nodes in the abdomen are commonly involved.2
Q: How is EATL diagnosed?
A: Work-up of EATL must include immunohistology, T-cell flow cytometry, T-cell rearrangement and adequate imaging with CT and PET scanning.3
Management of EATL requires a combination of early diagnosis and treatment by surgical resection followed by chemotherapy to achieve treatment success. Overall however, the treatment completion rate remains at 50% and EATL carries a poor prognosis with a 5-year survival rate of <20%.4
What Is Enteropathy-Associated T-Cell Lymphoma In Celiac Disease and/or Gluten Sensitivity?
Sources:
Pun AH, Kasmeridis H, Rieger N, Loganathan A. Enteropathy associated T-cell lymphoma presenting with multiple episodes of small bowel hemorrhage and perforation. J Surg Case Rep. 2014 Mar 20;2014(3). pii: rju013. doi: 10.1093/jscr/rju013. [↩]
Yang DH, Myung SJ, Chang HS, et al. A case of enteropathy-associated T-cell lymphoma presenting with recurrent hematochezia. Korean Journal of Gastroenterology = Taehan Sohwagi Hakhoe Chi. Dec 2003;42(6):527-32. [↩]
Meijer JWR, Mulder CJJ, Goerres MG, Boot H, Schweizer JJ. Coeliac disease and (extra)intestinal T-cell lymphomas: definition, diagnosis and treatment. Scandanavian Journal of Gastroenterology. Dec 2004;39(Suppl 241):78,7p. [↩]
Pun AH, Kasmeridis H, Rieger N, Loganathan Enteropathy associated T-cell lymphoma presenting with multiple episodes of small bowel hemorrhage and perforation.A. J Surg Case Rep. 2014 Mar 20;2014(3). pii: rju013. doi: 10.1093/jscr/rju013. [↩]
Bread is a Major Source of Maltose. Courtesy Johnson Mathey Catalyst
What Is Maltose Intolerance?
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?
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 [↩]
Pitting edema. Right photo shows that indent remains from pressing. Courtesy wikimedia.
What Is Edema?
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?
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?
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?
C ancer 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:
Feldman M, Friedman LS, Brandt LJ. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease. ed 9. Philadelphia: Saunders; 2010. pp. 745–767. [↩]
