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As I am sure you are aware,
Chronic lesions of the oral mucosa are disorders of the mouth that are characterized by soreness and sores of the soft mucosal lining of the mouth.
C hronic ulcerative jejunitis is a disease of the small intestine that is characterized by inflammation and ulceration of the mucosal lining of the jejunum.
Q: How do inflammation and ulceration affect digestion in the jejunum?
A: Inflammation swells the lining and this impairs absorption of nutrients. Together with ulceration the inflamed and swollen jejunum hampers peristalsis, or the rhythmic movement of food by intestinal muscles.
Impaired peristalsis promotes constipation and/or diarrhea. Bacterial overgrowth may develop. Ulcerations may bleed which could cause the development of iron deficiency anemia.
What Is Prolonged Prothrombin Time?Prolonged prothrombin time (PT) is a laboratory blood test result showing that blood clots too slowly which makes the patient subject to abnormal bleeding.
Q: What does the prothrombin time (PT) test measure?
A: The prothrombin test measures the clotting ability of blood protein factors I, II (prothrombin), V, VII, and X. If any of these factors are too low, it takes longer than normal for the blood to clot. Prothrombin is a vitamin K dependent factor meaning a deficiency of vitamin K will cause low prothrombin.
Blood is drawn into a blood collection tube with a light blue stopper which has a buffering additive. Tubes must be completely filled.
Anti-endomysium antibodies (EmA) are connective tissue autoantibodies produced in persons who have inherited the genes for celiac disease, an autoimmune disease, and are reacting to gluten in their diet.
Autoantibodies are abnormal in that they attack the body’s own tissue.
Q: What is endomysium?
A: Endomysium is the delicate connective tissue that surrounds individual muscle fibers. The autoantigen, or target, that stimulates the autoimmune response is the naturally occuring enzyme in endomysium called tissue transglutaminase (tTG), or more specifically tranglutaminase-2 (TG2). Anti-tissue transglutaminase antibodies recognize the same antigen as EmA, from which they differ in terms of detection method.
Anti-endomysium antibodies (EmA) are tested by the indirect immunofluorescence method and directed against “reticulin-like” fibres in connective tissue around smooth muscle fibres in the esophagus, liver, stomach, and bladder of monkeys, in the sections of the jejunum and kidneys of rats and in sections of the human umbilical cord. In comparison, for the determination of anti-tissue transglutaminase IgA and IgG antibodies, ELISA with human extractive or recombinant transglutaminase is recommended.1
EmA‐binding patterns in serum samples from patients with celiac disease have proved to be exclusively TG2‐targeted and the correlation between EmA and TG2 antibodies is therefore good. Evidence shows that celiac autoantibodies are produced in the small‐bowel mucosa.2
What Is Primary Biliary Cirrhosis?P rimary 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.
Anti-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.
Gluten Sensitivity is an umbrella term that refers to any and all problematic health responses to gluten in any body system. We first defined gluten sensitivity in our ground breaking text, Recognizing Celiac Disease first published in 2006. Gluten Sensitivity includes celiac disease, gluten allergy, and non-celiac gluten sensitivity reactions.1
Under Pathophysiology in Recognizing Celiac Disease, we confidently published the fact, against the opinion of some noted specialists but in accord with others, that “non-celiac gluten sensitivity” exists as a condition distinct from celiac disease and which must be distinguished from celiac disease for proper treatment of both.
Today, although there lacks a general agreement for the term “gluten sensitivity,” the medical community has accepted the reality of non-celiac gluten sensitivity.
As a result, researchers are calling this condition the “new frontier.” As Dr. Lundin has stated, “We are still challenged with finding stricter clinical criteria for the condition, developing a usable clinical approach for gluten challenge in these individuals, and understanding the pathogenesis of the condition.”2
Non-celiac gluten sensitivity is an innate immune response producing mild inflammation (Marsh I class) of the small intestine lining to gluten when present in the diet but negative to production of the anti-EMA, and anti-tTG immunoglobulins (humoral response), which are autoantibodies mounted in celiac disease.
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H ypertransaminasemia is a chronic condition of elevated blood liver transaminase enzymes, commonly called “liver enzymes,” that signifies hepatocellular (liver) injury.
Q: What are serum transaminases?
A: Transaminases are the liver enzymes ALT and AST. ALT is the abbreviation for alanine aminotransferase enzyme and AST is the abbreviation for aspartate aminotransferase enzyme.
Transaminases are commonly measured in routine blood tests to determine liver function. Elevated ALT and AST transaminases indicate inflammation of the liver. Other specific tests must follow to determine the cause of inflammation.
P olymyositis is a body-wide connective tissue disease resulting from autoimmune attack of skeletal muscles that is characterized by inflammatory and degeneratory changes. The course is unpredictable being marked by spontaneous flare-ups and remissions.
Polymyositis can begin slowly or abruptly according to the factor that is triggering the onset such as infection, medications like phenytoin, and autoimmune disease.
Progressive muscle weakness starts in the proximal skeletal muscles (muscles closest to the trunk of the body).
Skeletal muscles, also called voluntary, are muscles that move the body as we want, such as walking and lifting objects, as opposed to those we cannot voluntarily control, such as the muscles of digestion.
Q: What are the degeneratory changes in skeletal muscles?
A: In polymyositis, degeneratory changes in skeletal muscles means that muscles are being destroyed (called necrosis), resulting in fibrosis, or scarring. When scar tissue takes the place of lost muscle tissue, it cannot act like muscle to contract and relax. Muscle destruction is what causes muscle pain and weakness.
After the clinical work-up of exams and blood studies to determine muscle damage, the diagnosis of polymyositis is confirmed by muscle biopsy. See image at above left. The black dots are inflammatory cells. Edema (fluid) between cells caused by inflammation pushes muscle fibers apart.
There is no cure for polymyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for polymyositis is a corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone.
Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with polymyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion.1
Diagnosis is based on elevated muscles enzymes, increased urinary creatine level, and electromyograph abnormalities.
Polymyositis can affect people at any age. It is most common in adults between ages 50 and 70, and in children ages 5 to 15. It affects women twice as often as men and is more common in African Americans than Caucasians.2 The major causes of death from polymyositis are cancer and lung disease, including pneumonia. The 5-year mortality rate can be as high as 1 in 5 patients.2