Celiac Sprue Disease Essay Research Paper What

Celiac Sprue Disease Essay, Research Paper

What if your doctor told you that eating a certain food say pizza would be devastating to your health. You might not like it, but you’d learn to live with it. But what if it was more than just pizza. What if you were told to avoid all bread, breadcrumbs, and pasta. And dozens of breakfast cereals, canned soups, luncheon meats, and salad dressings. And a wide variety of ice creams, ice cream cones, cookies, cakes, puddings, and pies. And most chewing gum, beer, canned tuna, and hot dogs.

That’s what it’s like for people who have celiac disease. Celiac disease, also known as gluten-sensitive enteropathy, celiac sprue, nontropical sprue, and idiopathic steatorrhea, is a disease whose extensive and variable symptoms challenge physicians to make a correct diagnosis in a timely fashion. The term “celiac sprue” has been applied to a clinical syndrome characterized by signs and symptoms of malabsorption, such as diarrhea and weight loss caused by eating grains. The term “gluten-sensitive enteropathy” more correctly defines the clinical pathologic disease caused by an immune-mediated sensitivity to gluten, a protein found in many cereal grains, principally wheat, barley, rye, and to a lesser degree oats. Most nutritionists agree that gluten is not present in rice, white or sweet potatoes, and corn.

Over 100 years ago a British physician named Samuel Gee described the “coeliac affection.” Dr. Gee observed the syndrome in people of all ages, but especially in children who had chronic diarrhea, weight loss, edema, and a distended abdomen. The led to death unless cured by various diets. Many other physicians followed in the footsteps of this pioneer, prescribing diets based on rice, bananas, and lamb, which often led to symptomatic improvement of these children with celiac sprue.

It wasn’t until the end of World War II that the connection between the consumption of wheat and rye flour and the incidence of celiac sprue was made. Dutch pediatricians noted that during the war, when these flours were in short supply, celiac patients improved and few new cases were seen. After the war, when adequate food supplies were restored to the civilian population, celiac disease reappeared with regularity.

Based on this clinical observation, scientist then determined that a water-insoluble protein component of these grains, gluten, was the substance that damaged the intestine in certain individuals. Not until the 1950s were the characteristic microscopic changes in the lining of the intestine documented. The arrival of techniques to obtain biopsy specimens of the small intestine opened the floodgates of research activity, which taught us much of what we know today about this disease.

Most recently, research has been conducted that describes the immunologic mechanisms causing this type of intestinal injury. The vast majority of patients with celiac sprue possess a particular tissue type, which can be thought of in a similar fashion to each person’s blood type. If one possesses the right, or more correctly, wrong tissue type, there is a likelihood of developing celiac sprue.

The exact mechanism for this phenomenon is unknown, but several theories have been proposed. First, patients with celiac sprue may lack an enzyme necessary to digest toxic fractions of gluten. Second, celiac disease-associated tissue-type antigens are found on the surface of the intestinal cells that face the lumen (the part of the tubular intestine that is exposed to dietary contents). It is believed that these cells may bind with the toxic fractions of gluten. On the surface of the intestinal cell, gluten acts as a foreign substance, eliciting an immune reaction that destroys the intestinal-lining cells. Of course, each individual’s tissue type is inherited. Because of this, if one of a pair of identical twins develops celiac disease, the other invariably will develop it as well.

Approximately 25% of Caucasians, in whom the disease is most common, possess the celiac disease-associated tissue-type antigens, but obviously not all of them develop the disease. Other unknown factors begin the chain reaction of immunologic injury. One possible cause is infection with common agents as viruses. At least one virus has been shown to posses a similar protein composition to toxic fractions of gluten. Theoretically, infection with this virus exposes the immune system to an antigen that is “shared” with the intestinal epithelium, or lining. Long after the virus has disappeared, the immune system continues to attack the body’s own tissue, which produces celiac disease.

Once the immune system is activated in this way, there is progressive destruction of the surface cells that are normally responsible for absorption in the small intestine. The injury is most severe in the proximal intestine (jejunum) and becomes progressively less severe in the more distal intestine (ileum).

The reason for this pattern of distribution is probably due to the fact that gluten is gradually digested and eliminated from the intestinal lumen as the meal literally progresses downstream. The most proximal intestine, called the duodenum, is the primary site for absorption of minerals such as iron, calcium, and magnesium.

Extensive injury to the small bowel results in decreased absorption of nutrients such as carbohydrates, protein, and fat. Wh