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Celiac sprue disease

Noninfectious causes of acute diarrhea include drugs and toxins (Table 18-3), laxative abuse, food intolerance, irritable bowel syndrome (IBS), inflammatory bowel disease, ischemic bowel disease, lactase deficiency, Whipple s disease, pernicious anemia, diabetes mellitus, malabsorption, fecal impaction, diverticulosis, and celiac sprue. [Pg.312]

There are several forms of intolerance to lactose and galactose. Primary adult lactase deficiency is a normal age-related decrease in lactase activity seen in the majority of adults. Secondary lactase deficiency is a transient state of low enzyme activity following injury to the intestinal mucosa as a result of diseases such as celiac sprue, infectious gastroenteritis, and protein-calorie malnutrition. The last two states are common conditions (Dahlqvist 1983). [Pg.328]

The Lundh test also includes intestinal intubation and direct measurement of enzyme output in duodenal juice but uses a standardized test meal as a pancreatic stimulus. Because this test requires release of physiological regulatory mediators from the duodenal mucosa, it is less specific than the SC test and may render falsepositive results in intestinal diseases such as celiac sprue. [Pg.284]

Measurement of stool weight and quantitative fecal fat excretion on three consecutive days during a balanced diet are common screening tests for both pancreatic insufficiency and other pathologies that result in malabsorption. However, these tests are insensitive and nonspecific for pancreatic malfunction Steatorrhea occurs only after loss of more than 90% of exocrine parenchyma, and other causes of malabsorption (e.g., celiac sprue or Crohn s disease) may also induce abnormal fecal fat excretion of more than 7 g/day or more than 5 g/100 g. [Pg.284]

Gray, G. (1997). Persistence of diarrhea in treated celiac sprue Refractory disease of another organ s malfunction Gastroenterology 112,2146-2147. [Pg.153]

Celiac Disease (Celiac Sprue, Gluten-Sensitive... [Pg.1859]

FarreU RJ, Kelly CP. Celiac sprue and refractory sprue. In Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger and Fordtran s gastrointestinal and liver disease, 7th ed. Philadelphia WB Saunders, 2002 1817-41. [Pg.1885]

Intrinsic diseases of the small intestinal mucosa may impair mineral absorption. Such conditions as celiac sprue, dermatitis herpetiformis, infiltrative lymphomas, and occasionally inflammatory bowel disease produce diffuse mucosal damage. Protein energy malnutrition causes similar damage, and tropical enteropathy affects part of the population of developing countries living under adverse nutritional and hygienic conditions. [Pg.55]

In patients with vitamin D deficiency, oral vitamin D 50,000 units daily for 10 days or once weekly for 8 weeks, or 50,000 to 500,000 units intramuscularly is recommended. Serum calcium and 25(OH) vitamin D should be monitored periodically. Once replete, daily intakes of 600 to 1000 units are usually required. In the community or nursing home, vitamin D 100,000 units once per quarter is reasonable. In patients with vitamin D malabsorption (e.g., gluten-sensitive celiac sprue), 25(OH) vitamin D (calcidiol) administration is needed. In patients with severe hepatic or renal disease, calcitriol therapy may be required. This drug requires careful titration and serum calcium and creatinine monitoring because of its hypercalcemic potential and the limited calciuric ability of the dysfunctional kidney. [Pg.1657]

Celiac disease (celiac sprue) is an allergic inflammatory condition caused by poorly digested proline-rich sequences of wheat gluten and related proteins (p. 74). The disease is usually not recognized, but it may occur in 3% or more of the United States population. A T-cell response that causes destruction of the smaller intestinal mucosa, celiac disease is characterized by malabsorption and diarrhea. It can cause death by starvation. A primary target of the autoantibodies is a transglutaminase. ... [Pg.952]

Celiac disease (Celiac sprue)— Celiac disease is due to a genetically-inherited intolerance to wheat gluten, a main constituent of wheat flour, which is also present to a small extent in rye, barley, and oats, but not in rice. Such persons develop lesions of the small intestine which lead to diarrhea and malabsorption. It is not known why gluten causes intestinal damage. Symptoms usually arise during the first 3 years of life, but it may affect adults. Fbtients are relieved if gluten is excluded completely from the diet. [Pg.30]

I hope I have given you a feel for the relevance of chemistry in orphan diseases. In the case of celiac sprue, it has been half a century since W. K. Dicke, a Dutch pediatrician, identified gluten as the principal environmental trigger of the disease. During this period, the prevalence and etiology of this disease have been extensively investigated by biologists and clinicians, but it has been completely overlooked as a therapeutic opportunity. I firmly believe that chemistry can fill this gap in the next decade. Celiac disease is by no means... [Pg.163]

R8. Rubin, C. E., Brandborg, L. L., Phelps, P. C., and Taylor, H. C., Jr., Studies of celiac disease. I. The apparent identical and specific nature of the duodenal and proximal jejunal lesion in celiac disease and idiopathic sprue. Gastroenterology 38, 28-49 (1960). [Pg.119]

R12. Rubin, C. E., Celiac disease and idiopathic sprue. Some reflections on reversibility, gluten and the intestine. Gastroenterology 39, 260-261 (1960). [Pg.119]

Parenteral Anticoagulant-induced prothrombin deficiency hypoprothrombinemia secondary to conditions limiting absorption or synthesis of vitamin K (eg, obstructive jaundice, biliary fistula, sprue, ulcerative colitis, celiac disease, intestinal resection, cystic fibrosis of the pancreas, regional enteritis) drug-induced hypoprothrombinemias due to interference with vitamin K metabolism (eg, antibiotics, salicylates) prophylaxis and therapy of hemorrhagic disease of the newborn. [Pg.74]

Normally there is very little fat in the feces. However, fat content in stools may increase because of various fat malabsorption syndromes. Such increased fat excretion is steatorrhea. Decreased fat absorption may be the result of failure to emulsify food contents because of a deficiency in bile salts, as in liver disease or bile duct obstruction (stone or tumor). Pancreatic insufficiency may result in an inadequate pancreatic lipase supply. Finally, absorption itself may be faulty because of damage to intestinal mucosal cells through allergy or infection. An example of allergy-based malabsorption is celiac disease, which is usually associated with gluten intolerance. Gluten is a wheat protein. An example of intestinal infection is tropical sprue, which is often curable with tetracycline. Various vitamin deficiencies may accompany fat malabsorption syndromes. [Pg.499]

Nontropical sprue (adult celiac disease) results from a reaction to gluten, a protein found in grains. Intestinal epithelial cells are damaged and malabsorption results. Common symptoms are steatorrhea, diarrhea, and weight loss. [Pg.12]

Malabsorption Syndromes. Patients at risk include those with celiac disease, tropical sprue, cystic fibrosis, and short bowel syndrome. Excessive intake of oral zinc supplements can cause anemia and hematological abnormalities in the absence of occult blood loss. The copper deficiency is caused by zinc induction of metallothionein in the mtesti-nal mucosa, which then sequesters dietary copper, blocking its absorption. [Pg.1128]

Small bowel disease Mucosal lesion e.g. Celiac disease Tropical sprue Bacterial overgrowth deconjugation of bile salts) Parasites e.g. Giardia Intestinal resection Ileal disease - Crohn s Abetalipoproteinemia Drugs... [Pg.1855]

Celiac disease is sometimes called nontropical sprue, cefiac sprue, or gluten-sensitive enteropathy. [Pg.1859]

Secondary lactose intolerance may occur as a result of reduced enzyme activity following diffuse intestinal damage from infections (giardiasis, bacterial overgrowth, or viral gastroenteritis), ulcerative colitis, celiac disease, and tropical sprue. This deficiency is usually reversible following recovery from the disorder. [Pg.1863]

Celiac disease, now called sprue or gluten enteropathy, is probably due to a genetic flaw that entails immune system dysfunction. The people who get this disease have bowel reactions to the chemical gliaden in the gluten of wheat, barley, rye, and oats, with inflammation and mild-to-severe damage to the small intestinal wall. Symptoms include irritability, abdominal distress and distention, vomiting, diarrhea, terrible gas problems, and weight loss. [Pg.118]

Hypocupremia and low serum ceruloplasmin levels were reported in celiac disease (A13, LI), and in tropical (B36) and nontropical sprue (Cl, S40). Oral administration of copper to the patients with tropical sprue resulted in a sustained rise of serum copper in only one of four patients (B36). Stemlieb and Janowitz (S40) have recently shown that in nontropical sprue the absorption of copper from the gut is impaired. [Pg.37]

Malabsorption syndromes (e.g., tropical sprue, celiac disease, radiation enteritis or intestinal lymphectasia)... [Pg.977]


See other pages where Celiac sprue disease is mentioned: [Pg.249]    [Pg.775]    [Pg.249]    [Pg.775]    [Pg.1373]    [Pg.237]    [Pg.1865]    [Pg.304]    [Pg.1933]    [Pg.1665]    [Pg.267]    [Pg.155]    [Pg.158]    [Pg.159]    [Pg.159]    [Pg.160]    [Pg.160]    [Pg.85]    [Pg.91]    [Pg.93]    [Pg.1878]    [Pg.59]    [Pg.63]   
See also in sourсe #XX -- [ Pg.103 , Pg.104 , Pg.743 ]




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