Malabsorption causing

Oelkers, P., et al. Primary bile acid malabsorption caused by mutations in the ileal sodium-dependent bile acid transporter gene (SLC10A2). J. Clin. Invest. 1997, 99, 1880-1887. 

Derfler K, Meryn S, Herold C, Neuhold N, Mostbeck G, Gangl A. Reversible malabsorption caused by high doses of cyclamate. Am J Med 1988 85(3) 446-7. 

Pernicious anaemia. End stage of 10-15% of autoimmune gastritis due to vitamin B12 malabsorption caused by depletion of gastric parietal cells and autoantibodies against intrinsic factor. Associated with a variety of autoimmune endocrine diseases (e.g. -Hashimoto thyroiditis, Addison disease) and autoimmune myasthenic syndromes. 

In one study in 10 healthy subjects, the bioavailability of a single 750-microgram dose of digoxin, using urinary excretion as a measure, was reduced by 20% by aminosalicylic acid 2 g four times daily for 2 weeks. This seems to be just another aspect of the general malabsorption caused by aminosalicylic acid. The importance of this interaction in patients is not known (it is probably small) but it would be prudent to monitor concurrent use. 

A number of genetic diseases that result in defects of tryptophan metabolism are associated with the development of pellagra despite an apparently adequate intake of both tryptophan and niacin. Hartnup disease is a rare genetic condition in which there is a defect of the membrane transport mechanism for tryptophan, resulting in large losses due to intestinal malabsorption and failure of the renal resorption mechanism. In carcinoid syndrome there is metastasis of a primary liver tumor of enterochromaffin cells which synthesize 5-hydroxy-tryptamine. Overproduction of 5-hydroxytryptamine may account for as much as 60% of the body s tryptophan metabolism, causing pellagra because of the diversion away from NAD synthesis. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

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. 

Stool may also be analyzed for mucus, fat, osmolality, fecal leukocytes, and pH. The presence of mucus suggests colonic involvement. Fat in the stool may be due to a malabsorption disorder. Fecal leukocytes can be found in inflammatory diarrheas including infections caused by invasive bacteria (e.g., E. coli, Shigella, and Campylobacter species). Stool pH (normally greater than 6) is decreased by bacterial fermentation processes. 

Small, D. M. Point mutations in the ileal bile salt transporter cause leaks in the enterohepatic circulation leading to severe chronic diarrhea and malabsorption. J. Clin. Invest. 1997,... 

Marcuard SP, Albemaz L, Khazanie PG Omeprazole therapy causes malabsorption of cyano-cobalamin (vitamin B12). Ann Intern Med 1994 120 211-215. 

EPEC causes a degeneration of the microvillus brush border, with cupping and pedestal formation of the plasma membrane at the sites of bacterial attachment and reorganization of cytoskeletal proteins [43, 44], Invasion has been observed in some clinical specimens, but the mechanism of how this bacteria produces diarrhea is not fully understood. Some possibilities include an increase in permeability and loss in microvilli leading to malabsorption. 

Malabsorption in SIBO is considered the consequence of abnormalities occurring mainly in the intraluminal environment in fact, the excessive number of intraluminal bacteria interfere with the absorption process. However, in some cases, the presence of bacterial species capable of more aggressive adhesion to small bowel epithelium is probably the cause of direct damage to the absorptive surface, in particular in the blind loop syndrome [10,11],... 

Moreover, adequate nutritional support is mandatory. The aim of this therapeutic measure should be the reintegration of both caloric and vitamin requirements, often defective in these patients. The nutritional defect is caused both by the predisposing condition and by the malabsorption syndrome. 

Radiographic study of the small intestine may provide useful information (A6, F12, F14, K4, L2, M2, P3). If a simple suspension of barium sulfate is used, the upper small intestine of a normal person usually displays a fine feathery appearance a similar pattern is seen in most patients with pancreatogenous malabsorption. In the patient with enteropathy, however, the opaque medium appears in massive clumps. This was at one time thought to be due to vitamin deficiencies, but it was demonstrated experimentally that the cause was flocculation of the barium sulfate with excessive secretion of mucus. This clumped appearance may be seen in normal children, possibly due to the... 

Chronic diarrhea is likely to result in a disturbance of water and salt balance. This has been shown to be so in the malabsorption syndrome (C9, F5). These changes, especially potassium deficiency, may cause some aggravation of the intestinal situation and increase of abdominal distension. Some improvement in absorption may consequently occur on appropriate rehabilitation. However, a residual defect of absorption will remain until more specific therapy is instituted. 

Calcium and magnesium deficiency also occur in some patients with the malabsorption syndrome and this may lead to tetany or bone changes. Low blood calcium levels may result from decreased absorption associated with lack of effective compensatory parathyroid activity. In patients in whom secondary hyperparathyroidism is effective, extensive loss of calcium from the bones may occur. The cause of the defective absorption of calcium in patients of the sprue group is complex and not yet fully understood (B3, Dl, Jl, M7, Nl). It is important that complications such as calcium or magnesium deficiency should be corrected before the final steps of definitive diagnosis are attempted. If this is not done, the secondary effects may obscure the results of other tests. 

The change in daily output of fecal fat forms the basis for the definitive diagnostic test for gluten induced enteropathy (F16, F21). This diagnosis is justified if the patient presented with the main features of the malabsorption syndrome, if the fecal fat output fell to normal levels on a gluten-free diet, and if subsequent reintroduction of gluten into the diet caused an unequivocal increase in fecal fat... 

The type of antibacterial therapy used is important. No effect need be expected from the use of a single chemotherapeutic agent. Successful use has been made of a triple combination of sulfonamide, chloramphenicol, and chlortetracycline (A8). It would seem advisable to avoid neomycin (FI, J2), since this can itself cause a malabsorption syndrome. 

Malnutrition can also cause secondary osteoporosis in persons with different deficiencies of substances such as calcium and vitamin D. Malnutrition due to starvation caused by most severe or terminal chronic diseases and malabsorption due to inflammatory bowel diseases (colitis, Mb Crohn) can give rise to rapidly diminishing bone tissue. 

Whipple s disease is a rare malabsorption syndrome, which usually occurs in men aged 30-60 years of age. It is caused by a bacterium, Tropheryma whippelii, which infiltrates the mucosa of the small intestine. The symptoms are characterised by arthritis, steatorrhea, weight loss, abdominal pain, fever and weakness. Treatment consists of prolonged administration of antibacterial drugs and the correction of nutritional deficiencies. 

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