Intestinal malabsorption, vitamin

Clinical stresses which interfere with vitamin metabohsm, can result in calcium deficiency leading to osteomalacia and osteoporosis (secondary vitamin D deficiency). These stresses include intestinal malabsorption (lack of bile salts) stomach bypass surgery obstmctive jaundice alcoholism Hver or kidney failure decreasing hydroxylation of vitamin to active forms inborn error of metabohsm and use of anticonverdiants that may lead to increased requirement. 

Hypolipoproteinemias Abetaiipoproteinemia No chylomicrons, VLDL, or LDL are formed because of defect in the loading of apo B with lipid. Rare blood acylglycerols low intestine and liver accumulate acylglycerols. Intestinal malabsorption. Early death avoidable by administration of large doses of fat-soluble vitamins, particularly vitamin E. 

Hypocalcemia - To correct plasma calcium levels (eg, neonatal tetany and tetany due to parathyroid deficiency, vitamin D deficiency, alkalosis) prevention of hypocalcemia during exchange transfusions conditions associated with intestinal malabsorption. 

Factors which tend to decrease the availability of this vitamin include (1) cooking losses, since the vitamin is heat labile (2) cobalt deficiency in ruminants (3) intestinal malabsorption or parasites (4) lack of intrinsic factor (5) intestinal disease (6) aging (7) vegetarian diet (8) excretion... 

In mild forms of malabsorption, vitamin D (25,000-50,000 units three times per week) should suffice to raise serum levels of 25(OH)D into the normal range. Many patients with severe disease do not respond to vitamin D. Clinical experience with the other metabolites is limited, but both calcitriol and calcifediol have been used successfully in doses similar to those recommended for treatment of renal osteodystrophy. Theoretically, calcifediol should be the drug of choice under these conditions, since no impairment of the renal metabolism of 25(OH)D to l,25(OH)2D and 24,25(OH)2D exists in these patients. Both calcitriol and 24,25(OH)2D may be of importance in reversing the bone disease. As in the other diseases discussed, treatment of intestinal osteodystrophy with vitamin D and its metabolites should be accompanied by appropriate dietary calcium supplementation and monitoring of serum calcium and phosphate levels. 

Gastrointestinal Incontinence of feces, intestinal malabsorption, fat-soluble vitamins, rectal discharge, rectal bleeding... 

Second the test is repeated with intrinsic factor added to the oral dose. The radioactive vitamin B is now absorbed in pernicious anaemia (but not in intestinal malabsorption) and is detected in plasma and urine. Both stages of the test are needed to maximise reliability of diagnosis of pernicious anaemia. 

Adverse effects include flatulence and liquid, oily stools, leading to faecal urgency, abdominal and rectal pain. Symptoms may be reduced by adhering to a reduced-fat diet. Low plasma concentrations of the fat-soluble vitamins A, D and E have been foimd. OrUstat is contraindicated where there is chronic intestinal malabsorption or cholestasis. 

Intestinal malabsorption of vitamin B12 may be caused by gastrectomy or ileal resection, with an inverse relationship between the length of ileum resected and the absorption of vitamin B12. Other causes of malabsorption are tropical sprue, inflammatory disease of the small intestine, intestinal stasis with overgrowth of colonic bacteria, which consume the vitamin 6,2 ingested by the host, and HIV infection. Another cause of vitamin B malabsorption is failure to extract cobalamin from food. Some patients fail to absorb cobalamin bound to food, whereas absorption of nonfood-bound cobalamin in the Schilling test is unimpaired. This is particularly a problem in patients with compromised gastric status or early in the course of development of pernicious anemia. 

The Schilling test is primarily a test of vitamin B12 absorption and not of status, but it permits differentiation of causes of vitamin B12 deficiency (pernicious anemia or intestinal malabsorption). The proportion absorbed from orally administered Co- or Co-labeled vitamin 6,2 is measured by determining the radioactivity in feces, urine, or serum or by externally scanning the liver. The usual procedure is to measure radioactivity in a 24-hour urine sample, which is collected after oral administration of 0.5 Xg of radioactive Co-labeled vitamin B12 after an overnight fast. In normal individuals, 8% or more of the dose administered is excreted in the urine, whereas in people with pernicious anemia, less than 7% (often 0% to 3%) is excreted. A confirmatory test for lack of IF requires mgestion of vitamin B,2 and IF. ... 

Lo CW, Paris PW, Clemens TL, Nolan J, Holick ME Vitamin D absorption in healthy subjects and in patients with intestinal malabsorption syndromes. 

The answer is c. (Murray, pp 627-661. Scriver, pp 3897—3964. Sack, pp 121-138. Wilson, pp 287-320.) Hemorrhagic disease of the newborn is caused by poor transfer of maternal vitamin K through the placenta and by lack of intestinal bacteria in the infant for synthesis of vitamin K. The intestine is sterile at birth and becomes colonized over the first few weeks. Because of these factors, vitamin K is routinely administered to newborns. Deficiencies of the fat-soluble vitamins A, E, D, and K can occur with intestinal malabsorption, but avid fetal uptake during pregnancy usually prevents infantile symptoms. Hypervltaminosis A can cause liver toxicity but not bleeding, and deficiencies of E (neonatal anemia) or C (extremely rare in neonates) have other symptoms besides bleeding. 

Treatment of osteomalacia from vitamin D deficiency is vitamin D therapy, with dose depending on severity. Supplements of 800 to 4000 units/day or 50,000 units weekly for 8 weeks may be necessary. For sprue, a gluten-free diet is necessary. With intestinal malabsorption, high oral doses (50,000 to 100,000 units/day) or daily intramuscular injections of 10,000 units of vitamin D may be initially required. With disordered vitamin D metabohsm caused by anticonvulsants or rifampin, supplemental vitamin D (4000 units/day) can be effective. Sun exposure can also be useful. Serum calcium and 25(OH) vitamin D monitoring is necessary with high vitamin D doses. 

Xenobiotic-induced pancreatitis may be accompanied by gross plasma lipid changes that may result from marked changes of carbohydrate metabolism (see Chapter 9). The observation of the presence of gross macroscopic fecal fat content (steatorrhea) can indicate effects on pancreatic function, biliary dysfunction, or intestinal malabsorption. In longer-term studies, malabsorption of fat-soluble vitamins may be reflected by the clinical condition of vitamin-deficient animals. 

Final vitamin B12 absorption is limited (< 3 pg per meal) except when the diet is rich in animal food (Baik and Russel 1999). Vitamin B12 low intake of from food may lead to a negative balance and finally to functional deficiency when tissue stores of vitamin B12 are depleted. In addition, several factors causing intestinal malabsorption may lead to eobalamin deficiency (Carmel 2011) ... 

A collective term for a group of nutritional deficiency diseases characterized by impaired absorption of nutrients from the small intestine, especially fats, glucose, and vitamins. Although all sprues exhibit the same general clinical manifestations of intestinal malabsorption and steatorrhea (fatty diarrhea), the following three etiologic classifications are presented in this book ... 

Formation of strictures, abscesses, fistulae, and obstructions in patients with CD is possible. Patients with CD may develop significant weight loss or nutritional deficiencies secondary to malabsorption of nutrients in the small intestine, or as a consequence of multiple small- or large-bowel resections. Common nutritional deficiencies encountered in IBD include vitamin B12, fat-soluble vitamins, zinc, folate, and iron. Malabsorption in children with CD may contribute to significant reductions in growth and development. 

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... 

Cholecalciferol Regulate gene transcription via the vitamin D receptor Stimulate intestinal calcium absorption, bone resorption, renal calcium and phosphate reabsorption decrease parathyroid hormone (PTH) promote innate immunity inhibit adaptive immunity Osteoporosis, osteomalacia, renal failure, malabsorption Hypercalcemia, hypercalciuria the vitamin D preparations have much longer half-life than the metabolites and analogs... 

In chylomicron retention disease (Anderson s disease) the secretory defect is restricted to intestinal apoB-containing lipoproteins (i.e., chylomicrons). This very rare recessively inherited disorder results from defects in a GTPase, Sarlb, which plays a critical role in the intracellular assembly and trafficking of chylomicrons. The affected patients present with fat malabsorption resulting in steatorrhea and deficiency of fat-soluble vitamins [46, 52, 54]. 

Vitamin B12 deficiency may result in the abnormal development of many body cells including the mucosal cells lining the intestine, and this in itself can result in malabsorption of the vitamin. This may be reversed following treatment and it is important therefore not to undertake tests of absorption until the patient has been adequately treated with vitamin B12 and a suitable period for recovery has elapsed. 

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. 

Deficiencies of vitamin B12 can result from either low dietary levels or, more commonly, from poor absorption of the vitamin due to the failure of gastric parietal cells to produce intrinsic factor (as in pernicious anemia) or to a loss of activity of the receptor needed for intestinal uptake of the vitamin.5 Nonspecific malabsorption syndromes or gastric resection can also cause vitamin B12 deficiency. The vitamin may be administered orally (for dietary deficiencies), or intramuscularly or deep subcutaneously (for pernicious anemia). [Note Folic acid administration alone reverses the hematologic abnormality and thus masks the B12 deficiency, which can then proceed to severe neurologic dysfunction and disease. Therefore, megaloblastic anemia should not be treated with folic acid alone, but rather with a combination of folate and vitamin B12.] Therapy must be continued for the remainder of the life of a patient suffering from pernicious anemia. There are no known adverse effects of this vitamin. 

Since vitamin E is absorbed from the intestines in chylomicrons, any fat malabsorption diseases can lead to deficiencies in vitamin E intake. Neurological disorders have been associated with vitamin E deficiencies associated with fat malabsorptive disorders. 

Naturally occurring vitamin K is absorbed from the intestines only in the presence of bile salts and other lipids through interaction with chylomicrons. Therefore, fat malabsorptive diseases can result in vitamin K deficiency. 

Vitamin K is absorbed by the small intestines, where it enters the lymph packaged in chylomicrons. A deficiency in vitamin K can occur in adults and children suffering from fat malabsorption syndromes, such as cystic fibrosis. 

Blockage of the bile duct caused by problems such as cholesterol-containing gallstones or duodenal or pancreatic tumors can lead to an inadequate concentration of bile salts in the intestine. Digestion and absorption of dietary lipids is diminished. Certain diseases that affect the pancreas can lead to a decrease in bicarbonate and digestive enzymes in the intestinal lumen. (Bicarbonate is required to raise the intestinal pH so that bile salts and digestive enzymes can function.) If dietary fats are not adequately digested, steatorrhea may result. Malabsorption of fats can lead to caloric deficiencies and lack of fat-soluble vitamins and essential fatty acids. 

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