Vitamins malabsorption

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, because 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. However, calcifediol is no longer available. 

Vitamin K is an essential cofactor for the synthesis of prothrombin and other blood-clotting factors. Vitamin K deficiency occurs due to liver disease, longterm antimicrobial therapy, and malabsorption. Vitamin K deficiency can lead to hemorrhages in newborns and development of hypoprothrombobinemia. Rapid intravenous injection of emulsified vitamin K produces flushing, breathlessness, hypotension, and may lead to death. 

Treatment of hypocalcemia associated with vitamin D-deficient states should be individualized. In patients with malabsorption, vitamin D requirements vary markedly, and large doses may be required. In contrast, vitamin D deficiency associated with anticonvulsant med-... 

Constipation (may lead to fecal impaction), exacerbation of hemorrhoids, abdominal pain, distention and cramping, nausea, increased bleeding related to vitamin K malabsorption, vitamin A and D deficiencies Constipation (may lead to fecal impaction), exacerbation of hemorrhoids, abdominal pain, distention and aamping, nausea, increased bleeding related to vitamin K malabsorption, vitamin A and D deficiencies Constipation (may lead to fecal impaction), exacerbation of hemorrhoids, abdominal pain, distention and cramping, nausea, increased bleeding related to vitamin K malabsorption, vitamin A and D deficiencies... 

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. 

In experimental animals, vitamin E deficiency results in resorption of femses and testicular atrophy. Dietary deficiency of vitamin E in humans is unknown, though patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic fiver disease suffer deficiency because they are unable to absorb the vitamin or transport it, exhibiting nerve and muscle membrane damage. Premamre infants are born with inadequate reserves of the vitamin. Their erythrocyte membranes are abnormally fragile as a result of peroxidation, which leads to hemolytic anemia. 

Several factors contribute to development of bone disease in CF (1) malabsorption of vitamins D and K and calcium (2) poor... 

Anemia may be present in some patients due to impaired erythropoietin regulation, nutritional factors (vitamin E and iron malabsorption), or chronic inflammation. With chronic pulmonary disease, increased cytokine production can lead to shortened red blood cell survival, reduced erythropoietin response, and impaired mobilization of iron stores. 

Additionally, with chronic hypoxia, normal hemoglobin and hematocrit values may represent relative anemia.12 Increased red blood cell production is a physiologic response to hypoxia however, this response may be blunted in CF and may result in symptoms of anemia despite normal lab values. Abnormal bleeding may also be observed as a result of vitamin K malabsorption or antibiotic-associated depletion of gastrointestinal flora and vitamin K synthesis. 

Fat-soluble vitamin supplementation is usually required in pancreatic insufficiency. Specially-formulated products for CF patients (ADEKs and Vitamax ) are usually sufficient to attain normal serum vitamin levels at a dose of 1 tablet daily for younger children and 2 tablets daily for teenagers and adults. Additional supplementation may be needed in uncontrolled malabsorption or for replacement of severe vitamin deficiency.5,15 Appetite stimulants such as cyproheptadine may be an option for promoting nutrition and weight gain, but efficacy has not been established. 

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. 

Patients with IBD, particularly those with CD, are also at risk for bone loss. This may be a function of malabsorption or an effect of repeated courses of corticosteroids. Patients with IBD should receive a baseline bone density measurement prior to receiving corticosteroids. Vitamin D and calcium supplementation should be used in all patients receiving long-term corticosteroids. Oral bisphosphonate therapy may also be considered in patients receiving prolonged courses of corticosteroids or in those with osteopenia or osteoporosis. 

As patients lose exocrine function of the pancreas, they have decreased ability to absorb lipids and protein ingested with normal dietary intake. Weight loss from nutritional malabsorption is a common symptom of chronic pancreatitis not often seen in acute pancreatitis. Fatty- or protein-containing stools are also common carbohydrate absorption is usually unaffected. Even though patients with chronic pancreatitis have decreased ability to absorb lipid from the gastrointestinal tract, there does not appear to be an increased incidence of fat-soluble vitamin deficiency in these patients.34... 

When treating folic acid deficiency, an initial daily dose of 1 mg/day by mouth typically is effective. Absorption of folic acid generally is rapid and complete. However, patients with malabsorption syndromes may require larger doses (up to 5 mg/day). Similar to vitamin B12 deficiency, resolution of symptoms and reticulocytosis is prompt, occurring within days of commencing therapy. Hgb will start to rise after 2 weeks of therapy and may take from 2 to 4 months to resolve the deficiency completely. Afterwards, if the underlying deficiency is corrected, folic acid replacement can be discontinued. However, in cases where folic acid is consumed rapidly or absorbed poorly, chronic replacement may be required. 

Abetalipoproteinemia or Bassen-Kornzweig syndrome, a potentially disabling, familial disease characterized by lack of plasma TGs, malabsorption of fat-soluble vitamins, liver steatosis, steatorrhea, and other symptoms, is linked to mutations in the MTP functional subunit [52,53],... 

The consequence of bacterial bile acid metabolism [66, 74,77] is hardly clinically significant malabsorption [6] in otherwise healthy individuals [32,79], but in predisposed individuals this may be different. Accordingly, omeprazole interferes with the absorption of vitamin B12 [80-83] and protein assimilation [84], The mechanism for altered vitamin B12 absorption is prevention of its cleavage from dietary protein [83], for which the importance of the concurrent bacterial overgrowth has not yet been ruled out. 

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

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. 

Methionine synthase deficiency (cobalamin-E disease) produces homocystinuria without methylmalonic aciduria 677 Cobalamin-c disease remethylation of homocysteine to methionine also requires an activated form of vitamin B12 677 Hereditary folate malabsorption presents with megaloblastic anemia, seizures and neurological deterioration 678... 

Vitamin A. To overcome the difficulty of identification, vitamin A can be used as a label. The changes in the blood vitamin A curve following the administration of vitamin A in oil provide similar information to that given by the chylomicrograph. In malabsorption due to enteropathy the curve is depressed and delayed, and in pancreatic lipase deficiency it is markedly flattened. The use of vitamin A in oil and in aqueous dispersion is similar in principle to the use of labeled triolein and oleic acid (B4, G3, L4). 

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... 

Nutritional deficiency diseases are relatively rare in the temperate zone. The etiology of numerous other clinical conditions involve vitamin deficiencies, due to faults in absorption, transfer, or utilization. Because of the central position of the vitamins as sources of coenzymes, such functional deficiencies are important in malabsorption, where the picture is often complicated by multiple deficiencies, in anemias where the defect is in general highly specific, and in many other diseases where the deficiency is secondary to other pathologic events, but nevertheless of grave consequences. 

The establishment of quantitative methods for the determination of vitamins in body fluids and tissues by microbiological assay techniques should stimulate the search for the significance of vitamins in disease, not only in nutritional deficiency, but in the much wider field of all metabolic disturbances. Functional vitamin deficiencies are produced by malabsorption, by inhibitors of the vitamin function through products of the body, and particularly through drugs and other toxic substances. Vitamin deficiencies may be relative deficiencies whenever an individual s metabolism is deranged so as to require enhanced quantities of a given vitamin to cure or to counteract certain symptoms as, e.g., in Darier s disease (keratosis follicularis) (P2a). 

Malabsorption Syndrome, with Special Reference to the Effects of Wheat Gluten (Frazer), 5, 69 Mellituria, Nonglucose (Sidbury), 4, 29 Microbiological Assay Methods for Vitamins (Baker and Sobotka), 5, 173 Organic Acids in Blood and Urine (Nordmann and Nordmann), 4, 53 Paper Electrophoresis Principles and Techniques (Peeters), 2, 1 Paper Electrophoresis of Proteins and Protein-Bound Substances in Clinical Investigations (Owen), I, 238 Parathyroid Function and Hyperparathyroidism, Biochemical Aspects of (Nordin), 4, 275... 

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. 

While the dog is a carnivore, it is able to adapt to an omnivorous diet. Requirements for dietary sources of energy, amino acids, glucose precursors, fatty acids, minerals, vitamins, and water have been established based on recommendations by the National Research Council (NRC, 1985). Adult beagles maintained in a laboratory environment function well with one feeding of standard laboratory chow per day. In safety assessment testing, however, some compounds may induce serious dietary deficiencies through induced loss of appetite, malabsorption, or vomiting, and, in these cases, it may be advisable to provide a dietary supplement. 

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