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Updated: 12/26/06 02:17 PM
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Malabsorption of calcium is usually only recognized late when clinical symptoms of hypocalcemia have developed, i.e., osteomalacia (calcium depletion causing bone pain) and tetany (muscle spasms and even convulsions relieved by intravenous calcium).
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Ca++ absorption is depressed when there is steatorrhea
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If dietary vitamin D is inadequate or if vitamin D is malabsorbed because of defective luminal micelle formation, then calcium is secondarily malabsorbed. Any type of steatorrhea may be accompanied by calcium malabsorption because calcium forms insoluble, unabsorbable salts with long-chain fatty acids. Calcium malabsorption occurs in chronic renal failure. Renal hydroxylation is required to activate vitamin D which promotes synthesis of a calcium-binding protein in intestinal absorptive cells.
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Mg++ deficiency often exists in chronic diarrhea
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Magnesium deficiency secondary to malabsorption is most frequent when there is massive malabsorption of water and electrolytes whatever the cause: extensive intestinal mucosal injury, intestinal bypass, resection, etc. Mg++ deficiency can present symptomatically as anorexia, psychiatric illness, muscle weakness or tetany. If hypomagnesemia is not corrected first, then it may be difficult to correct hypocalcemia.
When the duodenal and proximal jejunal mucosa are injured, Fe++ absorption is markedly impaired. In the U.S.A. this is most commonly seen in celiac sprue. Naturally, the duodenum and proximal jejunum are most injured by gluten in this hereditary disease because the proximal intestine is where ingested gluten is present in highest concentration after gastric emptying.
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Fe++ absorption is impaired in mucosal diseases, and after gastric resection
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Gastric operations which disrupt normal anatomy often impair Fe++ absorption. The major reason for iron malabsorption following gastric surgery is dumping and a less important reason is loss of acidity. Postgastrectomy iron deficiency responds to a sufficiently large dose of medicinal iron. Iron deficiency in celiac sprue responds neither to dietary iron nor medicinal iron administered orally because it is not absorbed by the injured mucosa; the iron deficiency of celiac sprue is only repaired by parenteral administration of iron or by a gluten-free diet which repairs the intestinal injury.
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Next Section (S): Normal Vitamin Absorption »
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