Sprue calcium absorption

When fat splitting and absorption is normal the ingestion of fats has in general been found to aid calcium absorption. In conditions in which there is excessive fat excretion, however, such as sprue or idiopathic steatorrhea, calcium is lost in the feces as calcium soaps. It has also been suggested... 

Excessive fat. Excessive levels of fat, especially those that are saturated, depress calcium absorption because the fats combine with calcium to form insoluble soaps, a process called saponification. These insoluble soaps are excreted in the feces, with consequent loss of the incorporated calcium. (They may also carry with them fat-soluble vitamin D.) This explains why patients with chronic intestinal disorders, such as sprue and celiac disease, leading to increased fat in the feces (steatorrhea) may develop osteomalacia in due time. 

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. 

Calcium and phosphate enter the body from the intestine. The average American diet provides 600-1000 mg of calcium per day, of which approximately 100-250 mg is absorbed. This figure represents net absorption, because both absorption (principally in the duodenum and upper jejunum) and secretion (principally in the ileum) occur. The amount of phosphorus in the American diet is about the same as that of calcium. However, the efficiency of absorption (principally in the jejunum) is greater, ranging from 70% to 90%, depending on intake. In the steady state, renal excretion of calcium and phosphate balances intestinal absorption. In general, over 98% of filtered calcium and 85% of filtered phosphate is reabsorbed by the kidney. The movement of calcium and phosphate across the intestinal and renal epithelia is closely regulated. Intrinsic disease of the intestine (eg, nontropical sprue) or kidney (eg, chronic renal failure) disrupts bone mineral homeostasis. 

Cooper and Castle have proposed a three-step sequence to explain the vitamin B12 absorption in the gastrointestinal tract. In the first step, vitamin B12 binds with the intrinsic factor in gastric juice. The affinity of the vitamin for the intrinsic factor is thought to be greater than its affinity for proteins in the intestinal content consequently, the intrinsic factor (IF) successfully displaces the vitamin from its weaker bonds with other proteins. Calcium facilitates and EDTA inhibits the absorption of vitamin B12 by the everted intestine. On the basis of these and related findings, workers proposed the second step in vitamin Bi2 absorption. At that stage it is assumed that the intrinsic factor-vitamin B12 complex is trapped in the intestinal wall by the intermediate of calcium bonds and absorbed by pinocytosis. This stage of the absorption process probably is interfered with in sprue and steatorrhea where calcicum soaps are formed in the intestinal lumen. 

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