Vitamin calcium retention

Age, calcium intake, hormonal status, exercise and vitamin status have all been implicated in the development of osteoporosis. Estrogen levels represent an important factor in skeletal calcium retention and homeostasis. In therapeutic trials in which post-menopausal women were given daily doses of estrogens, such therapy has been demonstrated to be partially effective in reducing the rate of bone resorption. However, this therapy has the concomitant hazard of endometrial cancer (10). Vitamin D and its hormones have been given considerable attention in the more recent studies. Without adequate dietary and tissue levels of such vitamins, calcium absorption and bone status will be impaired. 

In the normal infant a wide range of calcium retention has been reported by Hoobler (H8), Telfer (Tl), Daniels and Stearns (D2), Flood (F5), Stearns (S10), Jeans et al. (Jla), and Harrison (H4). From these authors we have obtained the results of 24 calcium balances in healthy infants (7-12 months), fed on cow s milk or on evaporated milk, with, so far as can be ascertained, a normal intake of vitamin D. On an average intake of 1.17 g calcium daily, the mean retention of calcium was 32 % (range 0-79 %) or 0.38 g. This agrees very closely with the daily retention of calcium in a similar age group reported by Sherman and Hawley (S3) from their study of German published reports and with the calculated requirements of the body at this age (LI). 

Vitamin D, apart from its availability in the diet, is produced in the body, in response to sunlight striking the skin, and really acts like a hormone. It helps to raise the blood levels of calcium and phosphorus in several ways. It stimulates calcium and phosphorus absorption in the gastrointestinal tract promotes transfer of calcium and phosphorus from bone to blood promotes calcium retention by the kidney. As a hormone it acts 1 entering the cell nucleus and interacting with DNA to regulate protein synthesis. 

Normal vitamin D, function. Vitamin D3 promotes calcium retention by ... 

Reports of lead-nutrient interactions in experimental animals have generally described such relationships in terms of a single nutrient, using relative absorption or tissue retention in the animal to index the effect. Most of the data are concerned with the impact of dietary levels of calcium, iron, phosphorus, and vitamin D. These interaction studies are summarized in Table 2-12. 

Most convincing with respect to variable needs, however, are well authenticated cases of "vitamin D-resistant rickets" which respond only when enormous doses of vitamin D, sometimes up to 100,000, 500,000 or even 1,500,000 units, are administered.39,40 Lower levels, which are wholly adequate even for mildly susceptible children, are without any beneficial effect on highly resistant cases so far as calcium and phosphorus retention is concerned. When extremely high levels are used, toxicity is liable to develop.40... 

Minerals found in milk which are insoluble remain in water in the curd and are more concentrated in the cheese than in milk. About two-thirds of the calcium and one-half of the phosphorus of milk remains in cheese. A major portion of the milk calcium is retained in the curd of cheese made with coagulating enzymes. Acid coagulation alone results in the loss of portions of both calcium and phosphorus salts in the acid whey, since these minerals are more soluble in the acidic medium. Most milk fat and fat-soluble vitamins are retained in the curd, but a considerable amount of water-soluble vitamins is lost during cheese manufacture. Retention of part of some B-complex vitamins in curd is due to their extended association with casein in the original milk. 

Vitamin D analogs Calcifediol (Calderol) Calcitriol (Rocaltrol) Dihydrotachysterol (DHT, Hytakerol) Ergocalciferol (Calciferol, Drisdol) Generally enhance bone formation by increasing the absorption and retention of calcium and phosphate in the body useful in treating disorders caused by vitamin D deficiency, including hypocalcemia, hypophosphatemia, rickets, and osteomalacia... 

The metabolism of phosphorus (P) is largely related to that of calcium (Ca). The Ca P ratio in the diet affects the absorption and excretion of these elements (Harper 1969). Any increase in serum phosphorus results in a decrease of serum calcium by mechanisms which are still unknown. For example, increased serum phosphorus levels and decreased serum calcium levels are seen in uremia (renal retention of phosphorus), hypoparathyroidism, hypocalcemia (decreased serum calcium levels), and hyperphosphatemia (increased serum phosphorus levels), and the reverse is seen in hypercalcemia (increased serum calcium levels) and hyperparathyroidism. Hypophosphatemia (low serum phosphorus levels) is seen in ricketts (vitamin D deficiency) (Harper 1969 Tietz 1970). 

Cd toxicity to kidneys can lead to degradation of vitamin D metabolism, which leads to osteoporosis Cd-induced nephotoxicity can also lead to decreased calcium and phosphate retention, which can produce osteomalacia (weakening of bones). 

Hypercalcemia is commonly encountered in clinical prac-results when the flux of calcium into the extracellular fluid compartment from the skeleton, intestine, or Iddney is greater than the efflux. For example, when excessive resorption of bone mineral occurs in malignancy, hy-percalciuria develops. When the capacity of the kidney to excrete filtered calcium is exceeded, hypercalcemia develops. Hypercalcemia can be caused by increased intestinal absorption (vitamin D intoxication), increased renal retention (thiazide diuretics), increased skeletal resorption (immobilization), or a combination of mechanisms (primary hyperparathyroidism). 

The most common cause of hyperphosphatemia is a decrease in urinary phosphorus excretion secondary to decreased glomerular filtration rate. ° Retention of phosphorus decreases vitamin D synthesis and induces hypocalcemia, which leads to an increase in PTH. This physiologic response inhibits further tubular reabsorption of phosphorus to correct hyperphosphatemia and normalize serum calcium concentrations. Patients with excessive exogenous phosphorus administration or endogenous intracellular phosphorus release in the setting of acute renal failure may develop profound hyperphosphatemia. Severe hyperphosphatemia is commonly encountered in patients with chronic kidney disease, especially those with GFRs less than 15 mL/ min per 1.73 m (see Chap. 44). 

If, for some reason, the diffusible Ca is lowered, the kidney conserves the serum level of calcium, partly because of a lowered filtration rate, but mostly by an increased reabsorption. At a total serum Ca concentration of less than 1.8 mmol/liter the net urinary excretion is almost zero. This regulatory function of the kidney can be disturbed by a low glomerular filtration rate, phosphate retention, acidosis, secondary hyperparathyroidism, and disturbances in the vitamin D metabolism [4],... 

Low phosphate levels, that is, levels less than 3.0 mg/dL (4.0 mg/dL in children) or 0.97 mmol/L (1.45 mmol/L in children), may result from poor absorption such as occurs with ingestion of antacids that bind to phosphate. Phosphate may be decreased with reduced renal reabsorption often secondary to high levels of parathyroid hormone (PTH), which causes a retention of calcium and loss of phosphate through the kidneys, or in high calcium levels and vitamin D deficiency. Low serum phosphate levels may be noted in alkalosis because phosphate is shifted into the cells to buffer the pH. 

In the kidney, the effect of PTH in promoting phosphate excretion does not depend on the presence of vitamin D. The vitamin itself, however, promotes retention of phosphate by reabsorption. High levels of vitamin D therefore enhance the blood levels of both calcium and phosphorus on account of the action of the vitamin on osteoclasts and kidney cells, respectively. Recent work suggests that the enzyme system which converts 25-HCC to 1,25-DHCC in the kidney is regulated by PTH rather than being controlled directly by the blood calcium level. It has been suggested that the formation of 1,25-DHCC may also be affected by the phosphate concentration in the kidney cells. 

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