Calcium Metabolism

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Calcium Metabolism

Post by Dr Sarhan on Sun Jan 06, 2008 12:23 pm

The normal range for serum calcium concentration (total calcium) is 8.8 to 10.4 mg/dL (2.2 to 2.6 mmol/L) and is no different in younger and older persons. About 45% of serum calcium is bound to serum proteins, 5% is complexed with anions (eg, phosphate, bicarbonate, citrate), and 50% is ionized. The ionized fraction affects cellular function and is normally between 4.8 and 5.2 mg/dL (between 1.2 and 1.3 mmol/L).

The proportion of ionized calcium to total calcium depends on the concentration of plasma protein (particularly albumin), the concentration of anion bound to ionized calcium, and blood pH (acidosis decreases protein binding, alkalosis increases it). In addition, pH affects the interaction between ionized calcium and the cell membrane. Thus, when the ionized calcium concentration is even moderately decreased, alkalosis can precipitate tetany and acidosis can prevent it. In respiratory alkalosis, tetany can occur even with a normal ionized calcium concentration. Changes in potassium and magnesium concentrations can also alter the response to calcium.

If the ionized calcium concentration is unavailable, total calcium and albumin concentrations should be measured simultaneously, and the total calcium concentration should be corrected to compensate for any albumin deficit. This correction is important in the elderly because hypoalbuminemia is common, particularly in chronically ill and malnourished persons. The correction consists of adding 0.8 mg/dL (0.2 mmol/L) to the total calcium concentration for each 1 g/dL decrease in albumin below its normal concentration of 4 g/dL.

The constancy of serum ionized calcium blood concentrations results from a complex interaction between three major calcium-regulating hormones: parathyroid hormone (PTH), 1,25-dihydroxycholecalciferol, and calcitonin. The PTH concentration needed to maintain a normal serum calcium concentration seems to increase with age, presumably because the elderly have a relative calcium deficiency. With age, the intrinsic capacity of the intestine to absorb calcium decreases, and the response to 1,25-dihydroxycholecalciferol is blunted. Moreover, PTH-mediated renal synthesis of 1,25-dihydroxycholecalciferol may be impaired because renal mass is reduced. Decreased intake of calcium and vitamin D and estrogen deficiency may also contribute to calcium deficiency. No evidence indicates that the increased tubular reabsorption of calcium, the decreased tubular reabsorption of phosphate, or the stimulation of bone resorption by PTH is impaired in the elderly. In fact, the catabolic effects of PTH on bone may be enhanced, because bone resorption is increased and bone formation is decreased with age.

Serum concentrations of 25-hydroxycholecalciferol (the precursor of 1,25-dihydroxycholecalciferol) tend to decrease with age, probably because of decreased dietary intake or decreased sun exposure. Moreover, sunlight in the winter in temperate latitudes is insufficient to activate vitamin D synthesis in the skin. Concentrations of 1,25-dihydroxycholecalciferol are normal, however, in elderly persons who take vitamin D supplements.
Dr Sarhan
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