Hypoparathyroidism Serum calcium

Oral calcium supplementation (e.g., 1 to 3 g/day of elemental calcium) is indicated for chronic hypocalcemia due to hypoparathyroidism and vitamin D deficiency. If serum calcium does not normalize, a vitamin D preparation should be added. 

Vitamin D preparations are also used to treat hypoparathyroidism, but they require even larger doses, often up to 2.5 mg (100,000 units) daily to increase the serum calcium back to normal. As in vitamin D deficiency, the dose must be carefully monitored. 

After resolution of the acute phase, maintenance levels of at least 0.8 mEq/L are necessary for optimal efficacy and should be checked once every 6 to 12 months, or more often if clinically indicated. Other follow-up tests include periodic thyroid function tests, blood urea nitrogen, serum creatinine, serum calcium (because lithium may cause hypoparathyroidism), and an EGG. Thyroid function tests and renal function should be monitored approximately every 6 to 12 months (see the section Maintenance/Prophylaxis Treatment in Chapter 10). 

In the absence of PTH (idiopathic or surgical hypoparathyroidism) or an abnormal target tissue response to PTH (pseudohypoparathyroidism), serum calcium falls and serum phosphate rises. In such patients, l,25(OH)2D levels are... 

As a brief introductory summary, vitamin D substances perform the following fundamental physiological functions (1) promote normal growth (via bone growth) (2) enhance calcium and phosphorus absorption from the intestine (3) serve to prevent rickets (4) increase tubular phosphorus reabsorpiion (5) increase citrate blood levels (6) maintain and activate alkaline phosphatase m bone (7) maintain serum calcium and phosphorus levels. A deficiency of D substances may be manifested in the form of rickets, osteomalacia, and hypoparathyroidism. Vitamin D substances are required by vertebrates, who synthesize these substances in the skin when under ultraviolet radiation, Animals requiring exogenous sources include infant vertebrates and deficient adult vertebrates, Included there are vitamin D (calciferol ergocalciferol) and vitamin D< (activated 7-dehydrocholesterol cholecalciferol). 

The principal therapeutic concern is to restore normocalcemia and normophosphatemia. Under most circumstances, vitamin D (25,000-100,000 units three times per week) and dietary calcium supplements suffice. More rapid increments in serum calcium can be achieved with calcitriol, though it is not clear that this metabolite offers a substantial advantage over vitamin D itself for long-term therapy. Many patients treated with vitamin D develop episodes of hypercalcemia. This complication is more rapidly reversible with cessation of therapy using calcitriol rather than vitamin D. This would be of importance to the patient in whom such hypercalcemic crises are common. Dihydrotachysterol and 25(OH)D have not received much study as therapy for hypoparathyroidism, though both should be effective. Whether they offer advantages over vitamin D sufficient to justify their added expense remains to be seen. 

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). 

A 31-year-old woman developed diffuse musculoskeletal pain. She had been taking calcium and dihydrota-chysterol up to 4 mg/day for 6 months for hypoparathyroidism after subtotal thyroid resection. She had severe hypercalcemia (4.1 mmol/1), no detectable intact parathyroid hormone, renal insufficiency (serum creatinine 486 pmol/l), and a normochromic anemia (6.6 g/dl). Rehydration and forced diuresis initially improved renal function and reduced the serum calcium concentration, but the calcium concentration after 4 weeks was still 3.0 mmol/1 and it did not normalize until she was given a single intravenous dose of pamidronate 15 mg. 

Other causes of low serum calcium are less common. Hypoparathyroidism is due most commonly to parathyroid gland destruction during neck surgery (90%), and less commonly is idiopathic. Pseudohypoparathyroidism is biochemically similar to hypoparathyroidism however, these patients have inherited resistance to PTH and elevated concentrations of PTH. The molecular basis for the most common form, pseudohypoparathyroidism type I (Albright s hereditary osteodystrophy), is a reduction in guanine nucleotide regulatory complex. Ns, in the adenylate cyclase complex. 

Once acnte hypocalcemia is corrected by parenteral administration, fnrther treatment modahties shonld be individnalized according to the canse of hypocalcemia. If hypomagnesemia is present, magnesium supplementation is indicated (see Chap. 50). Asymptomatic and chronic hypocalcemia associated with hypoparathyroidism and vitamin D-deflcient states may be managed by oral calcium and vitamin D supplementation (see Tables 44—6 and 44—7). Therapy is begnn with 1 to 3 g/day of elemental calcium. Average maintenance doses range from 2 to 8 g of elemental calcium per day in divided doses. If serum calcium does not normalize, a vitamin D preparation may need to be added. 

The fall in serum calcium which follows parathyroidectomy is associated with a rise in calcium excretion (T1). Taken in conjunction with the hypocalcemic hypercalcuria of clinical hypoparathyroidism (L5), this suggests that the apparent calcuric effect of parathyroid extract is simply a reflection of its calcemic action. In fact, administration of the hormone appears if anything to reduce urinary calcium. Evidence to this effect has been produced by Bernstein et al. (B6), who have demonstrated a steep rise in calcium/inulin clearance ratio in dogs after parathyroidectomy... 

The apparently reciprocal relationship between plasma calcium and phosphate which is seen in clinical practice is largely accounted for by the opposite effects of parathyroid activity upon the calcium and phosphate concentrations. Thus, hyperparathyroidism is associated with high calcium and low phosphate concentrations and hypoparathyroidism with the reverse this is not a biochemical but a physiological reciprocity. A true biochemical or physicochemical reciprocity exists above the solubility product of tricalcium phosphate and presumably explains the irreversible depression of serum calcium by phosphate in renal failure (see Section 4.2). 

The parathyroid glands secrete parathyroid hormone (PTH) that regulate calcium levels in the blood. A decrease in serum calcium stimulates the release of PTH. A decrease of PTH is called hypoparathyroidism and an increase in PTH is hyperparathyroidism. 

Hypoparathyroidism is treated with PTH drags and hyperparathyroidism is treated with calcitonin. Calcitonin decreases serum calcium levels by promoting renal excretion of calcium. 

Hypoparathyroidism, whatever its cause, is associated with decreased bone resorption and diminished renal clearance of phosphate as a result, the serum calcium levels are low and the serum phosphorus levels are high. 

Excess phosphorus in the blood serum, which may result (1) when the kidneys do not excrete phosphorus adequately, or (2) from hypoparathyroidism, which causes an insufficient secretion of parathyroid hormone. When serum phosphorus rises, serum calcium falls, causing tetany. 

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. 

Therapy for hyperphosphatemia is directed toward correcting the cause of the high serum phosphate. In renal failure and in hypoparathyroidism, dietary restriction of phosphate and agents that bind phosphate in the intestine (calcium carbonate and others) are useful in lowering the serum phosphate concentrations. 

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