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CMDT 2008
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Renal stones, polyuria, hypertension, constipation, fatigue, mental changes Bone pain; rarely, cystic lesions and pathologic fractures Serum and urine calcium elevated; urine phosphate high with low to normal serum phosphate; alkaline phosphatase normal to elevated Elevated PTH
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Primary hyperparathyroidism is characterized by chronic poorly regulated excessive secretion of PTH by one or more parathyroid glands that results in hypercalcemia It is an increasingly recognized disorder, present in up to 01% of adult patients examined It can be seen at any age but is more frequent in persons over the age of 50 years and is three times more common in women than in men The disease is caused by hypersecretion of PTH, usually by a single parathyroid adenoma (80%), and less commonly by hyperplasia by two or more parathyroid glands (20%), or carcinoma ( 1%) However, when hyperparathyroidism presents before age 30 years, there is a higher incidence of multiglandular disease (36%) and carcinoma (5%) The size of the parathyroid adenoma correlates with the serum PTH level Parathyroid adenomas or hyperplasia can be familial (about 5%) and may be part of MEN types 1, 2A, and 2B In MEN 1, multiglandular hyperparathyroidism is usually the initial manifestation and ultimately occurs in 90% of affected individuals Hyperparathyroidism in MEN 2A is less frequent that in MEN 1 and is usually milder Familial hyperparathyroidism can occur without MEN It can also occur in the hyperparathyroidism-jaw tumor syndrome, a rare autosomal dominant familial condition in which parathyroid cystic adenomas or carcinomas are associated with ossifying fibromas of the mandible and maxilla as well as renal lesions (cysts, hamartomas, Wilms tumors) (see Table 26 17) Hyperparathyroidism results in the excessive excretion of calcium and phosphate by the kidneys PTH stimulates renal tubular reabsorption of calcium; however, hyperparathyroidism causes hypercalcemia and an increase in calcium in the glomerular filtrate that overwhelms tubular reabsorption capacity, resulting in hypercalciuria At least 5% of renal stones are associated with this disease Diffuse parenchymal calcification (nephrocalcinosis) is seen less commonly Chronic bone resorption induced by excessive PTH in the circulation may produce diffuse demineralization, pathologic fractures, or cystic bone lesions throughout the skeleton ( osteitis fibrosa cystica ) In chronic renal failure, hyperphosphatemia and decreased renal production of 1,25-dihydroxycholecalciferol (1,25[OH]2D3) initially produce a decrease in ionized calcium The parathyroid glands are stimulated (secondary hyperparathyroidism) and may enlarge, becoming autonomous (tertiary hyperparathyroidism) The bone disease seen in this setting is known as renal osteodystrophy This syndrome seems somewhat less likely to develop in patients with diabetes Hypercalcemia often occurs after renal transplant but usually subsides spontaneously
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The outlook is good if the diagnosis is made promptly and treatment instituted Any dental changes, cataracts, and brain calcifications are permanent Periodic blood chemical evaluation is required, since changes in calcium levels may call for modification of the treatment schedule Hypercalcemia that develops in patients with seemingly stable, treated hypoparathyroidism may be a presenting sign of Addison s disease
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Tartaglia F et al Randomized study on oral administration of calcitriol to prevent symptomatic hypocalcemia after total thyroidectomy Am J Surg 2005 Sep;190(3):424 9 [PMID: 16105530] Tfelt-Hansen J et al The calcium-sensing receptor in normal physiology and pathophysiology: a review Crit Rev Clin Lab Sci 2005;42(1):35 70 [PMID: 15697170]
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CMDT 2008
helpful clinically The serum phosphate is often low (< 25 mg/dL) The urine calcium excretion may be high or normal (averaging 250 mg/g creatinine) but it is usually low for the degree of hypercalcemia There is an excessive loss of phosphate in the urine in the presence of hypophosphatemia (25% of cases) to low-normal serum phosphate (In secondary hyperparathyroidism due to renal failure, the serum phosphate is high) The alkaline phosphatase is elevated only if bone disease is present The plasma chloride and uric acid levels may be elevated Vitamin D deficiency is common in patients with hyperparathyroidism, and it is prudent to screen for vitamin D deficiency with a serum 25-OH vitamin D determination Low serum 25-OH vitamin D levels (< 20 mcg/L; < 50 nmol/L) can aggravate hyperparathyroidism and its bone manifestations; vitamin D replacement may be helpful in treating patients with hyperparathyroidism (See below) Elevated serum levels of PTH confirm the diagnosis of hyperparathyroidism The best immunoassay recognizes the intact molecule at two different sites the amino terminal and the carboxyl terminal ends with two different antibodies This assay, known as IRMA, is specific and sensitive, making it easier to distinguish primary hyperparathyroidism from other causes of hypercalcemia All patients with apparent hyperparathyroidism should be screened for familial benign hypocalciuric hypercalcemia with a 24-hour urine for calcium and creatinine Patients should discontinue thiazide diuretics prior to this test Calcium excretion of < 50 mg/24 hours (or < 5 mg/dL on a random urine) is not typical for primary hyperparathyroidism and indicates possible familial benign hypocalciuric hypercalcemia (See below)
Parathyroid carcinoma is a rare cause of hyperparathyroidism but is more common in patients with severe hypercalcemia About 50% of parathyroid carcinomas are palpable
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