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Hyperparathyroidism

Primary Hyperparathyroidism. Primary hyperparathyroidism is characterized by excessive production of PTH and hypercalcemia. In 80 percent of cases, it is caused by a benign solitary parathyroid adenoma. Surgical reports suggest multiple adenomas are present in 2 to 4 percent of cases. About 15 percent of patients have diffuse hyperplasia of all four parathyroid glands, a condition that is frequently hereditary.

Hyperparathyroidism is seen two to four times more commonly in women than men, and its incidence increases with age; 60 to 65 percent of cases occur.

Secondary Hyperparathyroidism. Secondary hyperparathyroidism occurs as a result of low serum calcium levels. Most cases have hyperplasia in all four parathyroid glands. It is most often seen in chronic renal disease, but can also occur with disorders of vitamin D metabolism.

The physician should consider the many causes of hypercalcemia (Table I0). More than two-thirds of patients with hyperparathyroidism are asymptomatic; a biochemical panel will reveal elevated serum calcium levels. The remaining patients present with complaints of nonspecific symptoms ranging from fatigue, mild "aches and pains," constipation.

Manifestations of Parathyroid Adenomas. Calcium oxalate or phosphate stones may develop. Polydipsia and polyuria are often reported and are secondary to hypercalcemia. Eventually, renal failure and nephrocalcinosis may result.

Although mild hypercalcemia is often asymptomatic, more severe cases can cause nausea, vomiting, thirst, and anorexia. A history of peptic ulcer disease or hypertension is not uncommon, and there may be accompanying constipation, anemia, and weight loss. Some patients present with a neuromuscular disorder, such as paresthesias.

Evaluation and Diagnosis. The hallmark of primary hyperparathyroidism is hypercalcemia (a corrected serum calcium level greater than 10.5 mg per dL). Serum PTH should be determined by measuring intact PTH using the newer two-site immunoassay. An elevated PTH level in the presence of hypercalcemia confirms the diagnosis.

Table 10

Causes of Hypercalcemia

Approximate

Cause Disease incidence

Endocrine Hyperparathyroidism, 46 percent

disorders hyperthyroidism, Addison's

disease, pheochromocytoma,

hypothyroidism, vipoma

Cancer Breast, metastatic, parathyroid 45 percent

hormone-related peptide

secreting (lung, kidney

cancer), multiple myeloma,

leukemias, others

Increased Milk alkali syndrome, vitamin A 4 percent

intake or D intoxication, drugs (e.g.,

thiazides, lithium, aluminum)

Granulomatous Sarcoidosis, tuberculosis, etc 3 percent

diseases

Benign familial Paget's disease, immobilization, 2 percent

hypocalciuric idiopathic hypercalcemia of

hypercalcemia, infancy, aluminum intoxication,

others dysproteinemias, rhabdomyolysis,

measurement artifact

A benign autosomal dominant disorder known as familial hypocalciuric hypercalcemia also deserves mention. This disorder is characterized by hypocalciuria (usually greater than 50 mg per 24 hours), hypermagnesemia, and normal.

Treatment. Hospitalization is necessary when hypercalcemia is symptomatic and severe (generally defined as a serum level greater than 14 mg per dL). Vigorous hydration and correction of underlying hyponatremia and hypokalemia should be undertaken. Restoration of blood volume with saline followed by administration of a loop diuretic, such as furosemide, causes increased calcium excretion with a resulting decline in serum calcium levels.