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Primary Hyperparathyroidism. Primary hyperparathyroidism is characterized by excessive production of PTH and hypercalcemia.27,2~ 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. Parathyroid carcinoma accounts for less than hyperparathyroidism, hypercalcemia, high calcium, parathyroid

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 in

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 of primary

Table 10

Causes of Hypercalcemia


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


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. In addition, any milk

A National Institutes of Health Consensus Development Conference on Diagnosis and Management of Asymptomatic Primary Hyperparathyroidism addressed the diagnosis and management of hyperparathyroidism (Table i 3J.3E

Some experts think that surgical management of primary hyperparathyroidism is the only viable treatment option. In 

Management of Hypercalcemia

Therapy Drug regimen Comments

Hydration Normal saline, 150 to 300 Mainstay of acute treatment to increase

mL per hour calcium excretion

Base hydration rate on patient's fluid and cardiovascular status:

Diuresis Furosemide (Lasix®), Use only with adequate hydration

40 to 80 mg intravenously Monitor electrolytes

every one to four hours

Calcitonin-salmon 4 IU per kg intramuscularly or Acute, use only for rapid reduction while

(Calcimar®, Osteocalcin®, subcutaneously every 12 hours awaiting response to other therapies

Salmonine®) or Rapid onset, but degree of calcium

(Miacalcin®) 2 to 18 IU per kg infusion reduction is unpredictable and often small

Calcitonin-human intravenously every 12 hours


Plicamycin 25 mcg per ~ infusion Use a~er hydration and diuresis

[mithramycin] intravenously over three to Peak drop in calcium levels seen within

(Mithracin®) six hours in saline solution 48 to 96 hours

or over three to four days

in dextrose solution

Glucocorticoids 40 to 80 mg per day Not for acute situations

Prednisone or Most effective in multiple myeloma,

Hydrocoisone 200 to 300 mg per day sarcoidosis, leukemia/lymphoma,

for three to five days hype~imminosis A and D

Not effective in primary hyperparathyroidism

Bisphosphonams 7.5 mg per ~ per day Inhibits osteoclast function

Etidronate (Didronel®) intravenously over threeHighly effective in controlling hypercalcemia

hours associated with malignancy

Pamidronate (Aredia®) 60- to 90-mg infusion

intravenously over 24 hours

Gallium nitrate 200 mg per m~ per day Indicated for symptomatic hypercalcemia of

(Ganite®) intravenously for five days malignancy not responsive to hydration

Oral phosphorus [lemental phosphorus, Especially effective with chronic hypercalcemia

(K-Phos Neutral®, I to 3 g per day due to hyperparathyroidism and malignancy