Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (228 page)

   Imaging Studies

Localization studies such as ultrasonography, technetium-99m sestamibi, CT, or MRI scanning should not be used to establish the diagnosis of primary hyperpara-thyroidism but are commonly used to facilitate unilateral neck exploration and minimally invasive surgeries.

Suggested Readings

Fuleihan GE, Arnold A. Pathogenesis and etiology of primary hyperparathyroidism. In: Rose B, (ed).
UpToDate
, Waltham, MA: UpToDate, Inc.; 2009.

Fuleihan GE, Silverberg SJ. Clinical manifestations of primary hyperparathyroidism. In: Rose B, (ed).
UpToDate
, Waltham, MA: UpToDate, Inc.; 2009.

Fuleihan GE, Silverberg SJ. Diagnosis and differential diagnosis of primary hyperparathyroidism. In: Rose B, (ed).
UpToDate
, Waltham, MA: UpToDate, Inc.; 2009.

Khan F, Sachs H, Pechet L, et al.
Guide to Diagnostic Testing
. Philadelphia, PA: Lippincott Williams & Wilkins; 2002.

Kronenberg HM, Melmed S, Polonsky KS, et al.
Williams Textbook of Endocrinology
, 11th ed. Philadelphia, PA: Saunders, Elsevier Inc.; 2008.

HYPERCALCEMIA

   Definition

Hypercalcemia refers an abnormally high concentration of calcium compounds in the circulating blood.

   Overview

Hypercalcemia is a relatively common clinical problem. It results when the entry of calcium into circulation exceeds the excretion of calcium into urine or deposition in bone. Hypercalcemia occurs when there is accelerated bone resorption, excessive gastrointestinal absorption, or deceased renal excretion of calcium. There are many causes of hypercalcemia, but hyperparathyroidism and malignancy are the most common, accounting for >90% of the cases.

   Common Causes

Hypercalcemia can be divided into major categories based on the mechanisms of increased bone resorption and increased calcium absorption.

  1.  Disorders with increased bone resorption

a.   Primary hyperparathyroidism

b.   Secondary and tertiary hyperparathyroidism

c.   Malignancy. The most common etiology with nonmetastatic solid tumor is secretion of PTHrP. Rarely, it is due to a result of ectopic production of PTH.

d.   Thyrotoxicosis

e.   Immobilization

f.   Paget disease of bone

g.   Tamoxifen used in patients with breast cancer and skeletal metastases

h.   Hypervitaminosis A

  2.  Disorders with increased calcium absorption

a.   Increased calcium intake. A high calcium intake alone rarely causes hypercalcemia, but it can lead to hypercalcemia when combined with decreased urinary excretion.

b.   Chronic renal failure. It occurs in patients who are treated with calcium carbonate or calcium acetate to bind dietary phosphate.

c.   Milk-alkali syndrome. Excess intake of calcium- and alkali-containing antacids (such as calcium carbonate or sodium bicarbonate) leads to hypercalcemia, metabolic alkalosis, and renal failure. It typically occurs in the situation of taking excess calcium carbonate supplementation to treat osteoporosis or dyspepsia.

  3.  Hypervitaminosis D can cause hypercalcemia by increasing calcium absorption and bone resorption. High concentration of either 25-hydroxyvitamin D (calcidiol) or 1, 25-dihydroxvitamin D (calcitriol) can lead to hypercalcemia. High serum concentration of 1, 25-dihydroxvitamin D is usually caused by ingestion of calcitriol as treatment for hypoparathyroidism or for the hypocalcemia and secondary hyperparathyroidism of renal failure, but it also can be due to increased endogenous production in patients with granulomatous disease and lymphoma.

  4.  Miscellaneous causes:

a.   Lithium

b.   Thiazide diuretics

c.   Pheochromocytoma

d.   Adrenal insufficiency

e.   Rhabdomyolysis and acute renal failure

f.   Theophylline toxicity

g.   Familial hypocalciuric hypercalcemia

h.   Metaphyseal chondrodysplasia

i.   Congenital lactase deficiency

   Who Should Be Suspected?

   Patients with mildly elevated serum calcium (<12 mg/dL) may be asymptomatic, particularly if the elevation is chronic, or they may report nonspecific symptoms, such as constipation, fatigue, and depression.

   Patients with moderately elevated serum calcium (12–14 mg/dL) may have symptoms of polyuria, polydipsia, nausea, anorexia, vomiting, constipation, muscle weakness, and change in sensorium. Acute hypercalcemia leads to a shortened QT interval, which reflects the shortened myocardial action potential.

   Severe hypercalcemia (>14 mg/dL) can lead to progression of above symptoms and confusion, lethargy, stupor, and even coma and death.

   Laboratory Findings (Table
6-8
; Figure
6-14
)