Approach To Hypercalcemia

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The diagnostic approach to hypercalcemia begins with a careful history, including the manifestations of elevated calcium levels. When the aforementioned etiologies are taken into consideration, it becomes clear that the history should include family history of calcium disorders, such as renal stones or malignancy. The patient's risk factors for malignancy, such as smoking, should be investigated. A careful review of medications should also take place, to include not only prescription medications but also over-the-counter supplements. At this

Table 17-1


Table 17-1


Increased Bone Resorption Primary hyperparathyroidism

Specific Example Sporadic or familial: Multiple endocrine neoplasia (types I and II)



Solid tumors of lung; squamous carcinoma of head and neck; renal carcinoma

Breast cancer; multiple myeloma: prostate cancer

Tumor secretion of PTH-rP

Direct osteolysis

Hypervitaminosis A (vitamin A intoxication)

Includes both vitamin A and its analogs (used to treat acne)

Increased bone resorption


Less common than above causes

Increased risk when underlying disorder of high bone turnover (e.g.. Paget disease)

Increased Calcium Absorption Hypervitaminosis D (vitamin D intoxication)

Increased calcitriol level leads to increased GI absorption of calcium and phosphate

Granulomatous disease

Tuberculosis; sarcoidosis; Hodgkin disease

Increase extrarenal conversion of 25-hydroxyvitamin D, to calcitriol

Milk alkali syndrome

Excessive intake of calcium-containing antacids

Miscellaneous Medications

Thiazide diuretics Lithium

Reduced urinary excretion of calcium Increased PTH secretion


Calcium released from injured muscle

Adrenal insufficiency

Increased bone resorption and increased protein binding of calcium

Thyrotoxicosis (usually mild hypercalcemia)

Increased bone resorption

Table 17-2


Table 17-2




Renal calculi


Bone pain, including arthritis and osteoporosis

Psychic groans

Poor concentration, weakness, fatigue, stupor, coma

Abdominal moans

Abdominal pain, constipation, nausea, vomiting, pancreatitis

point, if the hypercalcemia is mild and the patient asymptomatic, it is acceptable to stop the suspect medication and repeat the serum calcium level.

The next step, if a causative medication is not found, is to measure a serum intact PTH level. This level will either be suppressed, normal, or elevated. As with many endocrine disorders, it is useful not to think of normal or abnormal values; rather, one should understand what is appropriate for a given situation. For example, in normal subjects, an increased calcium load will normally depress the PTH hormone level, thus a low PTH level in this situation is normal, or appropriately suppressed. If a patient has an elevated calcium level and the PTH is "normal," it is said to be inappropriately normal, because in the face of hypercalcemia it should be low, or suppressed.

If our patient with hypercalcemia has a normal or elevated PTH level, then the normal feedback loop is not responding. In this situation, the pituitary is producing PTH without check, which, in turn, is elevating the calcium level. This is hyperparathyroidism. Primary hyperparathyroidism occurs when the parathyroid gland overproduces PTH and does not respond to the negative feedback of elevated calcium levels. The vast majority of primary hyperparathyroidism is caused by an adenoma (benign tumor) of one of the four parathyroid glands.

Secondary hyperparathyroidism occurs as the parathyroid glands overproduce PTH to respond to low serum calcium levels. This may occur as a response to low dietary calcium intake or a deficiency of vitamin D. Tertiary hyperparathyroidism occurs in patients who have renal failure. Patients in renal failure usually present with //ypocalcemia. hyperphosphatemia, and low vitamin D levels. If this is untreated, it leads to hyperplasia of the parathyroid glands, an increased PTH secretion, and subsequent hypercalcemia.

There is a condition that can produce inappropriately high PTH levels unrelated to the parathyroid production. This is familial hypocalciuric hypercalcemia (FHH), a genetic disorder related to a defect in a gene that codes for a calcium-sensing receptor. Consequently, simply measuring PTH alone may confound this diagnosis, which may be mistaken for primary hyperparathyroidism.

To distinguish these entities, a 24-hour urinary calcium level is obtained. In hyperparathyroidism, the kidneys spill calcium into the urine at a normal or elevated level. With FHH the urinary calcium level is low.

A PTH level that is low with an elevated serum calcium suggests that the parathyroid gland is responding appropriately to the high calcium environment. The etiology in this scenario must be some process that causes calcium to be released from bone or calcium to be absorbed from the gut despite the suppressed PTH. This is seen when tumors produce a hormone that mimics the active site of the PTH molecule, but that have no counter regulatory mechanism for suppression when calcium levels rise. This molecule is called parathyroid hormone-related peptide (PTH-rP). PTH-rP is produced by lung cancers, squamous cell cancers of the head and neck, and renal cell cancer. PTH-rP effects osteoclastic bone resorption, increases calcitriol, and promotes calcium resorption from the kidneys, resulting in increased levels of serum calcium. The continued production of PTH-rP effectively takes the parathyroid gland out of the loop in calcium homeostasis. Because cancer is a common etiology for hypercalcemia, the search for malignancy is paramount at this step in diagnosis, before other, less common, disorders are considered.

If a malignancy is not found, other etiologies must be considered. These fall into the category of endocrine disorders other than parathyroid and include hyperthyroidism, adrenal insufficiency, and acromegaly. The work-up thus includes thyroid-stimulating hormone (TSH), a Cortisol level, and a pituitary imaging study, respectively.

Treatment of Hypercalcemia

The treatment of hypercalcemia is directed at the underlying disorder.

Patients with mild hypercalcemia may be treated with preventative measures aimed at avoiding aggravating factors. These measures include adequate hydration (dehydration aggravates nephrolithiasis), avoiding thiazide diuretics or other offending medications, encouraging physical activity, and avoiding prolonged inactivity. Other interventions for mild hypercalcemia are disease specific.

For the treatment of primary hyperparathyroidism, surgical parathyroidectomy is the definitive treatment. Surgery is appropriate for patients with symptomatic hyperparathyroidism. Surgery may be an option for selected asymptomatic patients, including those who have developed osteoporosis or renal insufficiency, who have markedly elevated calcium levels, or who are younger than age 50 years.

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  • Mirrin
    What are the physical examination of hyper calcemia?
    8 years ago
  • cory
    What are the physical examinations of hyper calcemia?
    8 years ago
  • Natale
    Can rheumatoid arthritis cause hypercalcemia?
    1 year ago
  • karolin
    Can arthritis cause elevated calcium?
    3 days ago

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