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Hypercalcemia secondary to primary hyperparathyroidism
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Hypercalcemia secondary to Primary Hyperparathyroidism. Emily Kingsley, MD Med-Peds II. 90% of cases of hypercalcemia are due to hyperparathyroidism and malignancy

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Hypercalcemia secondary to Primary Hyperparathyroidism

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Hypercalcemia secondary to Primary Hyperparathyroidism

Emily Kingsley, MD

Med-Peds II

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  • 90% of cases of hypercalcemia are due to hyperparathyroidism and malignancy

    • HyperPTH: asymptomatic with chronic hypercalcemia, postmenopausal woman, normal physical examination, family history of hyperparathyroidism, and evidence of multiple endocrine neoplasia

    • Malignancy: Higher concentrations of and more rapid increases in serum calcium and subsequently are more symptomatic

  • Ambulatory: Healthy patients, usually due to primary hyperparathyroidism

  • Hospital: Usually due to malignancy

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Primary Hyperparathyroidism

  • Usually due to parathyroid adenoma

  • Typically have only small elevations in serum calcium concentrations (less than 11 mg/dL) and sometimes values are high-normal

    • May require multiple measurements

    • Parathyroid crisis: uncommon but acute onset of severe, symptomatic hypercalcemia

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Secondary HyperPTH

  • Seen in severe chronic kidney disease

  • Usually low or normal serum calcium values

  • Few with hypercalcemia have decreased bone turnover

  • Tertiary HyperPTH: Parathyroid hyperplasia to autonomous overproduction of PTH

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  • Mechanism of increased bone resorption depends on the cancer

    • Bony mets: direct induction of osteolysis by tumor cells through the use of cytokines (TNF, IL-1)

    • Nonmetastatic solid tumors: PTHrP

    • Lymphoma: PTH-independent extrarenal production of calcitriol from mononuclear cells

  • Hypercalcemia with values above 13mg/dL

    • Unusual in hyperparathyroidism

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Other causes of hypercalcemia

  • Thyrotoxicosis: usu. mild hypercalcemia

  • Immobilization

  • Paget disease of bone

  • Hypervitaminosis A

  • Hypervitaminosis D

    • Calcitriol used with renal failure has short half life

    • Calcidiol has longer half life so symptomatic pts. may need steroids and bisphosphonate

  • Sarcoidosis, Wegener’s granulomatosis

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  • Milk Alkali Syndrome: can occur in the setting of excess calcium carbonate supplementation to treat osteoporosis or dyspepsia

  • Lithium: increased secretion of PTH due to an increase in the set point at which calcium suppresses PTH release

  • Thiazide diuretics

  • Pheochromocytoma

  • Adrenal insufficiency

  • Theophylline toxicity

  • Familial hypocalciuric hypercalcemia: loss-of-function mutation in the calcium-sensing sensor on the parathyroid cells and in the kidneys

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Clinical Manifestations

  • Ranges from asymptomatic to obtundation and coma

  • Mild hypercalcemia (calcium <12 mg/dl): Asymptomatic or nonspecific symptoms (constipation, fatigue, and depression)

  • Moderate hypercalcemia (calcium 12 to 14 mg/dL):

    • may be well-tolerated chronically

    • Acute rise to these concentrations may cause marked symptoms: polyuria, polydipsia, dehydration, anorexia, nausea, muscle weakness, and changes in sensorium.

  • Severe hypercalcemia (calcium >14 mg/dL): progression of symptoms

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Cognitive dysfunction









Peptic ulcer disease


Bone pain

Profound muscle weakness


Shortening of the QT interval




Polyuria: decr. concentration in distal tub.


Acute/Chronic renal insuffic.

Serum calcium of 12 to 15 mg/dL can lead to a reversible fall in GFR from direct renal vasoconstriction

Long-standing hypercalcemia and hypercalciuria: Calcification, degeneration, and necrosis of the tubular cells →Tubular atrophy and interstitial fibrosis and calcification (nephrocalcinosis).

…Bones, stones, moans, and groans

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Normal or

  • Correction for the measured calcium concentration in hypoalbuminemia

    Ca = Serum Ca + 0.8 * (Normal Albumin – Pt Albumin)

Primary HyperPTH


Vitamin D levels



Vitamin A levels




Vit D intoxication

Granulomatous dis.

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Haden, ST, Brown, EM, Hurwitz, S, et al. The effects of age and gender on parathyroid hormone dynamics. Clin Endocrinol 2000; 52:329.

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  • 25-OH Vitamin D: Usually due to ingestion

  • 1,25-OH Vitamin D: Ingestion, granulomatous diseases, lymphoma, primary hyperparathyroidism

    • Increased: Recommend CXR → Sarcoidosis, Lymphoma

Granulomatous dis. Milk Alkali Syndrome

Vitamin D intoxication Metastatic bone dis.

Thyrotoxicosis Immobilization

Normal or



PTHrP malignancy

-Inhibition of renal proximal tubular

Phosphate resorption

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Treatment of Hypercalcemia

  • Degree of hypercalcemia and rate of rise determine symptoms and urgency of treatment

    • Calcium >14mg/dL: Require treatment regardless of symptoms

    • Calcium 12-14mg/dL:

      • Chronically maybe be tolerated

      • Acutely may lead to AMS

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Isotonic Saline

Treats volume depletion from calcium-induced urinary salt wasting

Increases renal perfusion and urinary calcium clearance

Administration: Initial rate of 200-300ml/hr adjusted for urinary output of 100ml/h

Limited in those with cardiac or renal disease

Should be discontinued with development of edema

Goal: Euvolemia

Rarely normalizes calcium level

Ways to Correct Hypercalcemia

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  • Bisphosphonates

    • Analogs of inorganic pyrophosphate that absorb to the surface of bone hydroxyapatite inhibiting calcium release by interfering with osteoclast-mediated bone resorption

    • More potent than Saline and Calcitonin

    • Administration: IV Zoledronic acid preferred due to potency and short administration time (15 min.)

      • Single dose due to risk of osteonecrosis of jaw with repeat doses

    • Effect: Seen in 2-4 DAYS

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  • Calcitonin

    • Decrease bone reabsorption by interfering with osteoclast maturation

    • Increase renal calcium excretion

    • Administration: IM or subcut, nasal not effective

    • Effect: Rapid with lowering within 4-6 HOURS

      • Decreases the serum calcium up to a maximum of 1 to 2 mg/dL

      • Efficacy limited to 48 HOURS

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  • Glucocorticoids

    • Useful with calcidiol ingestion

    • Useful with hypercalcemia from increased calcitriol production seen in granulomatous disease and lymphoma

      • Decreases calcitriol production by activated mononuclear cells in the lung and lymph nodes

    • Administration: 20-40mg/day

    • Effect: Seen in 2-5 days

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  • Dialysis

    • Indications:

      • Severe hypercalcemia (18 to 20 mg/dL) with neurologic symptoms

      • Limited use of IV hydration:

        • Renal insufficiency

        • Heart failure

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In Sum…

  • Mild (<12mg/dl): No therapy

    • Avoid thiazide diuretic, lithium, calcium ingestion (>1000mg/day), volume depletion, prolonged bedrest

  • Moderate (12-14mg/dl): Treat if symptomatic or an acute rise

  • Severe (>14mg/dl): IV saline (immediate effect), calcitonin (immediate effect), bisphosphonate (delayed but most effective)

  • Primary hyperparathyroidism: Parathyroidectomy

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And the calcium lived happily ever after…

(What would a Med-Peds presentation

be without a Sponge Bob reference?!?!)

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  • Develops in those with bone disease preoperatively due to a chronic increase in bone resorption from high levels of PTH

  • Sudden withdrawal of PTH causes increased osteoblast-mediated bone formation and marked net increase in bone uptake of calcium, phosphate, and magnesium

  • Syndrome most likely to be present if if the serum calcium concentration <8.5 mg/dL and the serum phosphate concentration <3.0 mg/dL on the 3rd postoperative day

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  • Hypocalcemia

    • Tetany, seizures, heart failure

    • Treatment:

      • Oral calcium (2 to 4 g per day): Between meals to avoid phosphate binding

      • IV calcium: With rapid reduction in serum calcium OR symptoms related to hypocalcemia OR plasma calcium concentration below 7.5 mg/dL

  • Hypophosphatemia: With significant bone disease

    • Replacement only in severe hypoPO4 (below 1 mg/dL): Combines with calcium to further reduce calcium concentration

    • BUT with lack of severe bone disease: See increase in phosphate due to reversal of PTH-induced phosphate loss in the urine

  • Hypomagnesemia

    • Can contribute refractory hypocalcemia by diminishing PTH secretion and inducing PTH resistance

  • Hyperkalemia

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  • Bilezikian, J. Clinical review 51: Management of hypercalcemia. J Clin Endocrinol Metab1993; 77: 1445-1449.

  • Haden, ST, Brown, EM, Hurwitz, S, et al. The effects of age and gender on parathyroid hormone dynamics. Clin Endocrinol 2000; 52:329.

  • Marx, S. Hyperparathyroid and hypoparathyroid disorders. N Engl J Med 2000; 343: 1863-1875.

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