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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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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
primary hyperparathyroidism
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
secondary hyperpth
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
  • 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
other causes of hypercalcemia
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
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
clinical manifestations
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
bones stones moans and groans



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

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.


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

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

treatment of hypercalcemia
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
ways to correct hypercalcemia
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
    • 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
    • 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
    • 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
    • Indications:
      • Severe hypercalcemia (18 to 20 mg/dL) with neurologic symptoms
      • Limited use of IV hydration:
        • Renal insufficiency
        • Heart failure
in sum
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
and the calcium lived happily ever after
And the calcium lived happily ever after…

(What would a Med-Peds presentation

be without a Sponge Bob reference?!?!)

hungry bone syndrome
  • 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
    • 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
  • 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.
  • Up-To-Date. www.utdol.com