Section 3: Calcium Disorders

Question 1

Most common cause of hypercalcemia

Answer 1

Primary hyperparathyroidism

Question 2

Causes of hypercalcemia

Answer 2

• Primary hyperparathyroidism
• Malignancy: Produces a parathyroid hormone– like particle
• Granulomatous disease: Sarcoid granulomas actually make vitamin D
• Vitamin D intoxication
• Thiazide diuretics: These increase tubular reabsorption of calcium
• Tuberculosis
• Histoplasmosis
• Berryliosis

Use the mnemonic “CHIMPANZEES. C=Calcium supplementation, H=Hyperparathyoidism, I=Infections (Histoplasmosis, Tuberculosis), M=Milk-Alkali syndrome, Medication (Thiazide Diuretic), P=Paget’s disease, A=Addison’s disease, N=Neoplasm (Metastasis), Z=Zollinger-Ellison’s disease, E=Excess Vit A, E=Excess Vit D, S=Sarcoidosis”

Question 3

Criteria for surgical removal of the parathyroid gland

Answer 3

• Any symptomatic disease (“stones, bones, psychic moans, GI groans”)
• Renal insufficiency, no matter how slight
• Markedly elevated 24-hour urine calcium
• Very elevated serum calcium (> 12.5)

Question 4

Normal serum calcium level

Answer 4

8.4 - 10.2 mg/dL

Question 5

Outline Rx for acute severe hypercalcemia

Answer 5

1. Hydration: High volume (3– 4 liters) of normal saline
2. Furosemide: Only after hydration has been given. Loop diuretics increase calcium excretion by the kidney
3. Bisphosphonate (pamidronate) is very potent but slow, taking a week to work
4. Calcitonin: If hydration and furosemide do not control the calcium and you need something faster than a bisphosphonate, then calcitonin is the answer
5. Steroid: Use if the etiology is granulomatous disease.

Question 6

Name the clinical features of acute severe hypercalcemia

Answer 6

• Confusion
• Constipation
• Polyuria and polydipsia from nephrogenic diabetes insipidus
• Short QT syndrome on the EKG
• Renal insufficiency, ATN, kidney stone

Question 7

CF of severe hypocalcemia

Answer 7

• Seizures
• Neural twitching (Chvostek’s sign and Trousseau’s sign)
• Arrhythmia: prolonged QT on ECG

Question 8

Outline the Rx of hypocalcemia

Answer 8

• Replace calcium
• Calcium + Vit D (for Vit D deficiency and hypoparathyroidism)

Question 9

List the causes of hypocalcemia

Answer 9

• Hypoparathyroidism
• Hypomagnesemia
• Infection
• Pancreatitis
• Overload (Rapid volume expansion)
• Chronic kidney disease
• Absorption abnormalities
• Loop Diuretic

Use the mnemonic “HIPOCAL”

Question 10

State the dietary allowance for calcium for the following group of perons:

1. Children aged 9-18 years
2. Adults 19-50 years
3. Adults 51 years and above

Answer 10

1. 1300mg
2. 1000mg
3. 1500mg

Question 11

A 52-year-old postmenopausal woman with a long-standing history of chronic obstructive pulmonary disease is evaluated during a follow-up office visit. She has had three acute exacerbations of her pulmonary disease in the past year. She was hospitalized on all three occasions and required high-dose methylprednisolone as part of the therapy. She continues to smoke despite requiring ipratropium bromide, salmeterol, and inhaled fluticasone. After her most recent hospital admission 3 months ago, she continued to require oral prednisone 10 mg/d. Every time a dose reduction of prednisone is attempted, there is an exacerbation of her pulmonary disease.

Which of the following should be done next as regards this patient’s bone health?

A Calcium supplementation
B Calcium and vitamin D supplementation
C Dual-energy x-ray absorptiometry (DEXA) scan and calcium and vitamin D supplementation
D Dual-energy x-ray absorptiometry (DEXA) scan, calcium and vitamin D supplementation, and bisphosphonate therapy
E Estrogen hormone replacement therapy

Answer 11

Answer and Critique (Correct Answer = D)

The best management for this patient is a dual-energy x-ray absorptiometry (DEXA) scan, calcium and vitamin D supplementation, and bisphosphonate therapy. Bone loss induced by exogenous corticosteroids is the most common form of secondary osteoporosis. There is a generalized decrease of bone mineral density, and 30% to 50% of patients develop vertebral fractures. The effect is determined by the dose and duration of corticosteroid therapy. Trabecular bone loss primarily occurs and is significant in the spine. After the initiation of corticosteroid therapy, there is a rapid phase of bone loss, followed by a slow continuous decline. The decreased bone formation is due to the toxic effects of glucocorticoids on osteoblasts. There is also decreased osteoblast recruitment and increased osteoblast apoptosis.

The prevention and treatment include oral calcium supplementation, 1500 mg/ d, and oral vitamin D, 800 IU/d. A DEXA scan should be performed at the initiation of corticosteroid therapy along with patient education and treatment of underlying risk factors. Bisphosphonates are recommended at the start of therapy for the prevention of bone loss if prednisone, 5 mg/d or higher (or its equivalent), is to be used for more than 3 months. Bisphosphonates should be started in patients with T scores < –1.0 who are receiving long-term corticosteroid therapy, regardless of the dose.

Hormone replacement therapy is no longer regarded as the mainstay of treatment for osteoporosis in women. In the Women’s Health Initiative study, the use of conjugated estrogens and medroxyprogesterone in postmenopausal women increased the risk of cardiovascular disease, invasive breast cancer, stroke, deep venous thrombosis, and pulmonary embolism.

Key Point

The prevention and treatment of corticosteroid-induced osteoporosis include calcium and vitamin D supplementation, a DEXA scan at the initiation of therapy, and bisphosphonates in patients taking prednisone, ≥5 mg/d (or its equivalent), for >3 months.

Bibliography

Maricic M. Glucocorticoid-induced osteoporosis: treatment options and guidelines. Curr Osteoporos Rep. 2005;3:25-9. [PMID: 16036098] [PubMed]