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Definition

The skeletal system undergoes constant tunover and is affected by a variety of stimuli. Hormones such as parathyroid hormone, calcitriol (1, 25 Vitamin D3), estrogens, and minerals such as calcium, phosphorus, and magnesium are all important in normal bone turnover. Abnormalities in any of these systems may adversely affect bone and cause metabolic disease such as osteomalacia, osteoporosis, and hyperparathyroid bone disease. Other derangements include renal bone disease, hypoparathyroidism, pseudohypoparathyroidism, and Paget’s disease.

History

Symptoms: Bone pain, proximal muscle weakness (seen with elevated parathyroid hormone) and symptoms of hypercalcemia such as constipation, pancreatitis, or peptic ulcer disease causing abdominal pain, polyuria, and if the calcium level is high enough, central nervous system changes.

General: Those deemed to be at risk for osteoporosis include those with a family history of osteoporosis, early menopause, lack of exercise, lack of adequate 1, 25 (OHh D3 levels and thin, white patients with a low-dietary intake of calcium. Osteomalacia may be encountered in patients with decreased sun exposure or decreased dietary intake of vitamin D. Paget’s disease is quite common, seen in approximately 3 percent of adults over the age of 50 in the United States.

Age: Any, but more common in adults.

Onset: Gradual.

Duration: Lifelong.

Intensity: Asymptomatic to severe pain.

Aggravating Factors: Fractures, advancing age, dietary lack of calcium or vitamin D, renal failure, chronic acidosis, inactivity, and menopause.

Alleviating Factors: Exercise, administration of calcium or estrogens for osteoporosis, correction of hyperparathyroidism, correction of vitamin D deficiency in osteomalacia and calcitonin or diphosphates for Paget’s disease.

Associated Factors: Hyperthyroidism, vitamin D deficiency, or lack of androgen may contribute to osteoporosis. Phosphate binding antacids,diphenylhydantoin (dilantin) or gastrointestinal malabsorbtion may contribute to osteomalacia. Hyperparathyroidism and pseudohyperparathyroidism may cause skeletal abnormalities in children (neck, metacarpals and metatarsals are short).

Physical Examination

• General: Patients may appear quite normal unless bone deformity is present.
• Cardiovascular: Calcium abnormalities may cause abnormal ECG findings (see Diagnostic Studies).
• Extremities: Pseudohypoparathyroidism may cause a short neck, metacarpals and metatarsals.
• Gentiourinary: Kidney stones may cause flank pain (associated with hyperparathyroidism and vitamin D excess).
• HEENT: Pseudohypoparathyroidism may cause rounded facies.
• Neurologic: Pseudohypoparathyroidism may cause mental retardation. Hypercalcemia can cause lethargy and, if the calcium is high enough, coma.
• Skin: Dry skin and brittle hair may be seen with chronic hypocalcemia or hypoparathyroidism. Subcutaneous calcium phosphate accumulation with renal failure may cause pruritus, dry skin, secondary infections due to scratching, and subcutaneous nodules.

Pathophysiology

• Osteomalacia: The inability to mineralize bone properly. The usual causes are the lack of vitamin D, calcium, and phosphorus.
• Osteoporosis: Decrease in the amount of normal bone mass. High-risk of fracture (especially back or hip fracture). May be due to advancing age, excess steroid use, lack of estrogen or androgen, inactivity, and low-calcium intake.
• Hyperparathyroidism: Primary hyperparathyroidism is usually caused by an adenoma and may be seen in conjunction with multiple endocrine neoplasia. Secondary hyperparathyroidism can be seen with renal failure or four gland hyperplasia. Both may cause osteitis fibrosa cystica.
• Hypoparathyroidism: May be idiopathic or encountered after neck surgery with the removal of the parathyroid gland.
• Pseudohypoparathyroidism: Is due to resistance to peripheral effects of parathyroid hormone.
• Renal bone disease: May be due to hyperparathyroidism, low 1, 25 (OH2) D3 or aluminum bone disease from aluminum oral phosphate binders.
• Paget’s Disease: Osteolytic bone formation followed by disorganized osteoblastic lesions with sclerosis. This bone structure is weak and prone to fractures. A viral etiology is suspected.

Diagnostic Studies

Laboratory

• Calcium (normal 8.5 to 10.5 mg/ dl): High to high normal in hyperparathyroidism, low in hypoparathyroidism and pseudohypoparathyroidism.
• Phosphate (normal 2.3 to 4.8 mg/dl): Low to low normal in hyperparathyroidism and osteomalacia. High in hypoparathyroidism and pseudohypoparathyroidism.
• Albumin (normal 3.5 to 5.0 mg/dl): To correct serum calcium (for every decrease of 1.0 mg/dl of albumin, calcium drops by 0.8 mg/dl).
• Intact parathyroid hormone (normal 10 to 65 pg/ml): High in hyperparathyroidism and in pseudohypoparathyroidism, low in hypoparathyroidism. May be high in secondary hyperparathyroidism.
• Serum I, 25 (OH2) D3 (normal 20 to 76 pg/ml): Low in hypoparathyroidism and renal failure, elevated in hyperparathyroidism.
• Serum alkaline phosphatase (normal 20 to 140 IU/L): May be high in osteomalacia and Paget’s disease.
• 24 hour urine for calcium (normal 100 to 300 mg/24 h): Used to document calcium intake; high in hyperparathyroidism and, at times, low in osteoporosis.
• Random urine for calcium (normal 1.0 to 11 .5 mmol/L): Elevated in hyperparathyroidism.

Radiology

• Bone radiographs: Osteopenia may be seen with osteomalacia and osteoporosis. Looser’s fracture seen in osteomalacia (scapula and long bones). Increased bone reabsorption in fingers and clavicle ends with hyperparathyroidism. Aids in the diagnosis of pseudohypoparathyroidism if short metacarpal changes are present. Paget’s disease changes usually seen in the pelvis or skull.
• Bone densometry: Quite helpful in determining bone density and fracture risk with osteoporosis.
• Bone scan: Will help in the diagnosis of Paget’s disease as affected areas will have a strong uptake of the isotope.

Other

ECG: Hypercalcemia causes a shortened S-T segment on decreased corrected Q- T interval. With very high calcium ( 16 mg/dl), the T wave widens. With hypocalcemia, the S-T segment is lengthened and the corrected Q-T interval may be prolonged.

Bone biopsy: Helpful in the management of renal bone disease or osteomalacia.

Differential Diagnosis

Traumatic

• Looser’s fractures: May appear like tree fractures (e.g., osteomalacia).
• Infectious Chronic osteomyelitis: Infection of bone.

Metabolic

• Hyperthyroidism: May be a cause of osteoporosis.
• Hypomagnesemia: May affect parathyroid hormone release. Neoplastic
• Multiple myeloma: May cause hypercalcemia, increased calcium loss, or renal failure.

Vascular

• Looser’s fractures: Nutrient arteries going to bone.

Congenital

• Hormone resistance patterns: In pseudohypoparathyroidism.

Acquired

• Alcoholism: May be a cause for osteoporosis or in conjunction with hepatic failure, or osteomalacia.

Treatment

Treatment of all forms of metabolic bone disease often requires calcium or vitamin D. Careful follow up of serum calcium is essential to avoid hypercalcemia.

Osteomalacia: Correction of underlying renal failure if present. Discontinue the use of aluminum hydroxide binders.

Vitamin D therapy: With normal renal function give vitamin D 25 to 50,000 u/d, With renal failure give 1,25 (OH2) D3, 0.25 to 0.5 mcg/d.

Osteoporosis: Recommendations include Increase the level of exercise if possible. Avoid prolonged bedrest. High-risk patients (thin, white females with a low-calcium intake) should be appraised of the risks of osteoporosis and increase dietary, jntake of calcium.

Milintain an intake of calcium 1.5 grams per day.

Consider estrogen therapy as menopause begins. Begin with 0.625 mg/d of estrogen. Thiazide diuretics (25 mg/d) help with renal retention of calcium. Calcitonin may help with bone pain. Dose 50 to 100 IU/d. Etidronate given cyclically at 400 mg/d for 2 weeks and repeat every 3 months.

Hyperparathyroidism: If adenoma is present, parathyroidectomy is indicated. If the patient presents with renal failure, treatment consists of phosphate control (to achieve P04 of 6.0), normalization of calcium and treatment with 1, 25 (OH2) D3 (oral dose 0.25 to 0.5 mcg/d, pulse biweekly dose of 2 ‘to 5.0 mEq, or intravenous 0.5 to 5 mcg/d 3 times a week). This will often suppress parathyroid hyperplasia (Usually not effective in nodular hyperplasia. In these patients parathyroidectomy may be necessary). Renal transplantation is often curative.

Hypoparathyroidism: Treatment with vitamin D 25 to 100,000 u/d or its analog I, 25 (OH2) D3 0.25 to 0.5 mcg/d. Calcium 1.0 to 2.0 g/d should be instituted.

Pseudohypoparathyroidism: Same as hypoparathyroidism.

Paget’s disease: Calcium 1.0 g/d.

Calcitonin: Start at 50 IU/d and increase up to 150 IU/d as needed, based on the symptoms and severity of disease. Diphosphates may be useful.

Pediatric Considerations

Osteopenia has been noted in premature infants especially those with birth weights under 1000 g and those with chronic diseases of prematurity. In such infants, the rate of fetal bone mineralization is not always maintained by breastfeeding infants or those feeding on standard formulas. X-rays reveal bone’ demineralization and fractures. Serum alkaline phosphatase levels may be as high as two to three times normal. Sequelae may be prevented with formulas containing higher levels of calcium, phosphate and Vitamin D. Such dietary supplements are also used for treatment when indicated.

Patients with metabolic disorders may appear normal at birth and indirectly develop signs of bone disease after or simultaneously with the manifestations produced by the underlying metabolic disorder. Treatment of inborn errors of metabolism must be aimed at correcting the specific disorder.

The key is to correct any vitamin D abnormalities rapidly to prevent abnormal bone growth.

Obstetrical Considerations

Osteoporosis: Almost always occurs during the postmenopausal period or postoophorectomy. If a patient develops clinically significant osteoporosis during the perimenopausal years and becomes pregnant, they will need to pay very careful attention to maintaining adequate calcium and vitamin D levels. The patient should also be followed as she is high risk for developing fractures. If a patient is suffering from a form of secondary osteoporosis, control of the underlying condition, along with adequate maintenance of calcium and vitamin D levels is appropriate.

Osteomalacia: Occurs secondary to nutritional vitamin D deficiency, renal failure, steatorrhea or vitamin D resistant ricketts. Pregnant patients need careful attention to the underlying disease process and vitamin D in doses sufficient to maintain adequate for the fetus and to control the osteomalacia.
Paget’s Disease: Calcitonin and disodium etidronate, both used for treatment of Paget’s disease, should be used only when necessary. Calcitonin is a Category C drug, and disodium etidronate is Category B. Mithramycin is contraindicated in pregnancy due to fetal effects.

Tagged under:calcitriol calcium level Diseases hypoparathyroidism menopause osteomalacia pancreatitis parathyroid hormone peptic ulcer disease pseudohypoparathyroidism renal bone disease risk for osteoporosis symptoms of hypercalcemia

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