Tumor biology and incidence
- Characterized by elevated serum PTH, hypercalcemia and hypophosphatemia
- Classified as primary, secondary or tertiary.
- Primary: Caused by parathyroid adenoma (approximately 80% of cases), multiple adenomas, hyperplasia or carcinoma of parathyroid tissues
- Secondary: Usually result of renal or intestinal losses of calcium
- Tertiary: Occurs when secondary hyperparathyroidism becomes autonomous
Presentation and physical findings
- Signs and symptoms: "Stones , bones, gastrointestinal groans, psychiatric moans, and fatigue overtones"
- Stones: Nephrolithiasis and nephrocalcinosis
- Bones: Often painful, tender, weak, and susceptible to pathologic fracture
- Patient may develop generalized osteitis fibrosa cystica (fibrous replacement of the marrow) or may develop a brown tumor
- Gastrointestinal: Abdominal pain possibly due to peptic ulcer or pancreatitis
- Psychiatric: May develop depression, psychosis
- Fatigue: Weakness or hypotonia of the muscles
- Elevated serum calcium, elevated serum PTH, and decreased serum phosphate
Radiographic appearance
- Early, generalized osteopenia; often overlooked
- Changes related to increased osteoclast activity, decreased thickness of trabeculae
- Best seen in X-rays of hands, spine
- May see soft tissue calcification, vascular calcifications
- Moderate osteopenia: Cortical resorption canals, subperiosteal resorption of bone and, loss of the terminal cortex of tufts of phalanges
- Severe osteopenia: Advanced cortical resorption canals, subperiosteal resorption of bone.
Pathology
- May observe brown tumor of hyperparathyroidism
- Contain abundance of giant cells in a mononuclear stroma
- Histologically indistinguishable from giant cell tumors; diagnosis based on combination of clinical, radiologic, and pathologic data
Diagnosis and treatment
- Correct life-threatening electrolyte disturbances
- Identify and treat cause of increased PTH levels
Last Updated on June 27, 2024
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