Causes and Risks

Parathyroid hormone helps maintain blood calcium by regulating bone turnover, absorption of calcium from the gut, and urinary calcium excretion.

Numerous disorders may lead to secondary hyperparathyroidism by causing hypocalcemia, disordered phosphate homeostasis, or both. These include:

• disorders of Vitamin D: examples are osteomalcia (rickets in children), caused by Vitamin D deficiency, malabsorption, abnormal Vitamin D metabolism induced by drugs
• disorders of phosphate metabolism: malnutrition, malabsorption, aluminum toxicity, kidney disease, cancers (phosphate depletion may also cause osteomalacia/rickets)
• calcium deficiency
• inhibitors of mineralization: chronic renal failure

Chronic kidney failure is an important cause of secondary hyperparathyroidism. The disorder is complex. Phosphate clearance is impaired, phosphate is released from bone, Vitamin D is not produced, intestinal calcium absorption is low and blood levels of calcium are lowered. A positive feedback loop leads to increased bone resorption (bone is broken down in an attempt to regulate abnormal levels of these chemicals) and hyperphosphatemia (high levels of phosphates in the blood) which causes further secondary hyperparathyroidism.

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