Hyperparathyroidism

Basics

Description

  • Parathyroid hormone (PTH) excess with symptoms owing to PTH actions, including:
    • Decreases urinary Ca2+ loss
    • Increases urinary PO42− loss
    • Stimulates vitamin D conversion from 25(OH)-D to 1,25(OH)-D in kidney
    • Liberates Ca2+ and PO42− from bone
    • Hypercalcemia is the primary metabolic finding
  • Hypercalciuria from hypercalcemia (despite decreased urinary loss) produces increased magnesium loss in urine
  • Hypomagnesemia (due to negative feedback to prevent hypercalcemia):
    • Cofactor in the production of PTH
    • Essential for action of PTH in target tissues
  • Genetics:
    • Associated with multiple endocrine neoplasia type 1:
      • Hyperparathyroidism
      • Pancreatic islet disease
      • Pituitary disease
    • Associated with multiple endocrine neoplasia type 2:
      • Hyperparathyroidism (type 2A, rare in 2B)
      • Medullary carcinoma of the thyroid (type 2A and 2B, less virulent in type 2A)
      • Pheochromocytoma (type 2A and 2B)
      • Mucosal neuroma (type 2B)

Etiology

  • Excess secretion of PTH owing to:
    • Primary hyperparathyroidism (parathyroid single benign adenoma 85%, hyperplasia 14%, carcinoma <1%)
    • Secondary hyperparathyroidism (response to vitamin D deficiency or chronic renal failure with hyperphosphatemia):
      • Calcium is low or normal, but PTH levels are elevated

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