Hyperparathyroidism

Basics

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)

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

There's more to see -- the rest of this topic is available only to subscribers.