Nodular hyperplasia of the parathyroid glands is characterized by several biochemical changes that reflect the underlying pathophysiology of the condition. Here are the key biochemical features:

1. Elevated Parathyroid Hormone (PTH) Levels: In nodular hyperplasia, there is an increase in the number of parathyroid cells, leading to overproduction of PTH. This can result in hyperparathyroidism, which is often classified as primary hyperparathyroidism.

2. Hypercalcemia: The elevated levels of PTH lead to increased calcium release from bones, increased renal tubular reabsorption of calcium, and increased intestinal absorption of calcium (via vitamin D activation). This results in elevated serum calcium levels.

3. Hypophosphatemia: PTH promotes renal excretion of phosphate, which can lead to low serum phosphate levels in patients with nodular hyperplasia.

4. Increased Alkaline Phosphatase: This enzyme may be elevated due to increased bone turnover associated with the effects of elevated PTH on bone metabolism.

5. Vitamin D Metabolism: There may be alterations in vitamin D metabolism, as PTH influences the conversion of vitamin D to its active form (calcitriol), which in turn affects calcium and phosphate homeostasis.

6. Calcium and Phosphate Balance: The biochemical profile often shows a characteristic imbalance, with high calcium and low phosphate levels, which is typical in primary hyperparathyroidism due to nodular hyperplasia.

In summary, nodular hyperplasia of the parathyroid glands is biochemically characterized by elevated PTH, hypercalcemia, hypophosphatemia, and increased alkaline phosphatase levels, reflecting the dysregulation of calcium and phosphate metabolism.