Malignancy-associated hypercalcemia: This is often due to the production of parathyroid hormone-related protein (PTHrP) by tumor cells, leading to hypercalcemia and suppressed PTH levels. Common malignancies include lung, breast, and kidney cancer.

Vitamin D intoxication: Excessive intake of vitamin D can lead to increased absorption of calcium from the gut, resulting in hypercalcemia and low PTH levels due to negative feedback.
Familial hypocalciuric hypercalcemia (FHH): A genetic disorder characterized by inactivating mutations in the calcium-sensing receptor, leading to increased PTH secretion and hypercalcemia. However, PTH levels may be inappropriately normal or slightly low in the context of hypercalcemia.
Lithium therapy: Lithium can increase PTH secretion, but in some cases, it may also lead to hypercalcemia with low or normal PTH levels.

Hypercalcemia of malignancy with PTHrP production and concomitant primary hyperparathyroidism: Although rare, it's crucial to consider the possibility of co-existing primary hyperparathyroidism and malignancy-associated hypercalcemia, as the management and prognosis differ significantly.
Multiple myeloma: A type of blood cancer that can cause hypercalcemia through various mechanisms, including bone destruction and production of osteoclast-activating factors.

Sarcoidosis: A systemic granulomatous disease that can lead to hypercalcemia due to increased conversion of vitamin D to its active form, which enhances calcium absorption. PTH levels are typically low due to negative feedback.
Williams syndrome: A genetic disorder characterized by hypercalcemia, elfin facies, and intellectual disability. The hypercalcemia is thought to be due to increased sensitivity to vitamin D.
Jansen's metaphyseal chondrodysplasia: A rare genetic disorder caused by constitutively active PTH/PTHrP receptors, leading to hypercalcemia and skeletal abnormalities. However, PTH levels are typically low due to negative feedback.