With normal or elevated PTH levels-

• Primary or tertiary hyperparathyroidism (most common)
• Li- induced hyperparathyroidism
• Familial hypocalciuric hypercalcemia

With low PTH levels-

• Malignancy (most common)
• Elevated 1, 25 (OH)₂ vitamin D
• Thyrotoxicosis, sarcoidosis, bone metastasis, multiple myeloma
• Paget’s disease with immobilisation
• Milk- alkali syndrome
• Thiazide diuretics
• Glucocorticoids deficiency

 Etiology-

With normal or elevated PTH levels-

• Primary or tertiary hyperparathyroidism (most common)
• Li- induced hyperparathyroidism
• Familial hypocalciuric hypercalcemia

With low PTH levels-

• Malignancy (most common)
• Elevated 1, 25 (OH)₂ vitamin D
• Thyrotoxicosis, sarcoidosis, bone metastasis, multiple myeloma
• Paget’s disease with immobilisation
• Milk- alkali syndrome
• Thiazide diuretics
• Glucocorticoids deficiency

 Clinical features-

• General- anorexia, fatigue, nausea, pancreatitis
• Renal- polyuria, polydipsia, renal stones
• GIT- dyspepsia, peptic ulcer, constipation
•  CNS- impaired cognition, hypertension
• Metabolic- metastaticcalcification, bone pain, fracture, nephrocalcinosis

 Investigations-

• Most common investigation is serum PTH level.
• PTH increased- primary hyperparathyroidism
• High plasma phosphate & alkali phosphatise- tertiary hyperparathyroidism
• Low urine calcium excretion- FHH
• Tests used to distinguish Primary Hyperparathyroidsm from Familial Benign Hypercalcemia- urinary calcium levels
• Hypercalcemia in ECG is diagnosed by decreased QT interval.

 Treatment-

• Volume expansion- 4-6 lt. Intravenous saline
• Hypercalcemia of malignancy – Zoledronic acid, pamidronate
• 1, 25 (OH)₂ D mediated hypercalcemia- glucocorticoids
• Calcitonin- for life threatening hypercalcemia
• Bisphosphonates- decreased serum calcium