Primary Hyperparathyroidism: Symptoms, Causes, and Management

Primary hyperparathyroidism (PHPT) results from autonomous parathyroid hormone (PTH) overproduction, leading to hypercalcemia. It is most commonly caused by a single parathyroid adenoma (80–85%), with hyperplasia (15%) or carcinoma (<1%) being less frequent.

Clinical Manifestations ("Stones, Bones, Groans, Moans")

• Renal: Nephrolithiasis (calcium phosphate/oxalate), nephrocalcinosis, polyuria/polydipsia.
• Skeletal: Osteopenia/osteoporosis (cortical > trabecular), subperiosteal resorption, brown tumors, increased fracture risk.
• GI: Nausea, constipation, peptic ulcer disease, pancreatitis.
• Neuropsychiatric: Fatigue, depression, anxiety, cognitive fog, weakness.
• Cardiovascular: Hypertension, vascular calcification, shortened QT interval.

Diagnosis

• Elevated serum calcium (albumin-corrected or ionized) + inappropriately normal or high PTH.
• 25-OH vitamin D (often low), 24-hour urine calcium/creatinine (to rule out familial hypocalciuric hypercalcemia).
• Sestamibi scan + neck ultrasound for preoperative localization.

Treatment

• Surgery (parathyroidectomy): Curative; minimally invasive focused approach if localized. Intraoperative PTH drop >50% confirms cure.
• Medical management (if non-surgical candidate): Cinacalcet (calcimimetic) lowers calcium; bisphosphonates/denosumab for bone protection.

Normocalcemic PHPT (high PTH, normal calcium) may precede overt hypercalcemia and warrants monitoring.