Primary Hyperparathyroidism: Understanding the Overactive Parathyroid

Introduction

Primary hyperparathyroidism (PHPT) is one of the most common endocrine disorders, especially in adults over 50. It arises from excessive secretion of parathyroid hormone (PTH) by one or more parathyroid glands, leading to elevated blood calcium levels. This imbalance can affect bones, kidneys, and multiple organ systems.

Normal Parathyroid Function

The parathyroid glands are four small glands located behind the thyroid. Their main job is to maintain calcium balance. When blood calcium falls, they release PTH, which:

• Increases bone resorption, releasing calcium into the bloodstream.

• Enhances renal calcium reabsorption and phosphate excretion.

• Stimulates conversion of vitamin D to its active form (calcitriol), increasing intestinal calcium absorption.

Pathophysiology of Primary Hyperparathyroidism

In primary hyperparathyroidism, the feedback control system malfunctions. One or more glands autonomously produce excess PTH regardless of calcium levels.

Common causes include:

1. Parathyroid adenoma (≈85%) – a benign tumour in a single gland.

2. Parathyroid hyperplasia (≈10–15%) – enlargement of multiple glands.

3. Parathyroid carcinoma (<1%) – a rare malignant cause.

Consequences of excess PTH include bone demineralization, kidney stones, and systemic effects on mood and digestion. Classic symptoms can be remembered by the mnemonic: ‘Bones, stones, groans, and psychic overtones’.

Diagnosis

Laboratory Findings:

• Elevated serum calcium

• Inappropriately elevated PTH

• Low to normal serum phosphate

• High urinary calcium excretion

Imaging: Neck ultrasound and sestamibi scans help localize abnormal glands. 4D-CT or MRI may assist in complex cases.

Bone and renal assessments include DEXA scanning and renal ultrasound.

Treatment

1. Surgical Management (Definitive Treatment)

Parathyroidectomy is the gold standard. Indications include symptomatic disease, young patients (<50), or those with significant hypercalcaemia, renal dysfunction, or osteoporosis. Minimally invasive parathyroidectomy guided by imaging is preferred.

2. Medical Management

For patients unfit or unwilling for surgery, treatment focuses on controlling calcium levels and protecting bone density:

• Maintain hydration and avoid thiazide diuretics or lithium.

• Use bisphosphonates to preserve bone density.

• Use calcimimetics (e.g., Cinacalcet) to reduce PTH secretion and serum calcium.

• Regular monitoring of calcium, renal function, and bone density is essential.

Postoperative Considerations

After parathyroidectomy, transient hypocalcaemia (‘hungry bone syndrome’) may occur as bones rapidly absorb calcium. Calcium and vitamin D supplementation are often needed. Long-term prognosis is excellent with normalization of calcium and PTH.

Summary Table

Conclusion

Primary hyperparathyroidism is a common but often underdiagnosed cause of hypercalcaemia. Understanding its pathophysiology helps clinicians identify subtle cases early and prevent complications. Surgery remains the cornerstone of cure, offering lasting restoration of calcium balance and improved quality of life.