Hyperparathyroidism

Medicine > Endocrine & metabolic

Background knowledge 🧠

Definition

Hyperparathyroidism is a condition characterised by excessive secretion of parathyroid hormone (PTH) from the parathyroid glands.
PTH regulates calcium, phosphate, and vitamin D metabolism.
Results in hypercalcaemia and hypophosphatemia.
Divided into primary, secondary, and tertiary types based on the underlying cause.

Epidemiology

More common in women, particularly postmenopausal.
Prevalence increases with age.
Primary hyperparathyroidism is the most common cause of hypercalcaemia in the general population.
Secondary hyperparathyroidism is common in patients with chronic kidney disease.
Tertiary hyperparathyroidism occurs in long-standing secondary hyperparathyroidism, often post-renal transplantation.

Pathophysiology

PTH increases bone resorption, renal calcium reabsorption, and intestinal calcium absorption via vitamin D activation.
Results in elevated serum calcium and low serum phosphate.

Aetiology

Primary: parathyroid adenoma (most common), hyperplasia, or carcinoma.
Secondary: chronic kidney disease, vitamin D deficiency, malabsorption syndromes.
Tertiary: autonomous parathyroid hyperplasia following prolonged secondary hyperparathyroidism.

Clinical Features 🌡️

Symptoms

Often asymptomatic, discovered on routine blood tests.
Fatigue and weakness.
Depression and cognitive disturbances.
Polyuria and polydipsia.
Bone pain and fractures.
Abdominal pain and constipation.
Kidney stones.

Signs

Hypercalcaemia on blood tests.
Low serum phosphate.
Elevated serum PTH.
Subperiosteal bone resorption on X-rays.
Osteopenia or osteoporosis on DEXA scan.
Renal stones on imaging.
Shortened QT interval on ECG.

Investigations 🧪

Tests

Serum calcium: elevated.
Serum phosphate: low.
Serum PTH: elevated in primary and tertiary, normal to elevated in secondary.
24-hour urinary calcium: elevated in primary, low in familial hypocalciuric hypercalcaemia (FHH).
Renal function tests: to assess kidney function.
Vitamin D levels: to check for deficiency.
DEXA scan: to assess bone density.
Imaging: ultrasound, sestamibi scan for parathyroid adenomas.
ECG: shortened QT interval.

Management 🥼

Management

Surgical removal of parathyroid adenoma or hyperplastic glands (primary and tertiary hyperparathyroidism).
Monitor asymptomatic patients with mild disease.
Bisphosphonates for osteoporosis.
Calcimimetics (e.g., cinacalcet) in secondary and tertiary hyperparathyroidism.
Vitamin D and calcium supplements in secondary hyperparathyroidism due to deficiency.
Hydration and avoidance of thiazide diuretics to prevent hypercalcaemia.
Regular monitoring of serum calcium, phosphate, renal function, and bone density.

Complications

Osteoporosis and fractures.
Nephrolithiasis (kidney stones).
Renal impairment and nephrocalcinosis.
Peptic ulcer disease.
Pancreatitis.
Cardiovascular complications (hypertension, arrhythmias).
Neuropsychiatric disturbances (depression, confusion).

Prognosis

Depends on the underlying cause and effectiveness of treatment.
Surgical treatment of primary hyperparathyroidism usually curative.
Secondary hyperparathyroidism improves with management of underlying condition.
Regular monitoring essential to prevent complications.
Prognosis poorer in tertiary hyperparathyroidism without effective treatment.
Quality of life can be significantly improved with appropriate management.

Key Points

Hyperparathyroidism causes hypercalcaemia and hypophosphatemia.
Primary hyperparathyroidism is the most common type.
Surgical removal of adenoma or hyperplastic glands is often curative.
Monitor asymptomatic patients with regular blood tests and bone density scans.
Manage complications like osteoporosis and renal stones actively.
Refer to UK guidelines for specific management protocols.

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