Health condition
Parathyroid gland disorders, from too much PTH to too little.
Hyperparathyroidism and hypoparathyroidism sit at opposite ends of the same axis - calcium control. Understanding one helps make sense of the other.
Why trust this guide
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Editorial team
Written by our editorial team from the UK sources listed on each page.
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Sourced from guidance
Checked against NICE, SIGN and Society for Endocrinology sources you can see at the end.
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Current for 2026
Reflects modern UK practice for both hyperparathyroidism and hypoparathyroidism, including surgical and medical pathways.
Key facts
Parathyroid disease at a glance.
The essentials, in plain English - what the parathyroid glands do, how they misbehave, and how it’s managed in the UK today.
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What it is
The parathyroid glands set blood calcium by releasing PTH. Disease means either too much PTH (hyperparathyroidism) or too little (hypoparathyroidism).
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Primary hyperpara
Usually a single benign parathyroid adenoma driving excess PTH and hypercalcaemia - the most common form seen in clinic.
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Secondary hyperpara
A compensatory response, most often to chronic kidney disease or vitamin D deficiency - PTH rises to defend a low or borderline calcium.
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Tertiary hyperpara
Autonomous, unregulated PTH secretion that persists after long-standing secondary disease, usually in advanced kidney disease.
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Hypoparathyroidism
Insufficient PTH, most commonly after thyroid or neck surgery, causing hypocalcaemia and its characteristic neuromuscular symptoms.
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Shared thread
Both directions are diagnosed on the same core bloods - calcium, PTH, vitamin D and phosphate - interpreted together, not in isolation.
Why this guide matters
One axis, two directions.
Hyperparathyroidism and hypoparathyroidism are often explained separately, but they share the same biochemistry and the same testing pathway. The three points below shape everything else on this page.
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Calcium and PTH are read together
Neither number means much alone - it’s the relationship between calcium and PTH that tells the story.
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Cause changes the treatment
A benign adenoma, chronic kidney disease and post-surgical injury all call for a different plan, even when the biochemistry looks similar.
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Most cases are manageable
Surgery is curative for many with primary hyperparathyroidism, and replacement therapy controls most hypoparathyroidism well.
How the diagnosis is made
From an abnormal blood test to a clear plan.
The steps a UK GP or endocrinologist will normally follow, in order - whichever direction the calcium is out of range.
Phase 1 · Assessing
Core bloods and pattern classification
Phase 2 · Confirming
Urine testing and imaging
Phase 3 · Preparing
Bone scan and specialist referral
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Assessing
Serum calcium and PTH
The starting pair for any suspected parathyroid problem - a high or low calcium is only meaningful once PTH is checked alongside it.
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Assessing
Vitamin D, phosphate and renal function
Vitamin D deficiency and kidney function both shape the picture, especially in secondary and tertiary hyperparathyroidism.
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Assessing
Classify the pattern
High calcium with high PTH points to primary or tertiary disease; low calcium with low PTH points to hypoparathyroidism.
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Confirming
24-hour urinary calcium
Helps distinguish primary hyperparathyroidism from familial hypocalciuric hypercalcaemia, which does not need surgery.
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Confirming
Neck ultrasound and sestamibi scan
Imaging to localise a parathyroid adenoma before surgery is considered - not needed to make the diagnosis itself.
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Preparing
DEXA scan for bone density
Assesses skeletal impact in hyperparathyroidism and helps decide between surgery and watchful waiting.
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Preparing
Specialist endocrinology referral
Confirmed or borderline cases in either direction are best managed jointly with endocrinology, and surgery where indicated.
Typical timeline: an incidental blood result to a settled plan in a matter of weeks.
Symptoms
“Bones, stones, groans - and the opposite.”
Hyperparathyroidism’s classic mnemonic, alongside the very different neuromuscular picture of hypoparathyroidism.
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Often found incidentally
Mild primary hyperparathyroidism is frequently picked up on routine bloods, with no symptoms at all.
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Bones - bone pain
Excess PTH draws calcium from bone, causing aches, reduced density and a raised fracture risk.
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Stones - kidney stones
Persistently high calcium increases the risk of renal calculi and, over time, nephrocalcinosis.
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Groans - abdominal symptoms
Constipation, nausea, abdominal pain and reduced appetite are classic hypercalcaemic features.
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Psychiatric overtones
Low mood, poor concentration, fatigue and confusion can all be traced back to a raised calcium.
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Muscle cramps and tetany
Hallmarks of hypocalcaemia in hypoparathyroidism - cramping, twitching and, in severe cases, spasm.
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Perioral tingling and positive signs
Numbness around the mouth and fingertips, with Chvostek’s and Trousseau’s signs on examination.
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Red flag - crisis or seizures
Severe hypercalcaemic crisis or hypocalcaemic seizures need same-day emergency assessment.
Treatment
How each direction is treated in the UK.
Surgery or watchful waiting for hyperparathyroidism, and calcium replacement for hypoparathyroidism - with medical options either side.
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Watchful waiting
Mild, asymptomatic primary hyperparathyroidism with only modestly raised calcium can often be monitored rather than operated on.
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Parathyroidectomy
Curative for a solitary adenoma - the treatment of choice for symptomatic or significantly abnormal biochemistry.
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Cinacalcet
A calcimimetic used when surgery is unsuitable or declined, lowering PTH and calcium medically.
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Treating the underlying cause
In secondary hyperparathyroidism, correcting vitamin D deficiency or optimising chronic kidney disease care addresses the driver.
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Surgery for tertiary disease
Once secretion becomes autonomous after prolonged secondary disease, parathyroidectomy is often needed.
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Calcium and alfacalcidol
The mainstay of hypoparathyroidism - oral calcium with active vitamin D, titrated against regular blood levels.
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Recombinant PTH
Reserved for severe, refractory hypoparathyroidism not adequately controlled on calcium and vitamin D alone.
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Emergency IV calcium
For acute severe hypocalcaemia or tetany - a same-day hospital treatment, not a routine outpatient step.
What this guide is based on
The sources behind every claim on this page.
UK national guidance and specialist society standards, current at the time of last review.
Key references
Guidelines and standards we relied on.
A quiet reminder
This guide is for information, not medical advice.
Your GP or endocrinologist knows your history and bloods and can tell you which parts apply to you. If in doubt, get seen.
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NICE. Hyperparathyroidism (primary): diagnosis, assessment and initial management (NG132).
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SIGN. Guidance referenced in the management of endocrine and metabolic bone disease.
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Society for Endocrinology. Clinical guidance on calcium and parathyroid disorders.
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British Association of Endocrine and Thyroid Surgeons (BAETS). Parathyroid surgery standards.
Red flags
When calcium problems need urgent attention.
Most parathyroid disease is manageable in outpatient care. These are the situations that aren’t - and where same-day help is needed.
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Hypercalcaemic crisis
Very high calcium with confusion, dehydration and drowsiness is a medical emergency needing same-day hospital care.
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Severe hypocalcaemic tetany or seizures
Uncontrolled muscle spasm, laryngospasm or seizures from low calcium need emergency IV calcium replacement.
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Cardiac arrhythmia
Both very high and very low calcium can provoke dangerous arrhythmias - an ECG is part of any severe case.
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Acute kidney injury
Obstructing renal stones or nephrocalcinosis from long-standing hypercalcaemia can precipitate kidney injury.
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Unrecognised post-surgical hypoparathyroidism
Tingling or cramps in the days after thyroid or neck surgery should prompt an urgent calcium check.
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Fragility fracture
A low-trauma fracture in someone with untreated hyperparathyroidism signals significant bone loss and needs prompt review.
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Suspected parathyroid carcinoma
Very rare - a very high calcium with a palpable neck mass or rapid onset warrants urgent specialist assessment.
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Laryngeal nerve injury after surgery
Voice change or breathing difficulty after parathyroid or thyroid surgery needs same-day ENT or surgical review.
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Familial hypocalciuric hypercalcaemia missed
Operating on this benign, inherited condition by mistake achieves nothing - urinary calcium testing should rule it out first.
Living with it
A manageable condition, whichever direction yours runs.
Four things that make the biggest difference day to day - regular monitoring, protecting your bones, recognising a flare early, and understanding your long-term plan.
A quiet reminder
Steady monitoring beats reacting to a crisis.
Regular bloods catch drift in either direction long before it becomes an emergency.
- 01 Monitor
Keep up with blood tests
Calcium, PTH and kidney function are checked regularly whichever direction your condition runs - don’t skip the follow-up bloods.
- 02 Bones
Protect your bone health
Adequate calcium and vitamin D intake, weight-bearing exercise and avoiding smoking all support skeletal health long-term.
- 03 Recognise
Know your warning symptoms
Learn what a hypercalcaemic or hypocalcaemic flare feels like for you, and who to contact if it happens.
- 04 Plan
Understand your treatment pathway
Whether you’re heading towards surgery, medical management, or lifelong replacement, ask your team what the plan looks like a year from now.
Frequently asked
Everything we get asked about parathyroid disorders.
Quick answers on hyperparathyroidism, hypoparathyroidism, surgery and calcium emergencies.
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What is a parathyroid gland disorder?
A problem with the four small glands in the neck that control blood calcium via parathyroid hormone (PTH). Too much PTH causes hyperparathyroidism and hypercalcaemia; too little causes hypoparathyroidism and hypocalcaemia.
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What’s the difference between primary, secondary and tertiary hyperparathyroidism?
Primary is usually a benign adenoma secreting excess PTH independently. Secondary is a compensatory rise in PTH, often from chronic kidney disease or vitamin D deficiency. Tertiary is autonomous overactivity that develops after prolonged secondary disease.
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Do I need surgery for primary hyperparathyroidism?
Not always. Symptomatic disease or significantly abnormal biochemistry usually warrants parathyroidectomy, which is curative. Mild, asymptomatic cases can often be monitored with watchful waiting instead.
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What causes hypoparathyroidism?
The most common cause by far is damage to the parathyroid glands during thyroid or other neck surgery. Less commonly it can be autoimmune, genetic, or related to low magnesium.
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How is a severe calcium emergency treated?
Severe hypercalcaemia is treated in hospital with fluids and specific calcium-lowering treatment. Severe hypocalcaemic tetany or seizures need emergency intravenous calcium replacement - both are same-day presentations, not routine appointments.
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Can hyperparathyroidism be found without any symptoms?
Yes - it’s often picked up incidentally on routine blood tests showing a raised calcium, well before bone pain, stones or mood symptoms appear. This is now one of the most common ways it’s diagnosed.
Related content
Keep reading.
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Hyperparathyroidism
The full guide to excess PTH, adenomas and surgery.
Learn more -
Hypoparathyroidism
The full guide to low PTH and calcium replacement.
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Hypercalcaemia
The biochemical picture behind hyperparathyroidism.
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Osteoporosis
Bone loss linked to long-standing hyperparathyroidism.
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Chronic kidney disease
A common driver of secondary hyperparathyroidism.
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