Skip to main content

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.

A radiographer guides a patient onto the bed of an advanced 3 Tesla MRI scanner in a London imaging suite

Why trust this guide

  • 01

    Editorial team

    Written by our editorial team from the UK sources listed on each page.

  • 02

    Sourced from guidance

    Checked against NICE, SIGN and Society for Endocrinology sources you can see at the end.

  • 03

    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.

  • What it is

    The parathyroid glands set blood calcium by releasing PTH. Disease means either too much PTH (hyperparathyroidism) or too little (hypoparathyroidism).

  • Primary hyperpara

    Usually a single benign parathyroid adenoma driving excess PTH and hypercalcaemia - the most common form seen in clinic.

  • Secondary hyperpara

    A compensatory response, most often to chronic kidney disease or vitamin D deficiency - PTH rises to defend a low or borderline calcium.

  • Tertiary hyperpara

    Autonomous, unregulated PTH secretion that persists after long-standing secondary disease, usually in advanced kidney disease.

  • Hypoparathyroidism

    Insufficient PTH, most commonly after thyroid or neck surgery, causing hypocalcaemia and its characteristic neuromuscular symptoms.

  • 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.

  • Calcium and PTH are read together

    Neither number means much alone - it’s the relationship between calcium and PTH that tells the story.

  • 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.

  • 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.

  1. 01

    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.

  2. 02

    Assessing

    Vitamin D, phosphate and renal function

    Vitamin D deficiency and kidney function both shape the picture, especially in secondary and tertiary hyperparathyroidism.

  3. 03

    Assessing

    Classify the pattern

    High calcium with high PTH points to primary or tertiary disease; low calcium with low PTH points to hypoparathyroidism.

  4. 04

    Confirming

    24-hour urinary calcium

    Helps distinguish primary hyperparathyroidism from familial hypocalciuric hypercalcaemia, which does not need surgery.

  5. 05

    Confirming

    Neck ultrasound and sestamibi scan

    Imaging to localise a parathyroid adenoma before surgery is considered - not needed to make the diagnosis itself.

  6. 06

    Preparing

    DEXA scan for bone density

    Assesses skeletal impact in hyperparathyroidism and helps decide between surgery and watchful waiting.

  7. 07

    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.

  • Often found incidentally

    Mild primary hyperparathyroidism is frequently picked up on routine bloods, with no symptoms at all.

  • Bones - bone pain

    Excess PTH draws calcium from bone, causing aches, reduced density and a raised fracture risk.

  • Stones - kidney stones

    Persistently high calcium increases the risk of renal calculi and, over time, nephrocalcinosis.

  • Groans - abdominal symptoms

    Constipation, nausea, abdominal pain and reduced appetite are classic hypercalcaemic features.

  • Psychiatric overtones

    Low mood, poor concentration, fatigue and confusion can all be traced back to a raised calcium.

  • Muscle cramps and tetany

    Hallmarks of hypocalcaemia in hypoparathyroidism - cramping, twitching and, in severe cases, spasm.

  • Perioral tingling and positive signs

    Numbness around the mouth and fingertips, with Chvostek’s and Trousseau’s signs on examination.

  • 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.

  • Watchful waiting

    Mild, asymptomatic primary hyperparathyroidism with only modestly raised calcium can often be monitored rather than operated on.

  • Parathyroidectomy

    Curative for a solitary adenoma - the treatment of choice for symptomatic or significantly abnormal biochemistry.

  • Cinacalcet

    A calcimimetic used when surgery is unsuitable or declined, lowering PTH and calcium medically.

  • Treating the underlying cause

    In secondary hyperparathyroidism, correcting vitamin D deficiency or optimising chronic kidney disease care addresses the driver.

  • Surgery for tertiary disease

    Once secretion becomes autonomous after prolonged secondary disease, parathyroidectomy is often needed.

  • Calcium and alfacalcidol

    The mainstay of hypoparathyroidism - oral calcium with active vitamin D, titrated against regular blood levels.

  • Recombinant PTH

    Reserved for severe, refractory hypoparathyroidism not adequately controlled on calcium and vitamin D alone.

  • 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.

  • NICE. Hyperparathyroidism (primary): diagnosis, assessment and initial management (NG132).

  • SIGN. Guidance referenced in the management of endocrine and metabolic bone disease.

  • Society for Endocrinology. Clinical guidance on calcium and parathyroid disorders.

  • 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.

  • Hypercalcaemic crisis

    Very high calcium with confusion, dehydration and drowsiness is a medical emergency needing same-day hospital care.

  • Severe hypocalcaemic tetany or seizures

    Uncontrolled muscle spasm, laryngospasm or seizures from low calcium need emergency IV calcium replacement.

  • Cardiac arrhythmia

    Both very high and very low calcium can provoke dangerous arrhythmias - an ECG is part of any severe case.

  • Acute kidney injury

    Obstructing renal stones or nephrocalcinosis from long-standing hypercalcaemia can precipitate kidney injury.

  • Unrecognised post-surgical hypoparathyroidism

    Tingling or cramps in the days after thyroid or neck surgery should prompt an urgent calcium check.

  • Fragility fracture

    A low-trauma fracture in someone with untreated hyperparathyroidism signals significant bone loss and needs prompt review.

  • Suspected parathyroid carcinoma

    Very rare - a very high calcium with a palpable neck mass or rapid onset warrants urgent specialist assessment.

  • Laryngeal nerve injury after surgery

    Voice change or breathing difficulty after parathyroid or thyroid surgery needs same-day ENT or surgical review.

  • 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.

  1. 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.

  2. 02 Bones

    Protect your bone health

    Adequate calcium and vitamin D intake, weight-bearing exercise and avoiding smoking all support skeletal health long-term.

  3. 03 Recognise

    Know your warning symptoms

    Learn what a hypercalcaemic or hypocalcaemic flare feels like for you, and who to contact if it happens.

  4. 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.

  • 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.

  • 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.

  • 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.

  • 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.

  • 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.

  • 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.