Hypoparathyroidism

Also known as: Parathyroid hormone deficiency

Hypoparathyroidism is deficient parathyroid hormone secretion or action, producing hypocalcaemia with hyperphosphataemia: a combination that is itself a useful diagnostic signature, since most other causes of hypocalcaemia lower phosphate rather than raise it.

Post-surgical hypoparathyroidism is by far the commonest cause, following thyroidectomy, parathyroidectomy or radical neck surgery, and may be transient or permanent.

Other causes include autoimmune disease (isolated or as part of autoimmune polyglandular syndrome type 1), infiltrative disease, radiation, genetic syndromes such as DiGeorge, and functional hypoparathyroidism from severe hypomagnesaemia, which is fully reversible and must always be excluded.

Pseudohypoparathyroidism is a distinct entity of PTH resistance rather than deficiency, with the same biochemical picture but a raised rather than low PTH.

Corrected calcium (low), phosphate (high) and PTH (low or inappropriately normal) measured together establish the diagnosis. A PTH in the low-normal range is inappropriate in the presence of hypocalcaemia, and reporting it as "normal" is a recognised source of missed diagnosis
Magnesium is mandatory, since severe hypomagnesaemia causes a functional hypoparathyroidism that resolves completely with magnesium replacement and does not require lifelong treatment
Renal function, to distinguish from chronic kidney disease-related mineral disturbance
Vitamin D, to exclude coexisting deficiency
ECG for QT prolongation
24-hour urinary calcium, which is important for long-term monitoring, since treatment raises urinary calcium and risks nephrocalcinosis
Where the cause is not post-surgical, consider autoimmune screening, and imaging of the basal ganglia in long-standing disease, where calcification is common
A raised PTH with the same calcium and phosphate picture indicates pseudohypoparathyroidism rather than hypoparathyroidism

The therapeutic aim is deliberately modest: maintain calcium in the low-normal range and keep the patient symptom-free, rather than normalising calcium fully. Because PTH normally promotes renal calcium reabsorption, its absence means that raising serum calcium to mid-normal levels drives a large urinary calcium load, with consequent nephrocalcinosis, nephrolithiasis and chronic kidney disease.

Activated vitamin D (alfacalcidol or calcitriol) is the mainstay, since patients cannot adequately convert standard vitamin D without PTH
Oral calcium supplementation, in divided doses
Magnesium replacement where deficient, which may be all that is required in functional cases
Thiazide diuretics reduce urinary calcium loss and are a useful adjunct in patients with hypercalciuria
Recombinant PTH is available in some settings for patients inadequately controlled on conventional therapy or requiring unacceptably high supplement doses
Monitor calcium, phosphate, renal function and 24-hour urinary calcium long term, and arrange periodic renal imaging, since renal complications develop silently
Patients need clear sick-day and symptom guidance, since intercurrent illness, vomiting or changes in vitamin D dosing can precipitate acute hypocalcaemia

Acute severe hypocalcaemia is managed as in the hypocalcaemia entry, with intravenous calcium gluconate and cardiac monitoring.

Referral: endocrinology for all confirmed hypoparathyroidism, given the need for long-term titration and monitoring; nephrology if nephrocalcinosis or declining renal function develops.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Hyperparathyroidism

Also known as: Primary hyperparathyroidism, Secondary hyperparathyroidism

Hyperparathyroidism is excessive parathyroid hormone secretion, classified by mechanism:

Primary: autonomous overproduction, most often from a single parathyroid adenoma (around 85%), less often four-gland hyperplasia, and rarely parathyroid carcinoma. Produces hypercalcaemia with an inappropriately normal or raised PTH, and is the commonest cause of hypercalcaemia in the outpatient setting
Secondary: an appropriate compensatory response to hypocalcaemia, most often from chronic kidney disease or vitamin D deficiency. Calcium is low or normal with a raised PTH
Tertiary: long-standing secondary hyperparathyroidism in which the glands become autonomous, typically in advanced or dialysis-dependent chronic kidney disease, producing hypercalcaemia with a markedly raised PTH

Most primary hyperparathyroidism is now detected incidentally on routine biochemistry in an asymptomatic patient, which has changed the clinical question from "how do we treat this" to "does this need treating at all".

Corrected calcium and PTH measured together is the essential pairing, since PTH must always be interpreted against the prevailing calcium. A PTH within the reference range is inappropriate if the calcium is raised
Phosphate is typically low in primary hyperparathyroidism and high in the chronic kidney disease-related forms
Vitamin D, renal function, and alkaline phosphatase
24-hour urinary calcium and calcium-creatinine clearance ratio to exclude familial hypocalciuric hypercalcaemia, which produces a very similar biochemical picture but is benign and must not lead to parathyroidectomy. Missing this distinction results in unnecessary neck surgery that does not correct the calcium
DXA bone density including the distal third of the radius, which is preferentially affected in hyperparathyroidism and may be the only abnormal site
Renal imaging for nephrolithiasis and nephrocalcinosis, which may be silent and which alters the treatment threshold
Localisation imaging (sestamibi scintigraphy, ultrasound, four-dimensional CT) is performed once surgery is decided upon, to guide a minimally invasive approach. It is a surgical planning tool, not a diagnostic test, and a negative scan does not refute a biochemically confirmed diagnosis

Primary hyperparathyroidism:

Parathyroidectomy is the only curative treatment, and is indicated for symptomatic disease, and in asymptomatic patients meeting recognised criteria: age under 50, significantly raised calcium, reduced bone density or fragility fracture, nephrolithiasis or nephrocalcinosis, marked hypercalciuria, or reduced eGFR
Patients not meeting criteria may be monitored, with periodic calcium, renal function and bone density
Cinacalcet, a calcimimetic, lowers calcium where surgery is not appropriate or is declined, though it does not improve bone density
Ensure adequate hydration, avoid thiazides and lithium where possible, and maintain rather than restrict a normal dietary calcium intake, since restriction can paradoxically drive PTH higher
Correct coexisting vitamin D deficiency cautiously, monitoring calcium
Bisphosphonates or denosumab for bone protection where surgery is not undertaken

Secondary hyperparathyroidism:

Treat the underlying cause: vitamin D replacement for deficiency, and, in chronic kidney disease, phosphate control with dietary measures and phosphate binders, activated vitamin D analogues, and calcimimetics per renal bone disease protocols

Tertiary hyperparathyroidism:

Usually requires parathyroidectomy, particularly where hypercalcaemia is significant or calciphylaxis is a concern

Post-operatively: monitor calcium closely, anticipating hypocalcaemia and, where bone turnover was high, hungry bone syndrome.

Referral: endocrinology for diagnosis and treatment decisions; endocrine surgery for parathyroidectomy; nephrology for renal bone disease.

Hypoparathyroidism

Overview

Diagnosis

Management

Overview

Diagnosis

Management