Hypoparathyroidism

Hypoparathyroidism (HypoPT) is hypocalcemia occurring in the presence of an undetectable, low, or inappropriately normal parathyroid hormone (PTH) level, confirmed on two occasions at least two weeks apart.^[1] It is the mirror image of hyperparathyroidism rather than a milder point on the same spectrum: PTH normally raises serum calcium and lowers serum phosphate by mobilizing calcium from bone, increasing renal tubular calcium reabsorption while promoting phosphate excretion, and activating vitamin D in the kidney — so its deficiency produces the opposite biochemical picture, low calcium with high phosphate, rather than the high-calcium/low-phosphate pattern of an overactive gland.^[1] It is an uncommon condition, with an estimated prevalence of roughly 6.4-37 per 100,000 person-years and an incidence of about 0.8-2.3 per 100,000 person-years.^[1][2]

Post-surgical hypoparathyroidism is by far the leading cause, accounting for approximately 75% of all cases — it follows inadvertent damage, devascularization, or removal of the parathyroid glands during thyroid surgery (most often total or completion thyroidectomy, or any central neck dissection) or during parathyroidectomy itself.^[1] Most post-surgical hypocalcemia is transient, resolving over days to months as the remaining gland tissue recovers, but a meaningful minority becomes permanent — by convention, defined as persisting beyond 12 months after surgery.^[1] The remaining roughly 25% of cases are nonsurgical: autoimmune destruction, genetic causes, hypomagnesemia-driven functional PTH failure, infiltrative or other rarer causes, or idiopathic disease.^[1]

Chronic HypoPT carries a genuinely broad complication burden beyond the acute neuromuscular symptoms of hypocalcemia — renal (nephrocalcinosis, nephrolithiasis, chronic kidney disease), cardiovascular (QT prolongation, arrhythmia, and in some registry data an increased risk of ischemic heart disease and stroke), cataracts, basal ganglia calcification, seizures, and depression have all been documented at rates clearly above the general population.^[1] Much of this chapter's management logic — a deliberately low-normal rather than mid-normal calcium target, and vigilant urine calcium monitoring — exists specifically to minimize this long-term complication burden, not just to relieve symptoms.

The core presentation — neuromuscular irritability

Hypocalcemia lowers the threshold for neuronal depolarization, producing a spectrum of neuromuscular irritability: paresthesias (classically perioral, and in the fingers and toes), muscle cramps, and generalized muscle stiffness or tetany, reported in roughly 40-60% of patients with chronic HypoPT.^[1][3]

Severe presentation

More severe or acute hypocalcemia can progress to overt tetany, laryngospasm (a genuine airway emergency), generalized or focal seizures — seizures are a common presenting feature, particularly in younger patients and in nonsurgical disease — and cardiac manifestations, including a prolonged corrected QT (QTc) interval and arrhythmia, rarely progressing to cardiomyopathy or heart failure in severe, longstanding cases.^[3][1] See Red Flags & Referral.

Chronic, less specific symptoms

Fatigue, anxiety, depressed mood, and cognitive complaints ("brain fog") are common and often under-recognized as disease-related rather than incidental.^[1] Longstanding disease is also associated with cataracts, occurring earlier than in the general population, and basal ganglia calcification, which is usually asymptomatic but has been reported in over a third of nonsurgical HypoPT patients in a Canadian cohort.^[1]

Post-surgical presentation specifically

Post-surgical hypocalcemia is typically identified early — within the first 24-48 hours after thyroid or parathyroid surgery — through routine postoperative calcium monitoring, often before overt symptoms develop; a low or falling calcium trend, or an early low PTH level, should prompt starting calcium and active vitamin D promptly rather than waiting for symptoms to appear (see Risk Factors and the Clinical Decision Algorithm for the specific 12-24 hour PTH check that helps predict which patients will not need long-term therapy).

Post-surgical hypoparathyroidism (the leading cause, ~75% of all cases)

Follows inadvertent devascularization, damage, or removal of one or more parathyroid glands during neck surgery — most often total or completion thyroidectomy, any central neck dissection, or reoperative neck surgery, and less commonly parathyroidectomy itself.^[1] Risk rises with the extent of thyroid resection, central neck dissection, reoperation, underlying malignancy or thyrotoxicosis, larger parathyroid gland size, lower surgeon case volume, and — counterintuitively — parathyroid autotransplantation: a recent meta-analysis of 25 studies found autotransplantation was itself associated with an increased risk of post-surgical HypoPT, so current guidance is to avoid autotransplantation and instead leave viable parathyroid tissue in situ, reserving autotransplantation only for the situation where a gland has already been inadvertently removed.^[1]

Most post-surgical hypocalcemia is transient and recovers over days to months; it is considered permanent once it persists beyond 12 months after surgery.^[1] A PTH level measured 12-24 hours postoperatively is genuinely useful for prediction: a PTH above 10 pg/mL (1.05 pmol/L) at that point makes the development of permanent HypoPT very unlikely, meaning these patients do not need long-term treatment above the usual recommended daily allowance of calcium and vitamin D — whereas a PTH below that threshold still carries less than a 50% chance of going on to permanent disease, so it is not, on its own, proof that the patient will need lifelong therapy.^[1]

Autoimmune hypoparathyroidism

Can occur in isolation or as part of autoimmune polyendocrine syndrome type 1 (APS-1 / APECED), caused by mutations in the AIRE (autoimmune regulator) gene and classically presenting with the triad of chronic mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency (Addison's disease) — hypoparathyroidism is present in over 80% of APECED patients and may be the only endocrinopathy present at first diagnosis.^[1] Activating autoantibodies against the calcium-sensing receptor (CaSR) have also been reported in autoimmune HypoPT, sometimes in isolation without full APECED.^[1]

Genetic causes

Include disorders of parathyroid gland formation, PTH secretion, and PTH gland damage — for example DiGeorge syndrome (22q11.2 deletion), in which parathyroid gland agenesis or hypoplasia is one part of a broader syndromic picture, and autosomal dominant hypocalcemia (ADH) from activating mutations in the calcium-sensing receptor, in which the parathyroid gland is tricked into sensing calcium as higher than it actually is and suppresses PTH release inappropriately — these patients are specifically more prone to marked hypercalciuria in response to even standard calcium/vitamin D dosing and warrant extra caution.^[1] Genetic testing is advised in nonsurgical HypoPT when there is a positive family history of nonsurgical disease, syndromic features are present, or the patient is younger than 40 years; testing specifically for AIRE variants is advised when other clinical features of APECED are present.^[1]

Hypomagnesemia — functional hypoparathyroidism

Severe hypomagnesemia is a genuinely important and sometimes-missed cause of hypocalcemia, and it must be corrected before calcium and active vitamin D therapy will work at all.^[1] Magnesium is required both for PTH secretion by the parathyroid gland and for PTH's action at its target tissues — intracellular magnesium is a cofactor for the adenylate cyclase enzyme that mediates the PTH receptor's downstream signal, so severe deficiency produces a state of both impaired PTH release and end-organ resistance to whatever PTH is released, sometimes called functional hypoparathyroidism. (Severe hypermagnesemia, at the opposite extreme, can also suppress PTH secretion via the same calcium-sensing receptor pathway that magnesium activates, though this is a much less commonly encountered clinical scenario.)^[1] Correcting the magnesium deficit is not optional adjunct therapy here — it is the step that allows calcium homeostasis to respond to treatment at all.

Other causes

• Infiltrative or granulomatous disease, and deposition of iron (hemochromatosis, chronic transfusion) or copper (Wilson disease) within parathyroid tissue.^[1]
• Metastatic infiltration of the parathyroid glands, and neck irradiation.^[1]
• Immune checkpoint inhibitor therapy, which can rarely induce HypoPT through activating calcium-sensing receptor autoantibodies.^[1]
• Cinacalcet, a calcimimetic that increases the calcium-sensing receptor's sensitivity to extracellular calcium and can rarely cause HypoPT/hypocalcemia as an on-target drug effect.^[1]
• Transient causes unrelated to surgery: severe burns, and acute critical illness.^[1]
• Maternal hyperparathyroidism/hypercalcemia can suppress the fetal parathyroid axis in utero, producing transient hypocalcemia in the newborn.^[1]
• Idiopathic — a genuine diagnosis of exclusion once genetic, autoimmune, and metabolic causes have been reasonably evaluated.^[1]

Also escalate or refer for:

• Hypocalcemia that remains refractory despite doses of calcium and active vitamin D that would normally be considered adequate — check serum magnesium immediately; uncorrected hypomagnesemia is a classic, easily missed reason for apparent treatment failure (see Risk Factors and Treatment Failure).
• A newly suspected diagnosis, for full etiologic workup, genetic testing where indicated, and genetic counselling.
• Recurrent hospitalization or emergency visits for either hypocalcemia or hypercalcemia despite an apparently reasonable conventional regimen — over-replacement is genuinely as harmful in this disease as under-replacement, not merely a minor inconvenience to tolerate.
• Hypercalciuria, nephrocalcinosis, nephrolithiasis, or declining renal function on monitoring.
• Pregnancy in a patient with known HypoPT, for coordinated obstetric/endocrine care.
• Persistently poor quality of life, high pill burden, or poor tolerance of large calcium/active vitamin D doses, to assess candidacy for PTH replacement therapy.^[1]

Confirming the diagnosis

HypoPT is confirmed by hypocalcemia (low ionized calcium, or low total calcium adjusted for albumin) together with an undetectable, low, or inappropriately normal intact PTH level (using a second- or third-generation assay), demonstrated on two occasions at least two weeks apart.^[1] This PTH pattern is the key that separates HypoPT from every other cause of hypocalcemia: in secondary hyperparathyroidism from vitamin D deficiency, malabsorption, or chronic kidney disease, PTH rises appropriately in response to the low calcium; a low-or-inappropriately-normal PTH in the face of hypocalcemia means the gland itself (or its regulation) is the problem.^[1] A separate condition, pseudohypoparathyroidism (target-organ PTH resistance, with hypocalcemia, high phosphate, but an elevated rather than low PTH), produces a similar-looking clinical picture through a fundamentally different mechanism and is genuinely outside the scope of this chapter.^[1]

Supporting biochemical pattern

Beyond the core calcium/PTH pattern, look for elevation in serum phosphate (reduced renal phosphate excretion without PTH's normal phosphaturic effect), reduced 1,25-dihydroxyvitamin D (impaired PTH-driven renal activation), and an inappropriately elevated urinary fractional excretion of calcium — the kidney is losing calcium into the urine despite the body being calcium-deficient, the opposite of the calcium-conserving response that should occur.^[1]

Magnesium — check at diagnosis, and whenever control looks refractory

Measure serum magnesium in every newly diagnosed patient, both because severe hypomagnesemia is itself a cause of functional HypoPT and because it will block response to calcium/active vitamin D therapy if left uncorrected (see Risk Factors).^[1]

Post-surgical patients — the 12-24 hour PTH check

Measure PTH 12-24 hours after total or completion thyroidectomy: a value above 10 pg/mL (1.05 pmol/L) makes permanent HypoPT very unlikely (strong recommendation, moderate-quality evidence) and means long-term calcium/active vitamin D above the usual recommended daily allowance is probably not needed, while a lower value still carries less than a 50% chance of progressing to permanent disease.^[1]

Baseline evaluation, all newly diagnosed patients

Serum creatinine and estimated GFR, calcium (ionized or albumin-adjusted), magnesium, phosphorus, and 25-hydroxyvitamin D; a 24-hour urine collection for calcium and creatinine; and baseline renal imaging (ultrasound or CT) to assess for nephrocalcinosis or nephrolithiasis before treatment begins.^[1]

• Target serum calcium in the low-normal range — the lower half of the normal reference range, or just below it — genuinely not the mid-to-high normal range used as the target in most other conditions. The goal is enough calcium to control symptoms while minimizing the long-term risk of hypercalciuria, nephrocalcinosis, and renal impairment that comes from the combination of low PTH (which normally helps the kidney retain filtered calcium) and the calcium/vitamin D supplementation needed to correct the hypocalcemia in the first place.^[1]
• Alleviate symptomatic hypocalcemia while actively avoiding hypercalciuria — a specific 24-hour urinary calcium target of <6.25 mmol/24h (250 mg/24h) in adult women and <7.5 mmol/24h (300 mg/24h) in adult men is proposed, not merely "keep calcium in range."^[1]
• Keep serum phosphorus in the high-normal range and avoid hyperphosphatemia; keep magnesium and 25-hydroxyvitamin D within the normal reference range (25(OH)D target 75-125 nmol/L).^[1]
• Avoid hypercalcemia just as deliberately as hypocalcemia — over-replacement is not a minor nuisance in this disease; it carries real symptomatic and renal risk, and is treated as a genuine adverse outcome to prevent, not merely a lab value to correct after the fact.
• Reduce long-term complication risk across every affected system — renal, skeletal, cardiovascular, ocular, and neuropsychiatric — through consistent target-range control and scheduled monitoring rather than symptom control alone (see Monitoring & Follow-Up).
• Support quality of life and reduce treatment (pill) burden where feasible — the rationale behind considering PTH replacement therapy once conventional therapy is judged unsatisfactory.^[1]

The modern advance — recombinant PTH replacement

Rather than simply treating the downstream calcium abnormality, PTH replacement genuinely restores the missing hormone itself. Full-length recombinant human PTH (1-84) (rhPTH(1-84), brand name Natpara) was approved by US and European regulators in 2015 as an adjunct for patients not well controlled on conventional therapy, dosed by once-daily subcutaneous injection starting at 50 mcg/day and titrated by 25 mcg increments every 4 weeks to a maximum of 100 mcg/day — but it was recalled from the US market in 2019 for a rubber-particulate manufacturing defect in the injection cartridge (the recall did not extend to Europe), and it was never marketed in Canada.^[4] The current PTH-replacement option actually available in Canada is palopegteriparatide (brand name Yorvipath) — a once-daily subcutaneous prodrug that provides sustained release of active PTH over roughly 60 hours — approved by US and European regulators in 2023-2024, and by Health Canada in February 2026.^[4][5]

Consider PTH replacement when conventional therapy is inadequate — inadequate control is defined as any one of: (i) symptomatic hypocalcemia; (ii) hyperphosphatemia; (iii) renal insufficiency; (iv) hypercalciuria; or (v) poor quality of life — or when the patient has poor compliance or malabsorption, is intolerant of large calcium/active-vitamin-D doses, or is already requiring high conventional doses (calcium above 2 g/day, or active vitamin D above 2 mcg/day).^[1] Clinical trials of PTH replacement (both rhPTH(1-84) and, in earlier proof-of-concept studies, synthetic PTH(1-34) — not itself a marketed HypoPT product) have shown a 50% or greater reduction in calcium and calcitriol dose while maintaining normal serum calcium in a majority of treated patients, reduced pill burden, and modest quality-of-life improvement; hypercalcemia episodes are more common on PTH therapy than on conventional therapy, which is an expected trade-off requiring continued monitoring rather than a reason to avoid PTH therapy outright.^[4] In palopegteriparatide's own trial data, complete cessation of active vitamin D was achieved in roughly 93% of treated patients while maintaining normal serum calcium, with a meaningful reduction in 24-hour urine calcium and improved quality-of-life scores.^[4]

• A calcium-containing, low-phosphate diet supports pharmacologic therapy rather than replacing it — moderate, not excessive, dietary calcium, and a genuinely low-sodium diet if a thiazide diuretic is in use, since high sodium intake works directly against the thiazide's calcium-retaining effect.^[1]
• Counsel every patient to recognize both hypocalcemia symptoms (perioral or extremity tingling, muscle cramps, unusual anxiety) and hypercalcemia symptoms (constipation, polyuria, unusual fatigue, confusion) — over-replacement is genuinely as important to catch early as under-replacement in this disease.
• Warn against unsupervised over-the-counter calcium or vitamin D supplement stacking on top of the prescribed regimen without informing the care team.
• A medical alert bracelet or card documenting the HypoPT diagnosis and calcium/active-vitamin-D dependence is genuinely useful if the patient ever presents confused or unconscious to an unfamiliar care team.
• Given the high pill burden of conventional therapy, proactively ask about adherence at every visit rather than assuming poor control is purely pharmacologic — persistent adherence difficulty is itself one of the recognized reasons to consider PTH replacement therapy.^[1]
• Offer genetic counselling where a genetic cause has been identified (DiGeorge syndrome, autosomal dominant hypocalcemia, familial isolated HypoPT), given the hereditary pattern and implications for family planning.^[1]
• Recommend periodic ophthalmology follow-up given the documented excess cataract risk, particularly with longer disease duration.^[1]
• For patients undergoing thyroid or parathyroid surgery, counsel before the operation that transient postoperative hypocalcemia is common and that a temporary calcium/active-vitamin-D regimen may be needed in the immediate recovery period — this reduces anxiety and supports adherence during a period when patients are otherwise focused on surgical recovery.

Lactation

The same close-monitoring approach continues through lactation: reassess serum calcium every 3-4 weeks, continue calcium and active vitamin D, and continue to avoid thiazide diuretics and PTH/PTH-analogue therapy.^[1]

Pediatrics

Genetic causes (DiGeorge syndrome, APECED, familial isolated HypoPT) often present in infancy or childhood. Management follows the same conventional-therapy principles with weight-based, specialist-directed dosing and close growth monitoring; PTH replacement has been studied in children with refractory disease under specialist protocols, maintaining normal linear growth in trial data, but pediatric management overall belongs with a pediatric endocrinology service rather than a general adult-oriented pathway.^[4]

Renal impairment

Because HypoPT itself carries an elevated baseline risk of chronic kidney disease, renal function monitoring is especially important in this population; calcitriol/alfacalcidol dosing may need adjustment as renal function changes, and thiazide efficacy for hypercalciuria falls off at lower eGFR — involve nephrology where renal impairment is significant.

Older adults

Comorbid renal impairment and polypharmacy — including concurrent diuretics or proton pump inhibitors, which reduce calcium carbonate absorption — make careful medication reconciliation especially important; blunted or atypical symptom reporting can also mask both hypo- and hypercalcemia in this group, arguing for closer biochemical monitoring rather than relying on symptoms alone.

Autoimmune polyendocrine syndrome (APECED/APS-1)

Actively screen for coexisting adrenal insufficiency in any patient with autoimmune HypoPT — as in Addison's disease, unrecognized adrenal insufficiency can destabilize calcium management under physiologic stress (illness, surgery), so coordinated endocrine care matters here just as much as it does for the reverse scenario.^[1]

Baseline (every newly diagnosed patient)

Serum creatinine/eGFR, calcium (ionized or albumin-adjusted), magnesium, phosphorus, and 25-hydroxyvitamin D; a 24-hour urine collection for calcium and creatinine; and baseline renal imaging (ultrasound or CT) to assess for nephrocalcinosis or nephrolithiasis before treatment begins.^[1]

Stable patients on established therapy

Repeat serum creatinine/eGFR, calcium, magnesium, and phosphorus every 6-12 months; 25-hydroxyvitamin D every 6-12 months; and a 24-hour urine calcium/creatinine every 6-24 months.^[1] Monitor more frequently during any dose titration, and recheck serum calcium within several days of any significant change in medical therapy.^[1] Unstable patients — those with fluctuating calcium — need more frequent monitoring to avoid both symptomatic swings and the long-term complications of poor control.^[1]

Complication surveillance

Chronic HypoPT carries a documented excess risk of complications across multiple organ systems, so routine follow-up should extend beyond biochemistry alone: nephrocalcinosis/nephrolithiasis (reported in a median of roughly 15% of patients across studies), chronic kidney disease/renal insufficiency (roughly 12%), cataracts (roughly 17%, a two- to fourfold higher risk than the general population, with an earlier average onset around age 35 — consider periodic ophthalmology referral), seizures (roughly 11%), depression (roughly 9%), ischemic heart disease (roughly 7%), and cardiac arrhythmias (roughly 7%), alongside basal ganglia calcification and QTc prolongation.^[1] Screen for mood symptoms and quality of life at routine visits, not only serum chemistry.^[1]

On a thiazide diuretic

Monitor blood pressure, serum potassium, magnesium, and renal function, given the additive hypokalemia/hypomagnesemia risk on top of the underlying disease.

Starting PTH replacement therapy

Follow the product-specific titration protocol as calcium and active vitamin D doses are tapered down in parallel — do not stop conventional therapy abruptly when starting PTH replacement, and watch specifically for hypercalcemia during the transition, which is more common on PTH therapy than on conventional therapy alone.^[4]

1. Confirm adherence, dose timing, and administration technique first — calcium carbonate absorption is reduced by concurrent proton pump inhibitor use or achlorhydria, and switching to calcium citrate (which does not depend on gastric acid) is often the fix rather than simply increasing the calcium dose further.
2. Check serum magnesium immediately if hypocalcemia remains refractory despite doses that would normally be considered adequate, and correct it if low — this is the single highest-yield step in apparent treatment failure, since hypocalcemia will not respond to calcium/active vitamin D until magnesium is corrected.
3. Confirm the patient is actually on an active vitamin D analogue (calcitriol or alfacalcidol) and not plain vitamin D3/D2 alone — a prescribing handoff error that will silently prevent the calcium from ever reaching target.
4. If hypercalciuria develops before serum calcium reaches the low-normal target, add a thiazide diuretic with dietary sodium restriction rather than continuing to escalate the calcium/active-vitamin-D dose and risking further urinary calcium loss and renal complications.
5. For a patient with known or suspected autosomal dominant hypocalcemia (activating CaSR mutation), recognize that even modest calcium/vitamin D doses can produce disproportionate hypercalciuria — target the low end of the acceptable calcium range and involve genetics/endocrinology early rather than escalating doses empirically to chase a higher calcium level.
6. If control remains poor, pill burden is high, renal function is declining, or hyper-/hypocalcemic episodes recur despite working through the steps above, reassess candidacy for PTH replacement therapy and refer to endocrinology rather than continuing to adjust conventional therapy indefinitely.

• Treating HypoPT-associated hypocalcemia with plain cholecalciferol (vitamin D3) or ergocalciferol (vitamin D2) alone instead of an active vitamin D analogue (calcitriol or alfacalcidol) — it will not adequately correct calcium, since the PTH-dependent renal activation step is exactly what is missing.
• Targeting the mid-to-high normal serum calcium range used in most other hypocalcemia contexts, rather than deliberately aiming low-normal — this unnecessarily raises the risk of hypercalciuria, nephrocalcinosis, and renal impairment.
• Missing hypomagnesemia as the reason hypocalcemia will not correct despite seemingly adequate calcium and active vitamin D doses.
• Withholding IV calcium in a patient with convincing acute severe symptomatic hypocalcemia in order to wait for a confirmatory or repeat lab value.
• Escalating calcium/active-vitamin-D doses further before checking and treating hypercalciuria — add a thiazide and restrict sodium first.
• Starting a thiazide diuretic without also restricting dietary sodium and monitoring magnesium and potassium — sodium intake works directly against the thiazide's intended effect, and the diuretic can itself worsen hypomagnesemia.
• Missing the interaction between calcium carbonate and proton pump inhibitors/reduced gastric acid, and not switching to calcium citrate when absorption looks impaired.
• Failing to arrange closer monitoring — rather than a default dose change in either direction — during pregnancy, or using thiazide/PTH therapy during pregnancy.
• Assuming post-surgical hypocalcemia is permanent before the 12-month mark, or, conversely, never arranging the early 12-24 hour postoperative PTH check that helps identify which patients are unlikely to need long-term therapy at all.
• Treating a "normal" calcium result as reassurance that no further monitoring is needed, and skipping the routine renal imaging, ophthalmology, cardiovascular, and mood-symptom surveillance that this disease's documented complication burden actually warrants.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal function, weight, pregnancy status). Select any linked drug name to open its complete Pharmasist Drug Database page. Calcium citrate and ergocalciferol (vitamin D2) do not currently have their own published Drug Database entries, so both are named as text only below rather than linked — see the chapter note at the top of this source file for the full explanation.

Conventional therapy — oral calcium plus an active vitamin D analogue

First-line therapy for essentially every patient with chronic hypoparathyroidism. The active vitamin D analogue (calcitriol or alfacalcidol) is not optional or interchangeable with plain vitamin D3/D2 — see Choose Initial Treatment for why.

Adjunct for hypercalciuria

Add when 24-hour urine calcium exceeds target (women: 6.25 mmol/24h; men: 7.5 mmol/24h) despite a low-normal serum calcium — before pushing calcium/active-vitamin-D doses any higher.

Magnesium correction

Required before calcium/active vitamin D therapy will work if magnesium is low — magnesium is a cofactor for both PTH secretion and PTH-receptor signaling.

Acute severe hypocalcemia / tetany — emergency parenteral therapy

Treat on clinical suspicion in a convincing presentation — do not delay for a confirmatory lab result. Requires cardiac monitoring throughout.

PTH replacement therapy

For patients not adequately controlled on conventional therapy — see Choose Initial Treatment for the full indication criteria. Requires specialist initiation and structured monitoring as conventional therapy is tapered.