Tertiary hyperparathyroidism
Tertiary hyperparathyroidism is autonomous parathyroid hormone hypersecretion that develops after long-standing, poorly controlled secondary hyperparathyroidism, most often in end-stage kidney disease, causing eucalcemia or hypercalcemia despite hyperplastic glands that no longer respond to normal feedback. Cinacalcet is first-line medical therapy, and subtotal or total parathyroidectomy with autotransplantation is reserved for disease refractory to medical management or a markedly elevated PTH.
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What this article covers
- Overview
Definition: tertiary hyperparathyroidism is autonomous, PTH-independent-of-feedback hypersecretion that emerges after prolonged, poorly controlled secondary hyperparathyroidism, most commonly in patients with end-stage kidney disease.
- Epidemiology
Occurs after years of longstanding secondary hyperparathyroidism, almost exclusively in patients with chronic kidney disease, particularly those on long-term dialysis.
- Risk factors
Long-standing, poorly controlled secondary hyperparathyroidism: the essential precondition, reflecting years of sustained hypocalcemic/hypovitaminosis-D stimulation.
- Pathophysiology
Chronic stimulation drives glandular transformation: years of hypocalcemia and hyperphosphatemia in end-stage kidney disease sustain PTH secretion, and the resulting diffuse polyclonal hyperplasia…
- Clinical features
Often detected on routine post-transplant or dialysis monitoring labs: persistently elevated PTH with a normal or rising calcium, in contrast to the low/normal calcium expected with secondary hyperparathyroidism.
- Differential diagnosis
Secondary hyperparathyroidism: elevated PTH with a low or normal calcium, unlike the eucalcemia or hypercalcemia of established tertiary disease (secondary hyperparathyroidism).
- Diagnosis
The diagnostic basis is the biochemical transition, not a formal criteria set: markedly elevated PTH with eucalcemia or hypercalcemia in a patient with a documented history of long-standing secondary…
- Management
First-line, cinacalcet usually resolves the hypercalcemia: 30 mg PO once daily initially with food, titrated every 2 to 4 weeks (30 to 60 to 90 to 120 to 180 mg) to target PTH and calcium, continued…
- Complications
Hypercalcemic crisis: altered mental status, severe dehydration, and acute kidney injury with markedly elevated calcium.
- Prognosis
Cinacalcet controls hypercalcemia in most patients, avoiding the need for surgery in many cases.
- Prevention
Treat secondary hyperparathyroidism early, before PTH crosses roughly 300 to 600 pg/mL and becomes persistently elevated: control phosphorus to the normal range, correct 25-hydroxyvitamin D…
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Related articles
- Secondary hyperparathyroidism
Secondary hyperparathyroidism is an appropriate, physiologic rise in parathyroid hormone driven by hypocalcemia or impaired vitamin D activation, most commonly from chronic kidney disease and less often from vitamin D deficiency or malabsorption. Management targets the underlying stimulus with dietary phosphorus restriction, phosphate binders, vitamin D repletion or active vitamin D analogs, and calcimimetics, reserving parathyroidectomy for disease refractory to medical therapy.
- Primary hyperparathyroidism
Primary hyperparathyroidism is autonomous PTH oversecretion, most often from a solitary parathyroid adenoma, producing hypercalcemia with an elevated or inappropriately normal PTH and low or low-normal phosphorus. Most patients are asymptomatic and identified on routine labs; parathyroidectomy is curative and is first-line for symptomatic disease or when specific biochemical, skeletal, or renal criteria are met, while observation with annual monitoring suffices for mild, asymptomatic disease.
- Hypercalcemia
Hypercalcemia is an elevated serum calcium concentration, most often caused by primary hyperparathyroidism in ambulatory patients or malignancy in hospitalized patients. Mild disease requires only treatment of the underlying cause, while severe or symptomatic hypercalcemia is treated with aggressive IV isotonic fluids, followed by an IV bisphosphonate or denosumab for sustained control and subcutaneous calcitonin as a rapid but short-lived bridge.