PTH

Parathyroid Hormone

Hormones

What is Parathyroid Hormone?

Parathyroid hormone (PTH) is a peptide hormone produced by the four small parathyroid glands located behind the thyroid gland in the neck. PTH is the primary regulator of calcium and phosphorus homeostasis in the body. When blood calcium levels drop even slightly, the parathyroid glands detect this through calcium-sensing receptors and respond by secreting PTH. PTH then acts on three target organs to raise calcium: it stimulates osteoclasts in bone to release calcium and phosphorus into the bloodstream, increases calcium reabsorption in the kidney tubules while promoting phosphorus excretion, and activates vitamin D (converting 25-hydroxyvitamin D to its active form 1,25-dihydroxyvitamin D) in the kidneys to enhance intestinal calcium absorption.

PTH is measured using an intact PTH assay, which detects the full-length 84-amino-acid molecule. PTH levels must always be interpreted alongside calcium levels—this pairing is essential for correct diagnosis. In primary hyperparathyroidism, both PTH and calcium are elevated (the parathyroid gland is autonomously overproducing PTH). In secondary hyperparathyroidism (commonly from vitamin D deficiency or chronic kidney disease), PTH is elevated but calcium is normal or low—the parathyroid glands are appropriately responding to low calcium. PTH follows a circadian rhythm with peak levels in the early morning and nadir in the afternoon, and also fluctuates with meals.

Why It Matters

Primary hyperparathyroidism is the third most common endocrine disorder, affecting approximately 1 in 500 women and 1 in 2000 men, with incidence increasing with age. It is the most common cause of hypercalcemia in outpatients. If left untreated, chronic PTH excess leads to progressive bone loss (osteoporosis), kidney stones, kidney damage, cardiovascular disease, and neurocognitive symptoms. Many patients are asymptomatic at diagnosis, identified incidentally through routine blood work showing elevated calcium. At the other extreme, hypoparathyroidism (most commonly after thyroid or parathyroid surgery) causes hypocalcemia with potentially dangerous symptoms including muscle spasms, seizures, and cardiac arrhythmias. Correct PTH interpretation is critical for managing calcium disorders.

Normal Reference Ranges

GroupRangeUnit
Adults (intact PTH)15–65pg/mL
Adults (some labs)10–55pg/mL

Reference ranges may vary by laboratory. Always compare results to the ranges provided by your testing facility.

What High PTH Levels Mean

Common Causes

  • Primary hyperparathyroidism (parathyroid adenoma in 85% of cases, hyperplasia in 15%)
  • Secondary hyperparathyroidism (vitamin D deficiency, chronic kidney disease)
  • Tertiary hyperparathyroidism (autonomous PTH secretion after prolonged secondary hyperparathyroidism)
  • Lithium therapy
  • Familial hypocalciuric hypercalcemia (benign genetic condition)
  • Parathyroid carcinoma (very rare)

Possible Symptoms

  • Kidney stones (calcium oxalate or calcium phosphate)
  • Osteoporosis and fragility fractures
  • Fatigue and muscle weakness
  • Depression, anxiety, and cognitive dysfunction ("brain fog")
  • Abdominal pain, nausea, and constipation
  • Excessive thirst and frequent urination (polyuria)
  • Bone and joint pain
  • If severe hypercalcemia: confusion, cardiac arrhythmias, and coma

What to do: Elevated PTH should be interpreted alongside calcium. If both are elevated, primary hyperparathyroidism is the most likely diagnosis. 24-hour urine calcium should be measured to rule out familial hypocalciuric hypercalcemia (low urine calcium) and assess kidney stone risk. Vitamin D should be checked and repleted if low, even in primary hyperparathyroidism. DEXA bone density scan should be performed. Surgery (parathyroidectomy) is curative and recommended for symptomatic patients and asymptomatic patients meeting criteria (age <50, calcium >1 mg/dL above normal, osteoporosis, kidney stones, reduced kidney function). If PTH is elevated with normal or low calcium, secondary causes (vitamin D deficiency, CKD) should be investigated and treated.

What Low PTH Levels Mean

Common Causes

  • Post-surgical hypoparathyroidism (most common cause, after thyroid or parathyroid surgery)
  • Autoimmune hypoparathyroidism
  • Magnesium deficiency (impairs PTH secretion)
  • DiGeorge syndrome (congenital absence of parathyroid glands)
  • Infiltrative diseases (hemochromatosis, Wilson's disease, metastatic cancer)
  • Radiation to the neck
  • Activating mutations of the calcium-sensing receptor

Possible Symptoms

  • Muscle cramps, spasms, and tetany (involuntary muscle contractions)
  • Numbness and tingling around the mouth and in the fingers and toes (perioral and acral paresthesias)
  • Seizures (from severe hypocalcemia)
  • Dry skin, brittle nails, and coarse hair
  • Dental abnormalities
  • Fatigue and anxiety
  • QT prolongation on ECG (arrhythmia risk)
  • Chvostek's sign (facial muscle twitch when tapping facial nerve) and Trousseau's sign (carpopedal spasm with blood pressure cuff)

What to do: Low PTH with low calcium confirms hypoparathyroidism. Magnesium should be checked and corrected, as magnesium deficiency prevents appropriate PTH secretion and must be treated first. Acute symptomatic hypocalcemia is a medical emergency treated with IV calcium gluconate. Chronic hypoparathyroidism is managed with oral calcium supplements (1–3 g of elemental calcium daily in divided doses) and active vitamin D (calcitriol, 0.25–2 µg daily) since PTH is needed to activate vitamin D in the kidney. Recombinant PTH (teriparatide or PTH 1-84) is available for refractory cases. Monitoring includes regular serum and urine calcium to avoid hypercalciuria and kidney damage.

When Is PTH Testing Recommended?

  • When blood calcium is found to be elevated (hypercalcemia) on routine testing
  • When evaluating unexplained kidney stones, especially recurrent calcium stones
  • When assessing unexplained osteoporosis, particularly in younger patients
  • When monitoring calcium balance after thyroid or parathyroid surgery

Frequently Asked Questions

PTH and calcium exist in a tightly regulated feedback loop—interpreting either value in isolation can be misleading. In primary hyperparathyroidism, both PTH and calcium are elevated (PTH is inappropriately high for the calcium level). In secondary hyperparathyroidism (e.g., from vitamin D deficiency), PTH is elevated but calcium is normal or low—the parathyroid glands are appropriately compensating. In hypoparathyroidism, both PTH and calcium are low. A "normal" PTH in the presence of high calcium is actually abnormal—normal parathyroid glands should suppress PTH when calcium is elevated. Similarly, a "normal" PTH with low calcium is inappropriate—PTH should be elevated to correct the low calcium. This is why the PTH-calcium pair, not either value alone, drives diagnosis.
Primary hyperparathyroidism is a disease of the parathyroid glands themselves—usually a benign tumor (adenoma) in one gland that autonomously overproduces PTH regardless of calcium levels, resulting in elevated calcium. It is treated with surgical removal of the abnormal gland. Secondary hyperparathyroidism is a reactive condition where the parathyroid glands overproduce PTH in response to chronically low calcium, most commonly from vitamin D deficiency or chronic kidney disease (CKD). In CKD, the kidneys cannot convert vitamin D to its active form, calcium absorption decreases, and PTH rises to compensate. Treatment addresses the underlying cause: vitamin D supplementation for deficiency, or active vitamin D analogs and phosphate binders for CKD. Tertiary hyperparathyroidism occurs when longstanding secondary hyperparathyroidism causes the glands to become autonomous.
Generally, you should continue your usual supplements and inform your doctor about them, as the goal is to see your PTH level in its usual physiological context. However, avoid taking calcium supplements within a few hours of the blood draw, as the acute calcium load can transiently suppress PTH and give a falsely low result. Vitamin D supplements should be continued, as part of the diagnostic workup involves assessing whether PTH is elevated despite adequate vitamin D status. If your vitamin D is low, your doctor may want to recheck PTH after vitamin D has been repleted to normal levels, since vitamin D deficiency alone can cause elevated PTH (secondary hyperparathyroidism) that resolves with supplementation. Always follow your specific lab preparation instructions.

Related Biomarkers

CaCalcium25(OH)DVitamin DCrCreatinine

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Medical Disclaimer: This information is for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Reference ranges may vary between laboratories. Always consult your healthcare provider for interpretation of your specific test results.

Disclaimer: SymptomGPT is not a medical diagnosis tool and does not provide medical advice. Always consult a qualified healthcare professional. If you are experiencing a medical emergency, call 911 immediately.