Patient Education · Endocrinology
Parathyroid Disorders & Calcium Metabolism
A guide to understanding the parathyroid glands, primary hyperparathyroidism, and when treatment is needed.
Parathyroid disorders are among the most commonly missed diagnoses in medicine. If you have questions about calcium or parathyroid hormone, please contact our office.
The Parathyroid Glands
What are the parathyroid glands and what do they do?
There are four parathyroid glands — each about the size of a grain of rice — embedded in the back of the thyroid. They produce parathyroid hormone (PTH), the principal regulator of blood calcium. PTH acts on bone (releases calcium), kidney (reabsorbs calcium, activates vitamin D), and intestine (increases calcium absorption from food). This system maintains blood calcium within a narrow range — essential for cardiac function, nerve transmission, and muscle contraction.
Primary Hyperparathyroidism
What is primary hyperparathyroidism?
Primary hyperparathyroidism (pHPT) occurs when one or more parathyroid glands becomes autonomous — producing PTH independently of the body’s calcium level. Chronically elevated PTH drives calcium out of bone and elevates blood calcium. It is caused by a single benign adenoma in approximately 85% of cases, and is one of the most common endocrine conditions in women over 50.
Is “asymptomatic” hyperparathyroidism really symptom-free?
What are the symptoms and complications?
The classic “bones, stones, groans, and psychic moans” — Bones: Osteoporosis from PTH-driven calcium loss. Stones: Kidney stones from hypercalciuria. Groans: GI symptoms including nausea and constipation. Psychic moans: Depression, anxiety, cognitive impairment.
Nonspecific symptoms including fatigue, increased thirst, and musculoskeletal aches are also common and frequently dismissed.
What is normocalcemic hyperparathyroidism?
Normocalcemic hyperparathyroidism is a condition in which PTH is persistently elevated while blood calcium remains within the normal range — provided secondary causes have been excluded. It carries real consequences for bone density and requires surveillance and, in appropriate cases, treatment.
Diagnosis
How is primary hyperparathyroidism diagnosed?
The biochemical diagnosis is established by finding elevated or inappropriately non-suppressed PTH alongside elevated (or high-normal) blood calcium. Diagnostic workup includes: Repeated calcium and PTH measurements, 24-hour urine calcium, vitamin D levels, kidney function, DEXA scan, and renal imaging.
Treatment
When is surgery recommended?
Parathyroidectomy is the only definitive cure. Surgery is recommended when any of the following criteria are met: Calcium more than 1 mg/dL above the upper limit of normal, T-score below −2.5, history of fragility fracture, 24-hour urine calcium above 400 mg/day, nephrolithiasis, or age under 50.
We also consider surgery for patients with significant symptoms attributable to hyperparathyroidism — even if formal criteria are not met — after careful discussion.
What if surgery is not an option?
For patients who decline surgery or whose disease does not yet meet surgical thresholds, careful surveillance is appropriate — including annual calcium and creatinine, DEXA scan every 1–2 years, and periodic renal imaging.
Cinacalcet (Sensipar) reduces calcium levels by sensitizing the calcium-sensing receptor. It does not cure the disease or protect bone, but manages hypercalcemia in patients who cannot undergo surgery.
