What is the role of lab studies in the evaluation of primary hyperparathyroidism?

Updated: Oct 02, 2018
  • Author: Lawrence Kim, MD, FACS, FACE; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
  • Print
Answer

Answer

Total serum calcium and albumin levels or ionized calcium levels should be measured. Hypercalcemia should be documented on more than one occasion before a diagnostic workup is undertaken.

Testing of the intact parathyroid hormone level is the core of the diagnosis. An elevated intact parathyroid hormone level with an elevated ionized serum calcium level is diagnostic of primary hyperparathyroidism. A 24-hour urine calcium measurement is necessary to rule out FHH.

Older assays measured fragments of the parathyroid hormone molecule, such as the C-terminal or mid region of parathyroid hormone. These first-generation assays are considered obsolete for the clinical practice. Second-generation parathyroid hormone assays, globally called "intact" parathyroid hormone assays, and third-generation parathyroid hormone assays called "whole" or "biointact" parathyroid hormone assays use two different antibodies against two different segments of parathyroid hormone. Second- and third-generation parathyroid hormone assays are producing far more clinically satisfying data than the first-generation assays but have some limitations that continue to be assessed in several studies.

Other laboratory findings in primary hyperparathyroidism include mild hyperchloremic acidosis, hypophosphatemia, and mild to moderate increase in urinary calcium excretion rate.

Vitamin D levels should be measured in the evaluation of primary hyperparathyroidism. Vitamin D deficiency (a 25-hydroxyvitamin D level of less than 20 ng per milliliter) can cause secondary hyperparathyroidism, and repletion of vitamin D deficiency can help to reduce parathyroid hormone levels. [7]  In most studies, increasing serum 25-hydroxyvitamin D stores to at least 37.5 ng per milliliter is sufficient for parathyroid hormone suppression and prevention of secondary hyperparathyroidism in persons with normal renal function (although some studies have suggested increasing stores to 50 ng per milliliter). [8]


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!