
Health Dictionary
Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Hypoparathyroidism laboratory findings
Introduction
Overview
Overview
Diagnosis of hypoparathyroidism is made by measurement of serum calcium (total and ionized), serum albumin (for correction), phosphate, intact parathyroid hormone (PTH), and 25-hydroxy vitamin D levels. Normal or inappropriately low serum intact parathyroid hormone (PTH) concentration in patients with subnormal serum albumin corrected total or ionized calcium concentration diagnostic of hypoparathyroidism.
Laboratory Findings
Laboratory Findings
- Diagnosis of hypoparathyroidism is made by measurement of serum calcium (total and ionized), serum albumin (for correction), phosphate, intact parathyroid hormone (PTH), and 25-hydroxyvitamin D levels.[1]
- PTH degrades rapidly at ambient temperatures and the blood sample therefore has to be transported to the laboratory on ice.
- Normal or inappropriately low serum intact parathyroid hormone (PTH) concentration in patients with subnormal serum albumin corrected total or ionized calcium concentration diagnostic of hypoparathyroidism.
- Hypomagnesemia and vitamin D deficiency should be ruled out as cause of hypocalcemia before making a diagnosis of hypoparathyroidism.
- Calculation of corrected total calcium:
- In this formula, serum calcium is measured in mg/dL and serum albumin is measured in gm/dL.
- Laboratory findings consistent with the diagnosis of hypoparathyroidism include:
- Low parathyroid hormone
- Low serum calcium level
- Normal to elevated serum phosphate concentration
| Disorder | Hypoparathyroidism | Classic vitamin D deficiency | Pseudohypoparathyroidism | Hypomagnesemia |
|---|---|---|---|---|
| Laboratory findings | ||||
| Serum calcium concentration | ↓ | ↓ | ↓ | Slightly ↓ |
| Intact PTH | ↓ | ↑ | ↑ | Inappropriately ↓ |
| Serum phosphate concentration | ↑ | ↓/Low-normal | ↑ | — |
Biochemical Tests
Biochemical Tests
Serum Calcium
- Measurement of total serum calcium with automatic techniques has similar or even more reliability than serum ionized calcium measurement.[2]
- An low serum calcium should be confirmed by repeat measurement.
- Serum albumin should be measured and if found low, corrected calcium should be measured.
Serum Parathyroid Hormone
- Method of choice for measuring intact parathyroid hormone include Immunoradiometric assay (IMRA) or Immunochemiluminescent assay (ICMA).[3]
Serum Magnesium
- Serum magnesium concentration should be measured to rule out hypomagnesemia (or sometimes hypermagnesemia) as a cause of hypocalcemia.
- Hypomagnesemia as a contributor to hypocalcemia may be difficult to rule out as serum magnesium levels may be normal even if there depletion of intracellular magnesium stores.
- Serum magnesium decreases to subnormal levels as magnesium depletion progresses.
Serum 25-Hydroxy Vitamin D
- Serum 25-hydroxy vitamin D should be measured to rule out vitamin D deficiency as a cause of hypocalcemia.
Serum Albumin
- Serum albumin should be measured as low albumin will give falsely low total serum calcium.
24-Hour Urinary Calcium
- 24-Hour urinary calcium excretion is indicated by the urinary calcium:creatinine clearance ratio.
- Hypoparathyroidism and vitamin D deficiency have low urinary calcium excretion.
- Hypocalcemic patients with activating mutations in the extracellular calcium-sensing receptor have a substantially higher urinary calcium:creatinine clearance ratio.[4]
24-Hour Urinary Magnesium
- 24-hour urinary magnesium level measurement before initiation of treatment for hypocalcemia is useful if magnesium deficiency is detected as a cause of hypocalcemia.
- Elevated or even detectable urinary levels of magnesium suggest magnesium depletion due to renal losses since kidney should conserve magnesium in depleted body stores.
References
References
- ↑ Shoback D (2008). “Clinical practice. Hypoparathyroidism”. N. Engl. J. Med. 359 (4): 391–403. doi:10.1056/NEJMcp0803050. PMID 18650515.
- ↑ Silverberg SJ, Bilezikian JP (1996). “Evaluation and management of primary hyperparathyroidism”. J. Clin. Endocrinol. Metab. 81 (6): 2036–40. doi:10.1210/jcem.81.6.8964825. PMID 8964825.
- ↑ Endres DB, Villanueva R, Sharp CF, Singer FR (1991). “Immunochemiluminometric and immunoradiometric determinations of intact and total immunoreactive parathyrin: performance in the differential diagnosis of hypercalcemia and hypoparathyroidism” (PDF). Clin. Chem. 37 (2): 162–8. PMID 1993319.
- ↑ Yamamoto M, Akatsu T, Nagase T, Ogata E (2000). “Comparison of hypocalcemic hypercalciuria between patients with idiopathic hypoparathyroidism and those with gain-of-function mutations in the calcium-sensing receptor: is it possible to differentiate the two disorders?”. J. Clin. Endocrinol. Metab. 85 (12): 4583–91. doi:10.1210/jcem.85.12.7035. PMID 11134112.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]
