Hypoparathyroidism laboratory findings: Difference between revisions
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*Hypomagesemia 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. | *Hypomagesemia 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 magnesium decreases to subnormal levels as magnesium depletion progresses. | ||
===24-Hour Urinary Magnesium=== | |||
*24-hour urinary magnesium level measurement before initiation of treatment is useful, if magnesium deficiency is detected as a cause of hypocamcemia. | |||
*Elevated or even detectable urinary levels of magnesium suggest magnesium depletion due to renal losses since kidney should conserve magnesium in depleted body stores. | *Elevated or even detectable urinary levels of magnesium suggest magnesium depletion due to renal losses since kidney should conserve magnesium in depleted body stores. | ||
===Serum 25-Hydroxy Vitamin D=== | ===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 25-Hydroxy Vitamin D should be measured to rule out vitamin D deficiency as a cause of hypocalcemia. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
OR
Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
OR
[Test] is usually normal among patients with [disease name].
OR
Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
OR
There are no diagnostic laboratory findings associated with [disease name].
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 (25[OH] vitamin 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:
Corrected total calcium = measured total calcium + 0.8 (4.0 − serum albumin)
- 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
- Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
| Disorder | Hypoparathyroidism | Classic vitamin D deficiency | Pseudohypoparathyroidism | Hypomagnesemia |
|---|---|---|---|---|
| Laboratory findings | ||||
| Serum calcium concentration | ↓ | ↓ | ↓ | Slightly ↓ |
| Intact PTH | ↓ | ↑ | ↑ | Inappropriately ↓ |
| Serum phosphate concentration | ↑ | ↓/Low-normal | ↑ | -- |
If necessary, measuring cAMP (cyclic AMP) in the urine after an intravenous dose of PTH can help in the distinction between hypoparathyroidism and other causes.
Biochemical Tests
Serum Calcium
- Measurement of total serum calcium with automatic techniques has similar or even more reliability than serum ionized calcium measurement.
Serum Parathyroid Hormone
- Method of choice for measuring intact parathyroid hormone include Immunoradiometric assay (IMRA) or Immunochemiluminescent assay (ICMA).[2]
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 subtantially higher urinary calcium:creatinine clearance ratio.[3]
Serum Magnesium
- Serum magnesium concentration should be measured to rule out hypomagnesemia (or sometimes hypermagnesemia) as a cause of hypocalcemia.
- Hypomagesemia 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.
24-Hour Urinary Magnesium
- 24-hour urinary magnesium level measurement before initiation of treatment is useful, if magnesium deficiency is detected as a cause of hypocamcemia.
- Elevated or even detectable urinary levels of magnesium suggest magnesium depletion due to renal losses since kidney should conserve magnesium in depleted body stores.
Serum 25-Hydroxy Vitamin D
- Serum 25-Hydroxy Vitamin D should be measured to rule out vitamin D deficiency as a cause of hypocalcemia.
References
- ↑ Shoback D (2008). "Clinical practice. Hypoparathyroidism". N. Engl. J. Med. 359 (4): 391–403. doi:10.1056/NEJMcp0803050. PMID 18650515.
- ↑ 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.