What laboratory finding is expected in a child with high Parathyroid Hormone (PTH) levels and bone pain?

Laboratory Findings in a Child with High PTH and Bone Pain

In a child with elevated PTH and bone pain, you should expect hypophosphatemia (low phosphate), not hyperphosphatemia. The correct answer is none of the options as stated, but if forced to choose from typical findings: hypocalcemia would be expected if this is secondary hyperparathyroidism (from conditions like rickets or CKD), while hypercalcemia would suggest primary hyperparathyroidism from a parathyroid adenoma.

Understanding the Clinical Context

The key to answering this question is determining whether the elevated PTH represents primary or secondary hyperparathyroidism, as the laboratory patterns differ significantly:

Primary Hyperparathyroidism (PTH-Dependent Hypercalcemia)

In primary hyperparathyroidism caused by parathyroid adenoma:

• Hypercalcemia (elevated or high-normal calcium) is the hallmark finding 1, 2
• Hypophosphatemia or low-normal phosphorus due to PTH-mediated renal phosphate wasting 1, 3
• Elevated or inappropriately normal PTH in the setting of hypercalcemia confirms the diagnosis 1, 3
• Bone pain in children with primary hyperparathyroidism reflects active bone disease and increased bone turnover 4

Secondary Hyperparathyroidism (Compensatory PTH Elevation)

In secondary hyperparathyroidism from conditions like rickets, vitamin D deficiency, or CKD:

• Hypocalcemia or low-normal calcium drives the compensatory PTH elevation 5
• Hyperphosphatemia may occur, particularly in CKD stages 3-5 5
• Elevated PTH is an appropriate physiologic response to low calcium 5
• Bone pain reflects rickets activity or renal osteodystrophy 5, 6

Expected Laboratory Pattern by PTH Physiology

PTH has three primary actions that determine the laboratory findings 7:

• Increases renal calcium reabsorption (raises serum calcium)
• Increases renal phosphate excretion (lowers serum phosphate)
• Stimulates 1,25-dihydroxyvitamin D production (increases intestinal calcium absorption)
• Mobilizes calcium from bone through increased turnover

Therefore, when PTH is elevated and functioning appropriately:

• Serum calcium should be elevated or rising (unless there's resistance or overwhelming calcium loss)
• Serum phosphate should be LOW due to renal phosphate wasting 1
• This means hyperphosphatemia (option C) would be UNEXPECTED with high PTH unless there is concurrent renal failure

Addressing the Specific Options

Option A: Hypokalemia

• Not a typical feature of hyperparathyroidism
• PTH does not directly regulate potassium homeostasis
• This would not be an expected finding 1

Option B: Hypercalcemia

• Expected in primary hyperparathyroidism from parathyroid adenoma 1, 2, 4
• The distinguishing biochemical feature is high or inappropriately normal PTH with elevated calcium 2
• In pediatric primary hyperparathyroidism, patients present with symptomatic hypercalcemia including bone pain 8, 4

Option C: Hyperphosphatemia

• This is CONTRADICTORY to elevated PTH physiology 1
• PTH causes renal phosphate wasting, leading to hypophosphatemia or low-normal phosphorus 1, 7
• Hyperphosphatemia with elevated PTH suggests CKD with impaired phosphate excretion 5

Option D: Regarding 1,25(OH)₂D

• In primary hyperparathyroidism, 1,25-dihydroxyvitamin D is typically elevated due to PTH-stimulated renal 1α-hydroxylase activity 3
• In secondary hyperparathyroidism from vitamin D deficiency, 1,25(OH)₂D would be low initially 5

Clinical Algorithm for Interpretation

When you encounter a child with high PTH and bone pain, measure simultaneously 1:

1. Serum calcium (corrected for albumin)
2. Serum phosphorus
3. Serum creatinine (to assess renal function)
4. 25-hydroxyvitamin D level

Then interpret:

• High calcium + High PTH + Low phosphorus = Primary hyperparathyroidism (likely adenoma) 1, 2
• Low/normal calcium + High PTH + Variable phosphorus = Secondary hyperparathyroidism (rickets, vitamin D deficiency, CKD) 5
• High calcium + High PTH + High phosphorus = Consider CKD with tertiary hyperparathyroidism 8

Critical Pitfall to Avoid

Do not assume hyperphosphatemia is compatible with elevated PTH in the absence of renal failure. PTH physiologically lowers serum phosphate through renal phosphate wasting 1, 7. If both PTH and phosphate are elevated, suspect chronic kidney disease where impaired renal function prevents phosphate excretion despite high PTH 5.