No, hyperparathyroidism does not cause low calcium—it causes HIGH calcium.
Primary hyperparathyroidism (PHPT) is characterized by hypercalcemia (elevated serum calcium) due to excessive PTH secretion from parathyroid adenomas or hyperplasia. 1 The fundamental pathophysiology involves PTH increasing calcium through three mechanisms: enhanced bone resorption, increased renal calcium reabsorption, and stimulated intestinal calcium absorption via vitamin D activation.
Understanding the Different Types of Hyperparathyroidism
Primary Hyperparathyroidism (PHPT)
- Always associated with hypercalcemia (or at minimum normocalcemia in early/mild cases)
- PTH is inappropriately elevated relative to the calcium level
- Hypercalcemia results from increased digestive calcium absorption, increased bone resorption, and primarily from decreased renal calcium excretion 1
- Even during acute illness when hospitalized, only 7.4% of PHPT patients show calcium increases >0.5 mg/dL, while 65.7% show decreases in total calcium—but this represents a relative decrease that typically remains above normal or in the high-normal range 2
Secondary Hyperparathyroidism (SHPT)
This is where the confusion arises—secondary hyperparathyroidism occurs WITH low or low-normal calcium 3, 4:
- PTH elevation is an appropriate response to hypocalcemia
- The serum calcium is normal or low, and PTH is elevated as a compensatory mechanism
- Common causes include:
- Chronic kidney disease: Reduced 1-alpha-hydroxylase production leads to defective calcium absorption and hypocalcemia, stimulating PTH 1, 3
- Vitamin D deficiency: Impaired intestinal calcium absorption triggers PTH elevation 3
- Insufficient calcium intake: Particularly in restrictive diets (veganism), chronic negative calcium balance stimulates PTH 5, 6
- Malabsorption syndromes: Post-bariatric surgery or other GI disorders 7
Tertiary Hyperparathyroidism
- Develops after longstanding secondary hyperparathyroidism
- Parathyroid glands become autonomous and hypercalcemia develops despite the original stimulus being corrected
- Most commonly seen after kidney transplantation 4
Clinical Algorithm for Interpretation
When you see elevated PTH, check the calcium:
High calcium + High PTH = Primary hyperparathyroidism
- Proceed with parathyroid imaging and surgical evaluation 8
Low/Low-normal calcium + High PTH = Secondary hyperparathyroidism
- Check 25-OH vitamin D levels (target ≥30 ng/dL) 5
- Assess renal function (eGFR) 3, 9
- Evaluate dietary calcium intake (should be >1000 mg/day) 5, 6
- Check 24-hour urinary calcium (profoundly low suggests negative calcium balance) 6
- Treat underlying cause: vitamin D repletion, calcium supplementation (600 mg twice daily), or manage CKD 3, 5
High calcium + High PTH after long-standing SHPT = Tertiary hyperparathyroidism
- Consider parathyroidectomy if medical management fails 4
Common Pitfall to Avoid
Do not confuse secondary hyperparathyroidism (which has low calcium) with primary hyperparathyroidism (which has high calcium). The key distinguishing feature is whether the PTH elevation is appropriate (secondary) or inappropriate (primary) for the calcium level. In PHPT, even a "normal" PTH is considered inappropriately elevated when calcium is high—PTH should be suppressed in the presence of hypercalcemia 7, 1.
In patients with normal vitamin D levels and adequate renal function, a calcium challenge test (600 mg twice daily for 2-3 weeks) can confirm secondary hyperparathyroidism due to insufficient intake—PTH should normalize if this is the cause 5.