Parathyroid Hormone

When high (hyperparathyroidism):

Always interpret PTH alongside serum Calcium and Vitamin D. The pattern determines the cause.

Pattern 1: High PTH + Low/Normal Calcium + Low Vitamin D = Secondary Hyperparathyroidism (most common in athletes)

• Root cause is usually Vitamin D deficiency. The body elevates PTH to maintain calcium in the face of poor absorption.
• Vitamin D3 -- 5,000 IU/day for 8-12 weeks, then re-test. Target 25-OH Vitamin D of 100-150 nmol/L (40-60 ng/mL)
• Vitamin K2 (MK-7) -- 100-200 mcg/day (directs calcium to bone, not soft tissue)
• Magnesium Glycinate -- 400 mg/day (required cofactor for Vitamin D activation and PTH signalling)
• Adequate sun exposure: 15-20 minutes midday, 3-4x/week
• Recheck PTH, Calcium, and Vitamin D in 8-12 weeks

Pattern 2: High PTH + High Calcium = Primary Hyperparathyroidism

• Usually caused by a parathyroid adenoma. Requires endocrinology referral.
• Often asymptomatic, detected on routine bloodwork. Untreated cases risk kidney stones, osteoporosis, and cardiovascular disease.
• Do NOT supplement Vitamin D aggressively in this pattern without physician guidance. It can worsen hypercalcaemia.

Pattern 3: High PTH + High Calcium + Reduced eGFR = Tertiary Hyperparathyroidism

• Seen in chronic kidney disease. Requires nephrology involvement.

When low (hypoparathyroidism):

• Rare. May reflect post-surgical damage, autoimmune disease, or severe magnesium deficiency.
• Magnesium -- 400-600 mg/day (low magnesium suppresses PTH release)
• Check serum Calcium: if low, urgent medical evaluation is required
• Investigate neck surgery history or autoimmune conditions

AAS/PED considerations:

• High-dose GH or MK-677 increases bone turnover markers; PTH may rise modestly as calcium demand increases during bone remodelling
• Very high-protein diets (>3 g/kg) increase urinary calcium excretion and can subtly raise PTH; ensure calcium intake matches (1,000-1,200 mg/day)
• AAS users with elevated creatinine should have PTH checked; early kidney dysfunction can present as rising PTH before eGFR drops significantly

Pharmacological options (specialist-only):

• For Pattern 1 (secondary hyperparathyroidism from low Vitamin D), correct the Vitamin D deficiency first; pharmacology is not indicated unless calcium remains low after 12 weeks of adequate D3 replacement
• Cinacalcet (Sensipar) -- 30-60mg/day (up to 90mg 2x/day); calcimimetic, activates calcium-sensing receptor on parathyroid cells to suppress PTH release; for confirmed primary hyperparathyroidism in patients declining or ineligible for surgery; endocrinology-supervised; monitor for hypocalcaemia, nausea, seizures
• Bisphosphonates (alendronate 70mg weekly, zoledronic acid 5mg IV yearly) -- for concurrent osteoporosis from chronic PTH elevation; do not reduce PTH directly but protect bone density
• Parathyroidectomy -- surgical removal of the offending adenoma; the only curative intervention for primary hyperparathyroidism; indicated when calcium >0.25 mmol/L above upper limit, age <50, kidney stones, or reduced bone density; minimally invasive with high cure rates
• For Pattern 3 (tertiary hyperparathyroidism in CKD), nephrology manages with cinacalcet, phosphate binders, and active Vitamin D analogues (calcitriol, paricalcitol)

References:

• Bilezikian, J. P., Brandi, M. L., Eastell, R., et al. (2014). Guidelines for the management of asymptomatic primary hyperparathyroidism: Summary statement from the Fourth International Workshop. Journal of Clinical Endocrinology & Metabolism, 99(10), 3561-3569. DOI: 10.1210/jc.2014-1413
• Holick, M. F. (2007). Vitamin D deficiency. New England Journal of Medicine, 357(3), 266-281. DOI: 10.1056/NEJMra070553
• Khan, A. A., Hanley, D. A., Rizzoli, R., et al. (2017). Primary hyperparathyroidism: Review and recommendations on evaluation, diagnosis, and management. A Canadian and international consensus. Osteoporosis International, 28(1), 1-19. DOI: 10.1007/s00198-016-3716-2
• Rude, R. K., Singer, F. R., & Gruber, H. E. (2009). Skeletal and hormonal effects of magnesium deficiency. Journal of the American College of Nutrition, 28(2), 131-141. DOI: 10.1080/07315724.2009.10719764