Is Calcium Supplementation Always Needed in Patients With Hypoparathyroidism?

Ahmed Al-Sharefi; Elizabeth Glenister; Margaret Morris; Richard Quinton


Clin Endocrinol. 2019;90(6):775-780. 

In This Article

Abstract and Introduction


Oral calcium salts are recommended for the treatment of chronic hypoparathyroidism (HypoPT), although dosimetry is variable between individual patients and clinicians. However, patient feedback on calcium salts can be negative, particularly due to gastrointestinal side effects and hypercalciuria-related complications. We begin with a clinical case of a HypoPT patient taking oral calcium salts following thyroid surgery, who requested support in reducing her dose of these with a view to stopping entirely. To evaluate her request, we first describe the usual treatment of HypoPT according to current guidance and then present data from (a) a case note review of a cohort of 24 HypoPT patients managed with a "no calcium" treatment regimen by single physician (b) a comprehensive online survey of HypoPT patients' treatment and experiences (n = 330). The case note review found that target range serum calcium levels were successfully achieved in all 24 patients since transitioning to a "no calcium" regimen, without any breakthrough hypocalcaemia-related symptoms, the development of new renal stones, the occurrence of calcium-related hospital admissions or the finding of significant hypercalciuria. The online survey identified 36% of HypoPT patients who continued to take activated vitamin D, but had discontinued calcium supplements. HypoPT patients not currently taking calcium reported a significantly lower prevalence of adverse effects and outcomes, both compared with their previous experiences whilst taking calcium and also compared with the 64% of patients who continued to take oral calcium. We conclude that, subject to methodological limitations, there are significant issues of tolerability arising from conventional calcium-based treatment regimens for patients with chronic HypoPT. For selected patients, it may be reasonable to facilitate a managed therapeutic transition to "no calcium" regimen, and we also propose that calcium-based regimes be prospectively evaluated against calcium-free (or calcium-low) alternatives.


Hypoparathyroidism (HypoPT) is a rare endocrinopathy characterized by hypocalcaemia, with low or "inappropriately normal" serum levels of parathyroid hormone (PTH). It is estimated to affect 60 000 to 115 000 individuals in the United States.[1] Although sometimes congenital, it mostly occurs as a sequela of neck surgery, especially total thyroidectomy, where it can be transient or permanent.[2] Lifelong treatment of chronic HypoPT targets the avoidance of symptomatic hypocalcaemia, whilst avoiding biochemical hypercalcaemia and minimizing hypercalciuria-associated deterioration in kidney function.[1]

What Therapies are Currently Recommended for the Treatment of Chronic HypoPT?

All major guidelines recommend lifelong therapy with oral calcium and activated vitamin D (calcitriol or alfacalcidol); treatment of concomitant hypovitaminosis D with unhydroxylated D3 (colecalciferol) or D2 (ergocalciferol) is also recommended.[1,2] Thiazide diuretics also have a potential role in managing HypoPT (and non-HypoPT)-related hypercalciuria, given their effect to reduce urinary calcium excretion. However, their effectiveness in HypoPT has only been confirmed for patients adhering to dietary salt restriction and taking higher thiazide doses than those typically prescribed in the UK for the treatment of hypertension.[3]

Until recently, HypoPT was the only hormonal disorder where treatment did not involve replacing the missing hormone. However, based upon a study showing its ability to achieve stabilization of serum calcium concentrations and reduce the daily calcium and active vitamin D needed up to 50%,[4] the European Medicines Agency granted marketing authorization for full-length recombinant human parathyroid hormone Natpar® (rhPTH[1-84]) in adult patients with chronic HypoPT as an adjunctive, rather than sole therapy, and only for patients who meet certain criteria.[1] Nevertheless, in view of rhPTH drug cost and reimbursement issues, guidelines from major scientific societies continue to emphasize the centrality of oral calcium supplements to the treatment of chronic HypoPT;[1,2] albeit that European physicians seem to prescribe lower calcium doses than their North American colleagues.

What are the Particular Challenges in Managing Patients With Chronic HypoPT?

In HypoPT, the lack of PTH-mediated renal tubular calcium reabsorption necessarily predisposes to hypercalciuria when taking calcium or activated vitamin D supplements. Chronic hypercalciuria, in turn, predisposes patients to nephrocalcinosis, kidney stones, renal impairment or even death.[5,6] Thus, achieving this balance can be challenging even in expert hands.

We discuss a clinical case highlighting the narrative of a HypoPT patient taking oral calcium salts following thyroid surgery, who was later successfully transitioned to a calcium-free regimen. We follow this by presenting the results of a chart review data from 24 patients under our care who had also transitioned to a "no calcium" treatment regimen. Finally, we present data and analysis from the very first, comprehensive online survey of a large cohort (n = 330) of HypoPT patients—all of whom had originally received oral calcium salts—exploring their experiences whilst taking (or not taking) oral calcium.