Endocrine Abstracts

Introduction: Primary hyperparathyroidism causes accelerated bone turnover and the consensus is to measure and act upon the 25hydroxyvitamin D level in order to reduce the drive to PTH production, slow down BMD loss, and prevent hungry bone syndrome. How best to replace vitamin D is less clear so we chose to audit our current practice.

Method: In 12 months 120 patients with primary hyperparathyroidism were identified retrospectively, 98 of which were vitamin D insufficient (25hydroxyvitamin D <72.5 nmol/l). These were audited as to the action taken and the change in 25hydroxyvitamin D, calcium and PTH.

Results: 21.4% of the 98 cases were loaded with the equivalent to 300,000U over 10 weeks, this being the most common decision in the “deplete” subgroup. The majority (44.9%), especially in the subgroup 25-50 nmol/l were given 20,000 to 60,000U monthly. The remaining 33 cases were not given any vitamin D supplementation.

30% of cases referred for surgery were not supplemented but with no detrimental effects.

There was an increment in calcium in all groups except those given <1000U daily (−0.04 mmol/l). The largest mean difference of +0.13 mmol/l in the subgroup loaded to 300,000U by weekly doses coincided with the largest mean change in 25-OHvitD level (70.67 nmo/l) without a PTH decrement (mean+0.86 pmol/l). Those receiving a stat dose of 300,000U did however show reduction in the PTH (mean −2.03 pmol/l), and this was as safe as other regimens for calcium change (+0.05 mmol/l), even with influence by an outlying result of +0.9 mmol/l. A subgroup of nine patients on 1 g supplement of calcium a day demonstrated a mean rise in calcium of +0.12 mmol/l, but despite minimal impact on 25-OHvitD, reduced PTH by a mean of −12.47 pmol/l.

Discussion: There doesn’t appear to be one best regimen to use and none appear detrimental. The variable effects on PTH level would warrant further investigation.