Abstract

PurposeTo evaluate the influence of intravenous methylprednisolone (IVMP) pulse administration on bone mineral density (BMD) of the lumbar spine and the femoral neck in patients with moderate-to-severe Graves’ orbitopathy (GO).MethodsThirty-five patients with GO in euthyreosis were treated with 12 IVMP pulses (6 × 0.5 g, 6 × 0.25 g on a weekly schedule). Supplementation with 1.0 g of calcium and 800 IU of vitamin D was initiated in all patients before beginning therapy. BMD of the lumbar spine (L1–L4) and the femoral neck were assessed at baseline and after the last IVMP pulse using dual-energy X-ray absorptiometry. To determine differences in BMD between values at baseline and after treatment, we used the least significant change (LSC) methodology. LSC values were calculated to be 3 and 5% for the lumbar spine and the femoral neck, respectively. Change in BMD equal to or exceeding the LSC was assessed as either increase or decrease of BMD. We then compared pre-treatment and post-treatment mean BMD values at the lumbar spine and the femoral neck.ResultsWe did not observe a decrease of BMD at any site equal to or exceeding the LSC. We found an increase of BMD in at least one measurement site equal to or exceeding the LSC value in 43% of patients, mostly in the lumbar spine (31%). Mean femoral neck BMD did not change while mean lumbar BMD increased.ConclusionsIVMP given in weekly intravenous pulses does not lead to loss of BMD of the lumbar spine and the femoral neck.

Highlights

  • Therapy with high dose intravenous glucocorticoids (GCs) is an effective immunosuppressive treatment used in variousElectronic supplementary material The online version of this article contains supplementary material, which is available to authorized users.Endocrine (2019) 64:308–315 and thereby shortening the lifespan of osteoblasts and osteocytes [9, 13, 14]

  • We found that GCs given intravenously in weekly infusions do not lead to the loss of bone mineral density (BMD) of the lumbar spine and the femoral neck

  • We observed an increase of BMD in at least one measurement site in 43% of patients, as well as an overall increase in mean BMD in the lumbar spine

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Summary

Introduction

At the same time the opposite effect is taking place in osteoclasts, resulting in their prolonged lifespan [13, 14]. An excess of GCs stimulates the mineralocorticoid receptor within parathyroid chief cells [15]. The mineralocorticoid receptor stimulation impacts parathyroid hormone (PTH) secretion by the chief cells leading to an overall increase in PTH levels [15]. The catabolic effects, on the other hand, result from continuous excessive secretion of PTH leading to bone destruction [16, 17]. GCs provoke decreased calcium absorption in the gut [18] This decreased absorption of calcium results in hypocalcemia, which feeds back and further stimulates PTH secretion [15]. Summarizing, the effect of GCs on bone differs depending on the duration and dosage of therapy, as well as its route of administration [19]

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