Significant Loss of Areal Bone Mineral Density Following Prolonged Bedrest during Treatment with Teriparatide
Presentation Number: SUN 319
Date of Presentation: April 2nd, 2017
Christopher T Martin*1, Catherine B Niewoehner2 and Lynn A Burmeister1
1University of Minnesota, Minneapolis, MN, 2Minneapolis VA HCS, Minneapolis, MN
Bone density gain and decreased rates of vertebral fracture have been shown in postmenopausal women with teriparatide treatment. We present of a case of severe osteoporosis with thoracic myelopathy secondary to non-traumatic T8 compression fracture managed non-surgically with 3.5 months of bed rest. Despite treatment with teriparatide, one year follow-up dual energy x-ray absorptiometry (DXA) scan revealed an unexpected 19% reduction in lumbar spine bone mineral density (BMD) and a 6% reduction in total hip density.
A 79-year-old caucasian female was referred to Orthopedics with 5 weeks of thoracic back pain, leg paresthesias and delayed bladder emptying. Her exam was significant for BMI 22.3, and positive Babinski bilaterally. MRI showed a T8 compression fracture with evidence of thoracic myelopathy. Osteoporosis was confirmed by DXA scan demonstrating a lowest T-score of -3.7 at the left femoral neck.
Past medical history was significant for menopause at age 51 with a subsequent one year history of hormone replacement therapy. She underwent T12 kyphoplasty in 2009 and L2 kyphoplasty in 2015 for likely traumatic vertebral fractures due to falls. She was a former 40-pack year smoker and she consumed “a few” beers daily. She had not previously received bisphosphonate nor other pharmacologic osteoporosis treatment besides calcium and vitamin D supplement of unknown dosage. Laboratory tests did not show additional causes of osteoporosis.
She was treated with strict bedrest and started on teriparatide with the intention to build bone prior to possible surgery. Three months later she presented to clinic on a gurney confirming adherence to the bedrest order. After 3.5 months of bed rest deconditioning, she was unable to walk and required an additional 3 months of physical therapy. Active myelopathy had resolved at 6 month orthopedics follow up. By 1 year follow up she had returned to many of her past activities using a thoraco-lumbar-sacral orthosis. There were no new fractures. Repeat DXA showed 19% loss in lumbar and 6% loss in total hip BMD. Teriparatide compliance was reported by the patient, her family and pharmacy refill records.
In the Fracture Prevention Trial, greater than 4% loss of femoral neck BMD after 1 year of teriparatide treatment was reported in 10% of postmenopausal women. However, these women still had gain in lumbar BMD. Lumbar BMD loss despite teriparatide treatment has not been previously reported. Daily alcohol consumption, severe osteoporosis at baseline and immobilization osteoporosis secondary to transient myelopathy treated with strict bed rest all likely contributed to loss of BMD in our patient. We hypothesize that immobilization may have decreased or reversed the expected bone gain response to teriparatide. Therefore our findings raise caution regarding the use of teriparatide monotherapy in similar clinical settings.
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