Patients with Crohn’s disease frequently have low bone mineral density (BMD) at diagnosis and through follow-up.¹ Multiple factors contribute to this risk, including poor nutrition, inflammatory cytokines, glucocorticoid treatment, vitamin D deficiency, decreased activity and reduced muscle mass.² We present an interesting case of severe lower back pain due to vertebral compression fractures, in a newly diagnosed patient with Crohn’s disease, treated with systemic steroids.

A 11-year-old male, diagnosed with Crohn’s disease three months prior, presented to outpatient clinic with a two-week history of severe lower back pain. He had been treated initially with two weeks of oral steroid (40 mg) followed by a seven-week weaning regime. The pain started in the final week of this course and was described as constant and sharp with intermittent spasms. He had associated morning stiffness in the lower back and struggled getting out of bed. There was no significant past medical history. At time of Crohn’s diagnosis, his symptoms included abdominal pain, mouth ulcers, and weight loss. While he demonstrated clinical response to steroid, he was due to escalate to infliximab in view of extensive small bowel involvement on MRI.

On examination, there was a reduction of spinal mobility with mild paraspinal tenderness, especially in the thoracic region. An urgent referral was made to rheumatology who arranged an MRI spine to investigate for IBD-related arthropathy/sacroiliitis. This demonstrated multiple new compression fractures of the lumbar spine but no evidence of sacroiliitis. A subsequent x-ray showed wedge compression fractures of all the vertebrae from T11 to L5. This was associated with a 4 cm loss of vertical height. An urgent referral was made to the spinal surgeons although interestingly, the lower back pain had already improved at the time of the referral, having reported significant symptomatic improvement during Infliximab induction. At present, this patient remains under close monitoring, with a particular focus on his bone health and is establishing infliximab treatment. While a vitamin D level was not sent initially in this patient, subsequent blood tests showed an adequate vitamin D level (60nmol/L).

All clinicians managing children with IBD must remain vigilant for low BMD-associated complications. These can often mimic arthropathy. While glucocorticoid treatment often results in prompt induction of clinical remission of IBD, it can have a negative impact on bone health, further compounding the damage inflicted by chronic inflammation. Exclusive enteral nutrition or treatment with anti-TNF agents may be preferable in a selected group of patients, particularly those who have low-BMD at diagnosis.

References

1. Rozes S, Guilmin-Crepon S, Alison M, et al. Bone health in paediatric patients with Crohn’s disease. JPGN 2021;73(2):231–235.

2. Tsampalieros A, Lam CKL, Spencer JC, et al. Long-term inflammation and glucocorticoid therapy impair skeletal modeling during growth in childhood. J Clin Endocrinol Metabol 2013;98:3438–3445.