BackgroundThis study aimed to investigate whether the presence of low bone mineral density (BMD) in patients with axial spondyloarthritis (axSpA) predicts formation of new syndesmophytes over 2 years.MethodsOne hundred and nineteen patients fulfilling the imaging arm of the Assessment of SpondyloArthritis International Society axSpA criteria were enrolled. All patients were under 50 years of age. The modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) was assessed by two trained readers blinded to the patients’ data. BMD (lumbar spine, femoral neck or total hip) at baseline was assessed using dual-energy absorptiometry. Low BMD was defined as Z score ≤ − 2.0. Spinal radiographic progression was defined as worsening of the mSASSS by ≥ 2 points over 2 years. Logistic regression analyses were performed to identify predictors associated with development of new syndesmophytes and spinal radiographic progression.ResultsAt baseline, 19 (16%) patients had low BMD. New syndesmophytes had developed in 22 (21%) patients at 2-year follow-up. New syndesmophyte formation after 2 years occurred more in patients with low BMD than in those with normal BMD (p = 0.047). In the multivariable analysis, current smoking, existing syndesmophytes and low BMD at baseline were associated with spinal radiographic progression (OR (95% CI) 3.0 (1.1, 7.7), 4.6 (1.8, 11.8) and 3.6 (1.2, 11.2), respectively). The presence of syndesmophytes at baseline and low BMD were predictors of new syndesmophytes over the following 2 years (OR (95% CI) 5.5 (2.0, 15.2) and 3.6 (1.1, 11.8), respectively).ConclusionsLow BMD and existing syndesmophytes at baseline were independently associated with the development of new syndesmophytes in young axSpA patients.

We present a case of lung metastasis manifesting as lung infarction by mucin and tumor embolization. The radiograph and high-resolution CT showed multiple focal consolidations with ground glass attenuation in subpleural areas of both lungs. Diagnosis was made by open lung biopsy, which revealed pulmonary infarction caused by intravascular adenocarcinoma with numerous mucus emboli in pulmonary arteries. Subpleurally located consolidations on high-resolution CT correlated well with the histologic findings of lung infarction by mucin and tumor emboli.