Multiple pneumatoceles and lung abscesses caused by early-onset E. coli sepsis in a preterm neonate

Frozen shoulder (FS) is speculated to have an inflammatory etiology. On angiography, abnormal angiogenesis is observed around the affected shoulder, suggesting a possible source of inflammation and pain. The effectiveness and safety of transarterial embolization (TAE) targeting abnormally proliferating blood vessels have been reported. This study investigated changes in chronic inflammatory and hypoxic status before and after TAE in FS by 18-fluorine-fluoro-2-deoxyglucose (FDG) positron-emission tomography/computed tomography as a possible mechanism of the therapeutic response to TAE.

Fifteen patients with unilateral FS, persistent for more than 6 months, who were refractory to conservative treatments, underwent TAE using the temporary embolic agent imipenem/cilastatin. Patients underwent positron-emission tomography/computed tomography with FDG (as a biomarker of inflammation) before and 8 weeks after TAE. Regional uptake was evaluated by the maximum standardized uptake value. The lesion-side–to–(contralateral-) normal-side uptake ratio was also calculated. Pain and functional scales, range-of-motion, and laboratory tests, including white blood cell, C-reactive protein, interleukin 6, vascular endothelial growth factor, and tumor necrosis factor α were evaluated.

On FDG-PET, the average maximum standardized uptake value of the lesion-side was significantly greater than that of the normal-side (maximum standardized uptake value before TAE: 3.11 ± 1.25 vs 1.95 ± 1.15, P = .0001; 8-weeks post-TAE: 2.36 ± 0.74 vs 1.78 ± 0.69, P = .0002). The mean lesion-side–to–(contralateral-) normal-side uptake ratios before TAE (1.71 ± 0.60) decreased after TAE (1.37 ± 0.29, P = .011). The decrease of FDG uptake (−21.1 ± 12.2%) showed a significant correlation with the change in the pain scale score (r = −0.56, P = .039) and extension score (r = −0.59, P = .026).

Chronic inflammation in FS, as demonstrated by FDG uptake, was decreased after TAE. Thus, chronic inflammation is likely to be an underlying mechanism that should be targeted for symptomatic improvement of frozen shoulder.

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