Objective To correlate the thickness of the axillary recess capsule measured by ultrasound with magnetic resonance imaging signs of adhesive capsulitis in patients with shoulder pain. Materials and methods We prospectively evaluated 193 consecutive patients (141 women and 52 men, aged 40–69 years) with shoulder pain lasting 1–9 months from January 2015 to December 2016 who underwent shoulder ultrasound. All participants had routine shoulder ultrasound with additional measurement of axillary recess capsule thickness. After examinations, two groups were formed: negative ultrasound group, composed of patients with a capsule thickness of 2.0 mm or less, and positive ultrasound group, composed of individuals with a capsule thickness greater than 2.0 mm. All patients from the positive ultrasound group and 27 randomly chosen patients from the negative ultrasound group underwent shoulder magnetic resonance imaging. Results In all, 169/193 patients (88%) had an axillary recess capsule thickness of 2.0 mm or less (negative ultrasound group) and 24/193 patients (12%) had a capsule thickness greater than 2.0 mm (positive ultrasound group). Twenty-seven patients from negative ultrasound group (27/169) were randomly selected to undergo shoulder magnetic resonance imaging. None of them had magnetic resonance imaging criteria for adhesive capsulitis. All patients from positive ultrasound group (24/24) underwent shoulder magnetic resonance imaging and 23 of them (23/24) had magnetic resonance imaging signs of adhesive capsulitis, with a sensitivity of 100% and a specificity of 96%. Conclusion In patients with shoulder pain, a thickness greater than 2.0 mm of the axillary recess capsule measured by ultrasound correlates to magnetic resonance imaging signs of adhesive capsulitis with good sensitivity and specificity.

In an earlier article, we demonstrated that sydnone SYD-1 (3-[4-chloro-3-nitrophenyl]-1,2,3-oxadiazolium-5-olate) inhibits electron transport in the respiratory chain and uncouples oxidative phosphorylation, and postulated that these effects are probably involved in its antitumor activity. We now report the effect of SYD-1 on certain macrophage functions, considering the important role of these cells in inflammatory response and also the relevant anti-inflammatory activity reported for some sydnones. Incubation of macrophages with SYD-1 (5-100 μM) for 48 h did not affect the cell viability up to a concentration of 50 μM. However, at the highest concentration (100 μM), the compound decreased macrophage viability by ~20%. In assays involving 2 h and 24 h of incubation, SYD-1 (5-100 μM) did not affect the cell viability. The incubation of macrophages with the compound for 2 h promoted a dose-dependent reduction of phagocytic activity of up to ~65% (100 μM). SYD-1 (100 μM) was also able to increase the production of superoxide anion (~50%). In the absence of LPS, SYD-1 decreased NO production dose-dependently by up to ~80% (100 μM). When SYD-1 and LPS were incubated concomitantly, the decrease of NO promoted by SYD was the most pronounced, reaching up to ~98% at the same concentration (50 μM). SYD-1 dose-dependently suppressed IL-6 secretion by LPS-stimulated macrophages, reaching up to ~90% of inhibition at the highest concentration (100 μM). These results indicate that SYD-1 promotes effects similar to those described for anti-inflammatory and immunosuppressive drugs, thus motivating further studies to clarify the mechanisms involved in this activity.

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