Rotator cuff tear: clinical experience with sonographic detection.

Between June 1986 and April 1988, 86 sonographic examinations of the shoulder were performed on patients suspected of having rotator cuff tears. Major sonographic diagnostic criteria included (a) a well-defined discontinuity usually visible as a hypoechoic focus within the cuff, (b) nonvisualization of the cuff and (c) an echogenic focus within the cuff. Seventy-five patients underwent both sonography and arthrography. Compared with arthrography alone, ultrasound examinations enabled detection of 92% of rotator cuff tears (24 of 26 tears), with a specificity of 84% and a negative predictive value of 95%. Correlation was obtained in 30 of these patients who underwent surgery for rotator cuff tear or other soft-tissue abnormality. In this group, the sensitivity of sonography for detection of a tear was 93%, with a specificity of 73%, while for arthrography sensitivity was 87% and specificity was 100%. These data indicate that sonography is a useful, noninvasive screening procedure for patients suspected of having rotator cuff injury.

A feasibility study to determine if microbicidal activity can be measured in dexamethasone-treated macrophage cultures.

Dexamethasone action severely limits the ingestion of Saccharomyces cerevisiae in cultures of murine peritoneal macrophages. In spite of this inhibitory response, numbers of viable yeasts sufficient for microbicidal studies can be recovered shortly after their limited ingestion from lysed steroid-treated phagocytes.

Modulatory effects of heat-labile serum components on the inhibition of phagocytosis by dexamethasone in peritoneal macrophage cultures.

This investigation examined the effects of heat-labile serum substances on the suppression of yeast phagocytosis in dexamethasone-treated cultures of murine resident peritoneal macrophages. When 4-6 day old untreated control cultures were supplemented with either heat-inactivated (56 degrees C, 30 min) or intact (non-heat-inactivated) fetal bovine serum, more than 90% of the macrophage population ingested at least 1 yeast particle during 15 min phagocytosis assays. In cultures treated with 10(-6) M dexamethasone, approximately 30% of the macrophages were phagocytic. In contrast, approximately 70% of the steroid-treated population consisted of phagocytes in cultures supplemented with intact serum. Medium shift experiments demonstrated that the type of serum present during the 15 min yeast phagocytosis assays, but not the 4-6 day incubation periods, determined the size of the phagocytic subpopulations in the treated cultures. Whereas the majority of control phagocytes ingested more than 8 yeast particles, most dexamethasone-treated phagocytes ingested far fewer than 8 particles regardless of the size of the phagocytic subpopulations. In contrast to yeast, the ingestion of latex particles was inhibited to the same extent in dexamethasone-treated cultures that contained either heat-inactivated or intact serum. Thus, dexamethasone action impairs the ability of macrophages to accumulate yeast particles even though the phagocytic subpopulation is larger in treated cultures containing intact serum. This larger subpopulation may result from the activation of the alternative complement pathway by yeast during phagocytosis.

Inhibition of yeast phagocytosis by dexamethasone in macrophage cultures: reversibility of the effect and enhanced suppression in cultures of stimulated macrophages.

This investigation was initiated to characterize further the ability of 1 microM dexamethasone to suppress the ingestion of heat-killed Saccharomyces cerevisiae particles in cultures of murine resident peritoneal macrophages. Time course studies revealed that the inhibitory response required the continual presence of the steroid in the culture medium. In addition, increased inhibitory responses occurred after dexamethasone was supplied to previously untreated cultures of resident macrophages that became stimulated by differentiating in vitro. These findings indicate that glucocorticoids act directly on macrophages to decrease their phagocytic capacity, which in vivo would reduce host resistance.