A prospective evaluation of survivorship of asymptomatic degenerative rotator cuff tears

BACKGROUND: The purpose of this prospective study was to report the long-term risks of rotator cuff tear enlargement and symptom progression associated with degenerative asymptomatic tears. METHODS: Subjects with an asymptomatic rotator cuff tear in one shoulder and pain due to rotator cuff disease in the contralateral shoulder enrolled as part of a prospective longitudinal study. Two hundred and twenty-four subjects (118 initial full-thickness tears, fifty-six initial partial-thickness tears, and fifty controls) were followed for a median of 5.1 years. Validated functional shoulder scores were calculated (visual analog pain scale, American Shoulder and Elbow Surgeons [ASES], and simple shoulder test [SST] scores). Subjects were followed annually with shoulder ultrasonography and clinical evaluations. RESULTS: Tear enlargement was seen in 49% of the shoulders, and the median time to enlargement was 2.8 years. The occurrence of tear-enlargement events was influenced by the severity of the final tear type, with enlargement of 61% of the full-thickness tears, 44% of the partial-thickness tears, and 14% of the controls (p < 0.05). Subject age and sex were not related to tear enlargement. One hundred subjects (46%) developed new pain. The final tear type was associated with a greater risk of pain development, with the new pain developing in 28% of the controls, 46% of the shoulders with a partial-thickness tear, and 50% of those with a full-thickness tear (p < 0.05). The presence of tear enlargement was associated with the onset of new pain (p < 0.05). Progressive degenerative changes of the supraspinatus muscle were associated with tear enlargement, with supraspinatus muscle degeneration increasing in 4% of the shoulders with a stable tear compared with 30% of the shoulders with tear enlargement (p < 0.05). Nine percent of the shoulders with a stable tear showed increased infraspinatus muscle degeneration compared with 28% of those in which the tear had enlarged (p = 0.07). CONCLUSIONS: This study demonstrates the progressive nature of degenerative rotator cuff disease. The risk of tear enlargement and progression of muscle degeneration is greater for shoulders with a full-thickness tear, and tear enlargement is associated with a greater risk of pain development across all tear types. LEVEL OF EVIDENCE: Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence

Diagnostic performance and reliability of ultrasonography for fatty degeneration of the rotator cuff muscles

BACKGROUND: Diagnostic evaluation of rotator cuff muscle quality is important to determine indications for potential operative repair. Ultrasonography has developed into an accepted and useful tool for evaluating rotator cuff tendon tears; however, its use for evaluating rotator muscle quality has not been well established. The purpose of this study was to investigate the diagnostic performance and observer reliability of ultrasonography in grading fatty degeneration of the posterior and superior rotator cuff muscles. METHODS: The supraspinatus, infraspinatus, and teres minor muscles were prospectively evaluated with magnetic resonance imaging (MRI) and ultrasonography in eighty patients with shoulder pain. The degree of fatty degeneration on MRI was graded by four independent raters on the basis of the modified Goutallier grading system. Ultrasonographic evaluation of fatty degeneration was performed by one of three radiologists with use of a three-point scale. The two scoring systems were compared to determine the diagnostic performance of ultrasonography. The interobserver and intraobserver reliability of MRI grading by the four raters were determined. The interobserver reliability of ultrasonography among the three radiologists was determined in a separate group of thirty study subjects. The weighted Cohen kappa, percentage agreement, sensitivity, and specificity were calculated. RESULTS: The accuracy of ultrasonography for the detection of fatty degeneration, as assessed on the basis of the percentage agreement with MRI, was 92.5% for the supraspinatus and infraspinatus muscles and 87.5% for the teres minor. The sensitivity was 84.6% for the supraspinatus, 95.6% for the infraspinatus, and 87.5% for the teres minor. The specificity was 96.3% for the supraspinatus, 91.2% for the infraspinatus, and 87.5% for the teres minor. The agreement between MRI and ultrasonography was substantial for the supraspinatus and infraspinatus (kappa = 0.78 and 0.71, respectively) and moderate for the teres minor (kappa = 0.47). The interobserver reliability for MRI was substantial for the supraspinatus and infraspinatus (kappa = 0.76 and 0.77, respectively) and moderate for the teres minor (kappa = 0.59). For ultrasonography, the interobserver reliability was substantial for all three muscles (kappa = 0.71 for the supraspinatus, 0.65 for the infraspinatus, and 0.72 for the teres minor). CONCLUSIONS: The diagnostic performance of ultrasonography in identifying and grading fatty degeneration of the rotator cuff muscles was comparable with that of MRI. Ultrasonography can be used as the primary diagnostic imaging modality for fatty changes in rotator cuff muscles. LEVEL OF EVIDENCE: Diagnostic Level II. See Instructions for Authors for a complete description of levels of evidence

Development and analytical performance evaluation of an automated chemiluminescent immunoassay for pro-gastrin releasing peptide (ProGRP)

Background: Pro-gastrin releasing peptide ( ProGRP) concentrations in blood play an important role in the diagnosis and treatment of patients with small cell lung cancer (SCLC). The automated quantitative ARCHITECT (R) ProGRP assay was developed to aid in the differential diagnosis and in the management of SCLC. The purpose of this study was to evaluate the analytical performance of this chemiluminescent microparticle immunoassay at multiple sites. Methods: ARCHITECT ProGRP measures ProGRP using a two-step sandwich using monoclonal anti-ProGRP antibodies coated on paramagnetic microparticles and labeled with acridinium. Analytical performance of the assay was evaluated at four sites: Abbott Japan, Denka Seiken, the Johns Hopkins University, and the University of Munich. Results: Total precision (%CV) for nine analyte concentrations was between 2.2 and 5.7. The analytical sensitivity of the assay was between 0.20 pg/mL and 0.88 pg/mL. The functional sensitivity at 20% CV was between 0.66 pg/mL and 1.73 pg/mL. The assay was linear up to 50,000 pg/mL using a 1:10 autodilution protocol. The calibration curve was stable for 30 days. Comparison with the Fujirebio microtiter plate enzyme-linked immunosorbent assay (EIA) ProGRP assay gave a slope of 0.93 and a correlation coefficient (r) of 0.99. Conclusions: These results demonstrate that the ARCHITECT ProGRP assay has excellent sensitivity, precision, and correlation to a reference method. This assay provides a convenient automated method for ProGRP measurement in serum and plasma in hospitals and clinical laboratories. Clin Chem Lab Med 2009;47:1557-63

Interferonβ-1b Induces the Expression of RGS1 a Negative Regulator of G-Protein Signaling

We present evidence of a link between interferonβ-1b (IFN-β) and G-protein signaling by demonstrating that IFN-β can induce the expression of the negative regulator of G-protein signaling 1 (RGS1). RGS1 reduces G-protein activation and immune cell migration by interacting with heterotrimeric G-proteins and enhancing their intrinsic GTPase activity. In this study, IFN-β treatment resulted in the induction of RGS1 in peripheral blood mononuclear cells (PBMCs), monocytes, T cells, and B cells. Induction of RGS1 by IFN-β was concentration dependent and observed at both the RNA and protein level. Other members of the RGS family were not induced by IFN-β, and induction of RGS1 required the activation of the IFN receptor. In addition, RGS1 induction was observed in PBMCs obtained from IFN-β-treated multiple sclerosis patients suggesting a possible, as yet unexplored, involvement of G-protein regulation in disease treatment. The upregulation of RGS1 by IFN-β has not been previously reported