Differentiating optic disc edema from optic nerve head drusen on optical coherence tomography.

OBJECTIVE: To assess optical coherence tomography in differentiating optic disc edema (ODE) due to papilledema and other optic neuropathies from optic nerve head drusen (ONHD). METHODS: Optical coherence tomographic images from 60 subjects (20 with ODE, 20 with ONHD, and 20 control subjects) were assessed qualitatively and quantitatively. Qualitative criteria for ODE included an elevated optic nerve head with smooth internal contour and subretinal hyporeflective space (SHYPS) with recumbent "lazy V" pattern. Optic nerve head drusen displayed a "lumpy-bumpy" internal optic nerve contour and a rapid decline in SHYPS thickness. Quantitative comparisons included retinal nerve fiber layer and SHYPS thickness. RESULTS: Optical coherence tomography differentiated ODE from ONHD qualitatively (sensitivity, 63%; specificity, 63%) and quantitatively (sensitivity, 80%; specificity, 90%). Respective differences in mean retinal nerve fiber layer thickness between ODE and ONHD were significant (P < .002) superiorly (206.8 vs 121.7 microm), nasally (176.3 vs 78.6 microm), inferiorly (247.2 vs 153.8 microm), and temporally (180.0 vs 85.5 microm). Respective differences in mean SHYPS thickness between ODE and ONHD were significant (P < .001) at radii of 0.75 mm (512.1 vs 274.4 microm), 1.5 mm (291.4 vs 103.0 microm), and 2.0 mm (145.5 vs 60.7 microm). CONCLUSION: Optical coherence tomography can differentiate ODE from ONHD, particularly when the nasal retinal nerve fiber layer and SHYPS thickness at the 2.0-mm radius are greater than 86 microm and 127 microm, respectively.

Neutrophil elastase increases MUC4 expression in normal human bronchial epithelial cells.

In chronic obstructive pulmonary diseases, the airway epithelium is chronically exposed to neutrophil elastase, an inflammatory protease. The cellular response to neutrophil elastase dictates the balance between epithelial injury and repair. Key regulators of epithelial migration and proliferation are the ErbB receptor tyrosine kinases, including the epidermal growth factor receptor. In this context, we investigated whether neutrophil elastase may regulate expression of MUC4, a membrane-tethered mucin that has recently been identified as a ligand for ErbB2, the major heterodimerization partner of the epidermal growth factor receptor. In normal human bronchial epithelial cells, neutrophil elastase increased MUC4 mRNA levels in both a concentration- and time-dependent manner. RNA stability assays revealed that neutrophil elastase increased MUC4 mRNA levels by prolonging the mRNA half-life from 5 to 21 h. Neutrophil elastase also increased MUC4 glycoprotein levels as determined by Western analysis, using a monoclonal antibody specific for a nontandem repeat MUC4 sequence. Therefore, airway epithelial cells respond to neutrophil elastase exposure by increasing expression of MUC4, a potential activator of epithelial repair mechanisms.