Data sources for measuring colorectal endoscopy use among Medicare enrollees.

BACKGROUND: Estimates of colorectal cancer test use vary widely by data source. Medicare claims offer one source for monitoring test use, but their utility has not been validated. We compared ascertainment of sigmoidoscopy and colonoscopy between three data sources: self reports, Medicare claims, and medical records. MATERIALS AND METHODS: The study population included Medicare enrollees residing in North Carolina (n = 561) who had participated in a telephone survey on colorectal cancer tests. Medicare claims were obtained for the 5 years preceding the survey (January 1, 1998 to December 31, 2002). Information about sigmoidoscopy and colonoscopy procedures conducted in physician offices were abstracted from medical records. Sensitivity, specificity, positive predictive value, negative predictive value, agreement, and kappa statistics were calculated using the medical record as the gold standard. Agreement on specific procedure type and purpose was also assessed. RESULTS: Agreement between claim and medical record regarding whether an endoscopic procedure had been done was high (over 90%). Agreement between self report and medical record and between self report and claim was good (79% and 74%, respectively). All three data sources adequately distinguished the type of procedure done. None of the data sources showed reliable levels of agreement regarding procedure purpose (screening or diagnostic). CONCLUSION: Medicare claims can provide accurate information on whether a patient has undergone colorectal endoscopy and may be more complete than physician medical records. Medicare claims cannot be used to distinguish screening from diagnostic tests. Recognizing this limitation, researchers who use Medicare claims to assess rates of colorectal testing should include both screening and diagnostic endoscopy procedures in their analyses.     

Mitigation of hearing loss from semi-circular canal transection in pseudomonas otitis media with ciprofloxacin-dexamethasone irrigation.

HYPOTHESIS: Irrigation of the mastoid with a quinolone antibiotic-steroid solution may mitigate hearing loss caused by iatrogenic semicircular canal injury in the presence of Pseudomonas aeruginosa (PA) otitis media (OM). BACKGROUND: Studies have shown the cochlea to be more vulnerable to semicircular canal transection (SCT)-related hearing loss in the presence of PA OM. Prophylactic systemic antibiotics and steroids may decrease this hearing loss, but SCT is usually not planned. The aim of this study was to determine if irrigation with ciprofloxacin-dexamethasone (cipro-dex) could improve hearing outcomes following SCT in PA OM. METHODS: PA OM was induced in 28 animals. After three to five days, unilateral SCT was performed in each animal, with sham SCT on the contralateral ear. At surgery, half of the animals (n = 14) underwent irrigation of the both mastoid bullae with cipro-dex; the second group of animals (n = 14) underwent irrigation of the bullae with sterile saline. Auditory thresholds were obtained immediately prior to SCT and 7-10 days after SCT. RESULTS: SCT ears treated with cipro-dex showed a mean click threshold improvement of 4.6 dB from pre-transection to 7-10 days post-transection, whereas thresholds in the SCT ears treated with saline worsened by 7.5 dB (p = 0.15). CONCLUSION: Irrigation of the guinea pig bulla with cipro-dex following SCT in the setting of PA OM appears safe and may yield beneficial effects on hearing.     

Selective unresponsiveness of pancreatic beta-cells to acute sulfonylurea stimulation during sulfonylurea therapy in NIDDM

Patients with non-insulin-dependent diabetes mellitus (NIDDM) who have chronic hyperglycemia lose acute incremental insulin responses to glucose but are able to briskly respond to other beta-cell secretagogues. To investigate whether this is a defect specific for glucose or represents a more general phenomenon, we measured the insulin responses to acute intravenous tolbutamide in 10 obese patients with NIDDM both before and during sulfonylurea therapy with tolazamide. Comparable glycemia was achieved with oral dextrose 2 h before intravenous testing. To assess beta-cell responsiveness to a nonsulfonylurea secretagogue, 1 mg glucagon was administered intravenously during tolazamide therapy. In seven patients, the mean peak insulin increment 5 or 10 min after intravenous tolbutamide was 54 +/- 11 microU/ml when not receiving tolazamide (0.14 +/- 1.3 microU/ml) with tolazamide (P less than .001), even though serum insulin responded rapidly to intravenous glucagon. In four patients tested for reversibility of their refractoriness to intravenous tolbutamide during chronic tolazamide therapy, the mean peak insulin increment 1 wk after discontinuing tolazamide was 79 +/- 22 microU/ml. A relatively rapid development of refractoriness was documented in four patients who were tested only 12 h after beginning tolazamide therapy; the mean peak insulin increments 5-10 min after intravenous tolbutamide were undetectable (-0.5 microU/ml), yet responses to intravenous glucagon were evident. In these NIDDM patients, exposure of pancreatic beta-cells to sustained levels of sulfonylureas induces a reversible state of refractoriness to acute stimulation with sufonylureas but not to another secretagogue.(ABSTRACT TRUNCATED AT 250 WORDS)