A clinicoradiological presentation of thoracic sarcoidosis requires histopathology in order to establish the diagnosis. Flexible bronchoscopy has a reasonable diagnostic yield and is the procedure of first choice for diagnosis. Endoscopic ultrasound (endoscopic ultrasoundguided fine needle aspiration/endobronchial ultrasound-guided transbronchial needle aspiration) can help in the diagnosis of sarcoidosis.An implementation strategy of endoscopic ultrasound for the diagnosis of sarcoidosis following negative flexible bronchoscopy results was examined prospectively in 15 clinics.A total of 137 patients (92 males; median age 43 yrs) were included, and sarcoidosis was found in 115 (84%). Alternative diagnoses were tuberculosis, lymphangitis carcinomatosa, pneumoconiosis and alveolitis. All patients were sent for flexible bronchoscopy, which was performed in 121 (88%), resulting in a definite diagnosis in 57 (42%). A total of 80 patients were sent for endoscopic ultrasound, which could be performed in 72 (90%), yielding a definite diagnosis in 47 (59%). Endoscopic ultrasound following negative flexible bronchoscopy avoided a surgical procedure in 47 out of 80 patients. The sensitivity of flexible bronchoscopy for sarcoidosis was 45% (95% confidence interval 35-54%), but 62% (50-72%) if biopsy specimens were taken. The sensitivity of endoscopic ultrasound following negative flexible bronchoscopy results was 71% (58-82%). With this strategy, 97 out of 115 (84% (76-90%)) of proven sarcoidosis was diagnosed using endoscopy.This large prospective implementation study (trial number NCT00888212; ClinicalTrials.gov) shows that endoscopic ultrasound is valuable for diagnosing sarcoidosis after negative flexible bronchoscopy results.
Background: The best method for titration of continuous positive airway pressure (CPAP) therapy in obstructive sleep apnea (OSA) syndrome has not yet been established. The 90th or 95th percentiles of the pressure titrated over time by automatic CPAP (A-CPAP) have been recommended as reference for prescribing therapeutic fixed CPAP (F-CPAP). We compared A-CPAP to F-CPAP, which was determined by a common prediction formula. Methods: Forty-five patients who were habituated to F-CPAP underwent titration polysomnography. In a double-blind, randomized order, each patient used an A-CPAP device in the autotitration and in the fixed pressure mode during one half of the night. Apnea-hypopnea index (AHI) and pressure profiles were primary outcomes. Bias and precision were additionally assessed for both CPAP modes. Results: No significant differences in various sleep parameters or in subjective sleep quality evaluation were found. The AHI was effectively lowered in both CPAP modes (A-CPAP 7.7 [10.8] events/h versus F-CPAP 5.4 [9.0] events/h, p = 0.061). Comparison of group means showed that F-CPAP closely paralleled mean (Pmean) and median (P50), but not the 95th percentile (P95) pressure, of A-CPAP. While bias was lowest for Pmean and P50, there was a lack of precision in all A-CPAP pressure categories. Conclusions: We confirm that F-CPAP set by prediction formula is not worse in terms of AHI control than A-CPAP. On average, F-CPAP parallels Pmean and P50 but not P95. However, due to imprecise matching, individual F-CPAP values cannot be derived from Pmean or P50.
After completing this course, the reader will be able to:1. Employ the current standard of care for stage III NSCLC.2. Balance the relative merits and risks of IMRT in this disease and position its indication.3. Advocate the need for further research for improvement in this field.This article is available for continuing medical education credit at CME.TheOncologist.com.
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LOCALLY ADVANCED NON-SMALL CELL LUNG CANCER: PRESENT STATUS OF TREATMENT AND OUTCOMEMore than 80% of the 213,000 incidental cases of lung cancer in the U.S. are of the non-small cell variant-non-small cell lung cancer (NSCLC)-and approximately 37% of these present at diagnosis with locoregional involvement [1]. The latter means that the tumor has spread out of the confines of the lung into the surrounding structures without clinical evidence of dissemination. This extension varies from tumors locally abutting the chest wall, diaphragm, or mediastinum (T3) to frank invasion of the mediastinal tis-
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