Sleep alters respiratory mechanics and gas exchange, which can adversely affect arterial oxygenation. Whether sleep affects oxygenation in hepatopulmonary syndrome is unknown. The aim of this study was to assess oxygen desaturation during sleep in hepatopulmonary syndrome. Twenty adults with cirrhosis including 10 controls and 10 patients with hepatopulmonary syndrome underwent home pulse-oximetry during sleep. Subjects at high risk for obstructive sleep apnea were excluded through the Berlin questionnaire. Subjects who spent more than 10% of total sleep time with arterial oxygen saturation < 90% were classified as sleep-time oxygen desaturators. Sleep-time desaturation was correlated with clinical variables. The results showed that 7 of 10 hepatopulmonary syndrome subjects and none of the 10 controls had sleep-time oxygen desaturation. The median percentage of total sleep time with arterial oxygen saturation < 90% was significantly higher in hepatopulmonary syndrome subjects than in controls (medians 25% versus 0%, P ؍ 0.005). Hepatopulmonary syndrome subjects had significantly lower wake-time arterial oxygen saturation level (median, 97% versus 95%; P ؍ 0.003) and mean sleep-time arterial oxygen saturation level (median, 96% versus 91%; P ؍ 0.0008) than did the controls. Sleep-time desaturation directly correlated with alveolar-arterial oxygen gradient (P ؍ 0.0007) and inversely correlated with wake-time arterial oxygen tension (P ؍ 0.0007) and oxygen saturation (P < 0.0001). Conclusion: Oxygen desaturation occurred during sleep in 70% of hepatopulmonary syndrome subjects, the degree of which correlated with the severity of hepatopulmonary syndrome. Marked hypoxemia during sleep may occur in hepatopulmonary syndrome patients who, according to wake-time oxygen values, have only mild to moderate hypoxemia.
Nitric oxide has been implicated in the pathogenic mechanism of inflammatory bowel disease states. We evaluated indomethacin-induced enteropathy in rats, in relation to the expression of the inducible isoform of NO synthase (iNOS) using aminosalicylic acid (5-ASA), its isomer 4-ASA (10 or 50 mg/kg/day, po), and dexamethasone, an iNOS transcription inhibitor (3 mg/kg/day, sc). Enteropathy was induced by indomethacin (7.5 mg/kg/day, sc) for two days and the small intestine was examined for lesions over the next 14 days. Indomethacin-induced small-intestinal ulcer size, mucosal myeloperoxidase activity, iNOS expression and serum nitrite/nitrate levels were maximally increased by day 4 and gradually decreased by day 14. Treatment with 5-ASA, but not 4-ASA, decreased indomethacin-induced ulcer length, myeloperoxidase activity, serum nitrite/nitrate levels and iNOS expression at day 4. Dexamethasone had a greater effect than 5-ASA in reducing myeloperoxidase activity and ulcer length by 26 and 32%, respectively. Dexamethasone also reduced serum nitrate/nitrite and iNOS expression to their basal levels. In conclusion, inhibition of iNOS expression by 5-ASA appears to be associated with diminished intestinal ulceration in indomethacin-induced enteropathy.
There was good intraobserver agreement in the interpretation of EUS features of CP. The intraobserver agreement seems better than the published interobserver agreement for EUS features of CP and better than the published intraobserver agreement for endoscopic retrograde cholangiopancreatography imaging for CP.
Background: We developed a Markov model to simulate outcomes in different subgroups of patients with stage I NSCLC to help define the role of SBRT in this disease. Methods: We modeled the 5 year clinical history of (i) operable stage I NSCLC patients treated with either SBRT or lobectomy, and (ii) patients aged ≥75 years with COPD who undergo SBRT or best supportive care (BSC). Parameters for recurrence rates and Markov state utilities for appropriate AJCC stages of NSCLC were extracted from the literature and adapted to monthly time intervals. For operable patients, age-and sex-specific rates of death from all other causes were extracted from standard life tables and varied according to smoking habit. Surgical outcomes from the model were compared to Adjuvant! Online (AO). Elderly COPD patients were stratified into 4 classes according to T stage and COPD GOLD score. We report various treatment strategy overall and quality adjusted survival stratified by age, sex, smoking history, COPD, and T-stage. Sensitivity analyses on Markov utilities, treatment-related death, and the proportion of patients with recurrent disease treated radically were performed to determine thresholds for treatment modality preference. Results: For surgical patients, the 5-year overall survival, cancer specific survival, and other causes of death as predicted by our model correlated closely with AO, ranging from 0.0% to 3.8%. Differences between surgery and SBRT ranged from 2.2% to 3.0% in 5-year overall survival and 0.07 to 0.09 in quality adjusted life years, both in favor of surgery. The SBRT utility threshold for preferring SBRT over surgery was 0.90. Outcomes were sensitive to the SBRT utility, the proportion of recurrences treated radically, and the surgical and SBRT treatment related mortalities. For high risk patients, our model predicted for a benefit in 5-year overall survival of 4.0% to 38.2% and 8.8 to 17.4 quality-adjusted life months in favor of SBRT over BSC for the 4 classes. Outcomes were not sensitive to the SBRT utility or disease progression. Conclusions: Withholding SBRT based on age and/or COPD severity may be unjustified. SBRT may offer comparable overall survival and quality adjusted life expectancy compared to surgical resection in operable cases.
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