LBA-1 Introduction: Patients with pulmonary embolism (PE) are initially treated in the hospital with low molecular weight heparin (LMWH). The most recent guideline of the American College of Chest Physicians on Antithrombotic therapy 2008 reports some small studies on outpatient treatment in patients with pulmonary embolism, which suggest outpatient treatment in selected patients with PE is potentially effective and safe but firm recommendations for clinical practice are lacking. Clinicians urgently need reliable, easy-to-use selection criteria for selection of patients with pulmonary embolism eligible for outpatient treatment. Objective: To evaluate the efficacy and safety of outpatient treatment according to predefined criteria (Hestia criteria) in patients with acute PE. Patients and Methods: Open-label, single-arm, multicenter clinical trial of patients with objectively proven acute pulmonary embolism, conducted in twelve hospitals in the Netherlands from 2008 to 2010. Follow-up was completed in September 2010. Patients with acute PE were triaged with the predefined Hestia criteria for eligibility for outpatient treatment starting with therapeutic weight adjusted doses of LMWH (Nadroparin), followed by vitamin K antagonists. All patients eligible for outpatient treatment according to the Hestia criteria, were sent home either immediately or within 24 hours after PE was objectively diagnosed. Outcome: Outpatient treatment was evaluated with respect to recurrent venous thromboembolism (VTE), including PE or deep venous thrombosis (DVT), major haemorrhage and total mortality during initial LMWH treatment and 3 months follow up. We considered outpatient treatment to be effective if the upper limit of the 95% confidence interval of the incidence of recurrent VTE would not exceed 7%. Results: Of 297 included patients, who all completed follow-up, 6 patients (2.0%; 95% confidence interval [CI], 0.8–4.3) had recurrent VTE (5 PE (1.7%), 1 DVT (0.3 %)). Three patients (1.0%, 95% CI 0.2–2.9) died during three months follow-up, but none as a result of fatal PE. One patient died of fatal intracerebral haemorrhage, the other two patients died of progressive malignancy. In addition to the patient with intracranial bleeding, one other patient had a major bleeding event (0.7 %, 95% CI 0.08%-2.4%). Conclusion: Outpatient anticoagulant treatment is effective and safe for patients with pulmonary embolism who have been selected with the Hestia criteria. (Dutch Trial Register NTR1319). Disclosures: Huisman: GSK: Research Funding; Actelion: Research Funding; Bayer: Speakers Bureau; Boehringer Ingelheim: Speakers Bureau; Pfizer: Speakers Bureau.

OBJECTIVESleep restriction results in decreased insulin sensitivity and glucose tolerance in healthy subjects. We hypothesized that sleep duration is also a determinant of insulin sensitivity in patients with type 1 diabetes.RESEARCH DESIGN AND METHODSWe studied seven patients (three men, four women) with type 1 diabetes: mean age 44 ± 7 years, BMI 23.5 ± 0.9 kg/m2, and A1C 7.6 ± 0.3%. They were studied once after a night of normal sleep duration and once after a night of only 4 h of sleep. Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies with an infusion of [6,6-2H2]glucose.RESULTSSleep duration was shorter in the night with sleep restriction than in the unrestricted night (469 ± 8.5 vs. 222 ± 7.1 min, P = 0.02). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids (NEFAs), or endogenous glucose production. Endogenous glucose production during the hyperinsulinemic clamp was not altered during the night of sleep restriction compared with the night of unrestricted sleep (6.2 ± 0.8 vs. 6.9 ± 0.6 μmol · kg lean body mass−1 · min−1, NS). In contrast, sleep restriction decreased the glucose disposal rate during the clamp (25.5 ± 2.6 vs. 22.0 ± 2.1 μmol · kg lean body mass−1 · min−1, P = 0.04), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by ∼21% (P = 0.04). Sleep restriction did not alter plasma NEFA levels during the clamp (143 ± 29 vs. 133 ± 29 μmol/l, NS).CONCLUSIONSPartial sleep deprivation during a single night induces peripheral insulin resistance in these seven patients with type 1 diabetes. Therefore, sleep duration is a determinant of insulin sensitivity in patients with type 1 diabetes.

Background -Obstruction of a major airway by tumour causes serious morbidity.

OBJECTIVE -Sleep restriction results in decreased insulin sensitivity and glucose tolerance in healthy subjects. We hypothesized that sleep duration is also a determinant of insulin sensitivity in patients with type 1 diabetes.RESEARCH DESIGN AND METHODS -We studied seven patients (three men, four women) with type 1 diabetes: mean age 44 Ϯ 7 years, BMI 23.5 Ϯ 0.9 kg/m 2 , and A1C 7.6 Ϯ 0.3%. They were studied once after a night of normal sleep duration and once after a night of only 4 h of sleep. Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies with an infusion of [6,6-2 H 2 ]glucose.RESULTS -Sleep duration was shorter in the night with sleep restriction than in the unrestricted night (469 Ϯ 8.5 vs. 222 Ϯ 7.1 min, P ϭ 0.02). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids (NEFAs), or endogenous glucose production. Endogenous glucose production during the hyperinsulinemic clamp was not altered during the night of sleep restriction compared with the night of unrestricted sleep (6.2 Ϯ 0.8 vs. 6.9 Ϯ 0.6 mol ⅐ kg lean body mass Ϫ1 ⅐ min Ϫ1 , NS). In contrast, sleep restriction decreased the glucose disposal rate during the clamp (25.5 Ϯ 2.6 vs. 22.0 Ϯ 2.1 mol ⅐ kg lean body mass Ϫ1 ⅐ min Ϫ1 , P ϭ 0.04), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by ϳ21% (P ϭ 0.04). Sleep restriction did not alter plasma NEFA levels during the clamp (143 Ϯ 29 vs. 133 Ϯ 29 mol/l, NS).CONCLUSIONS -Partial sleep deprivation during a single night induces peripheral insulin resistance in these seven patients with type 1 diabetes. Therefore, sleep duration is a determinant of insulin sensitivity in patients with type 1 diabetes.

EBUS-TBNA offers an effective accurate, minimally invasive strategy for evaluating FDG avid hilar and mediastinal lymph nodes. However, negative findings should be confirmed by surgical staging.