Use of the gas exchange threshold to noninvasively determine the lactate threshold in patients with cystic fibrosis.

OBJECTIVE: The anaerobic threshold (AT) is a submaximal index related to endurance exercise performance, which is usually determined by the measurement of blood lactate concentration during an incremental exercise test (lactate threshold [LT]). The LT, and thus the AT, can also be detected noninvasively in normal subjects by means of the gas exchange threshold (GET). This study was undertaken to validate the use of GET in patients with cystic fibrosis (CF) with a wide range of disease severity, and to assess the reproducibility of this index. METHODS: In patients with CF (FEV(1) range, 23 to 118% of predicted) and control subjects, gas exchange was measured breath by breath during the incremental exercise tests to allow determination of the GET. Arterialized-venous blood was sampled for determination of the LT. The GET and LT were determined in a blinded manner. RESULTS: The mean differences (GET - LT) for control subjects (n = 18) and patients with CF (n = 23) were - 40 mL/min and + 10 mL/min, respectively, neither being significantly different from zero. The limits of agreement were +/- 550 mL/min and +/- 410 mL/min, respectively. The mean test-retest differences in GET for control subjects (n = 14) and patients with CF (n = 12) were - 50 mL/min and 0 mL/min, respectively, neither being significantly different from zero; the respective limits of reproducibility were +/- 450 mL/min and +/- 350 mL/min. CONCLUSIONS: This study demonstrates that in patients with CF, the GET can be used to obtain an unbiased estimate of the LT, and that the GET is reproducible.

Bronchial dentures as a cause of airway actinomycosis.

A 65-year-old man was referred to the respiratory clinic with recurrent chest infections on a background of stage 3 chronic obstructive pulmonary disease. On examination, there was wheeze bilaterally more marked on the left lower lobe. Subsequent imaging revealed an obstruction of the left main bronchus that was concerning for malignancy. Initially, on flexible bronchoscopy, a hard mass was found and multiple biopsies were positive for actinomycosis. Subsequent rigid bronchoscopy was undertaken and a set of dentures were removed from the airway.

The effects of hypoxia on markers of coagulation and systemic inflammation in patients with COPD.

BACKGROUND: It has been demonstrated that there is an increased risk of venous thromboembolism (VTE) during air travel on flights of long duration. Patients with COPD are also at increased risk of VTE, particularly during exacerbations, possibly because of a hypercoagulable state secondary to hypoxia and/or heightened systemic inflammation. We investigated the effects of hypoxia on indices of coagulation and systemic inflammation in patients with COPD. METHODS: Twenty clinically stable patients with mild COPD were recruited. Patients were randomized to receive either medical air or 100% nitrogen through a 40% venturi mask at a flow rate of 10 L/min for 2 h. Blood was sampled for thrombin-antithrombin complex (TAT), prothrombin activation fragments 1 + 2 (F(1 + 2)), von Willebrand factor antigen (VWF:Ag), D-dimer, and interleukin-6 (IL-6) at baseline and after 2 h. RESULTS: Patients in the hypoxia and control groups were similar in terms of age, sex, pack-years smoked, and severity of airflow obstruction. There was no difference in baseline TAT, F(1 + 2), VWF:Ag, D-dimer, or IL-6 levels between groups. In the control group, there was no change in markers of coagulation or systemic inflammation over the 2-h study. In patients who underwent hypoxic challenge, there was an increase in TAT (P < .001), F(1 + 2) (P < .01), and IL-6 (P < .01), whereas D-dimer and VWF:Ag levels were unchanged. CONCLUSIONS: This study demonstrates that a 2-h hypoxic challenge in patients with COPD results in coagulation activation in conjunction with an increase in systemic inflammation.