The decision-making process for the intensity of care delivered to patients with lung cancer and organ failure is poorly understood, and does not always involve intensivists. Our objective was to describe the potential suitability for intensive care unit (ICU) referral of lung cancer in-patients with organ failures.

We prospectively included consecutive lung cancer patients with failure of at least one organ admitted to the teaching hospital in Grenoble, France, between December 2010 and October 2012.

Of 140 patients, 121 (86%) were evaluated by an oncologist and 49 (35%) were referred for ICU admission, with subsequent admission for 36 (73%) out of those 49. Factors independently associated with ICU referral were performance status <=2 (OR 10.07, 95% CI 3.85–26.32), nonprogressive malignancy (OR 7.00, 95% CI 2.24–21.80), and no explicit refusal of ICU admission by the patient and/or family (OR 7.95, 95% CI 2.39–26.37). Factors independently associated with ICU admission were the initial ward being other than the lung cancer unit (OR 6.02, 95% CI 1.11–32.80) and an available medical ICU bed (OR 8.19, 95% CI 1.48–45.35).

Only one-third of lung cancer patients with organ failures were referred for ICU admission. The decision not to consider ICU admission was often taken by a non-intensivist, with advice from an oncologist rather than an intensivist.

Treatment of persons with latent tuberculosis (TB) infection at greatest risk of reactivation is an important component of TB control and elimination strategies. Biomarkers evaluating the effectiveness of treatment of latent TB infection have not yet been identified. This information would enhance control efforts and assist the evaluation of new treatment regimes.

We designed a two-group, two-arm, randomised clinical study of tuberculin skin test-positive participants: 26 with documented contact with TB patients and 34 with non-documented contact. Participants in each group were randomly assigned to the immediate- or deferred-isoniazid treatment arms. Assays of in vitro interferon (IFN)- secretion in response to recombinant Rv1737 and overlapping synthetic peptide pools from various groups of immunodominant proteins were performed.

During isoniazid therapy, a significant increase from baseline in the proportion of IFN- responders to the 10-kDa culture filtrate protein, Rv2031, Rv0849, Rv1986, Rv2659c, Rv2693c and the recombinant Rv1737 protein was observed (p<=0.05). The peptide pool of Rv0849 and Rv1737 recombinant proteins induced the highest percentage of IFN- responders after isoniazid therapy.

The in vitro IFN- responses to these proteins might represent useful markers to evaluate changes associated with treatment of latent TB infection.

Preschool rhinovirus-induced wheeze is associated with an increased risk of asthma. In adult asthma, exhaled volatile organic compounds (VOC) are associated with inflammatory activity. We therefore hypothesised that acute preschool wheeze is accompanied by a differential profile of exhaled VOC, which is maintained after resolution of symptoms in those children with rhinovirus-induced wheeze.

We included 178 children (mean±sd age 22±9 months) from the EUROPA cohort comparing asymptomatic and wheezing children during respiratory symptoms and after recovery. Naso- and oropharyngeal swabs were tested for rhinovirus by quantitative PCR. Breath was collected via a spacer and analysed using an electronic nose. Between-group discrimination was assessed by constructing a 1000-fold cross-validated receiver operating characteristic curve. Analyses were stratified by rhinovirus presence/absence.

Wheezing children demonstrated a different VOC profile when compared with asymptomatic children (p<0.001), regardless of the presence (area under the curve (AUC) 0.77, 95% CI 0.07) or absence (AUC 0.81, 95% CI 0.05) of rhinovirus. After symptomatic recovery, discriminative accuracy was maintained in children with rhinovirus-induced wheeze (AUC 0.84, 95% CI 0.06), whereas it dropped significantly in infants with non-rhinovirus-induced wheeze (AUC 0.67, 95% CI 0.06).

Exhaled molecular profiles differ between preschool children with and without acute respiratory wheeze. This appears to be sustained in children with rhinovirus-induced wheeze after resolution of symptoms. Therefore, exhaled VOC may qualify as candidate biomarkers for early signs of asthma.

Elevated loop gain, consequent to hypersensitive ventilatory control, is a primary nonanatomical cause of obstructive sleep apnoea (OSA) but it is not possible to quantify this in the clinic. Here we provide a novel method to estimate loop gain in OSA patients using routine clinical polysomnography alone. We use the concept that spontaneous ventilatory fluctuations due to apnoeas/hypopnoeas (disturbance) result in opposing changes in ventilatory drive (response) as determined by loop gain (response/disturbance). Fitting a simple ventilatory control model (including chemical and arousal contributions to ventilatory drive) to the ventilatory pattern of OSA reveals the underlying loop gain.

Following mathematical-model validation, we critically tested our method in patients with OSA by comparison with a standard (continuous positive airway pressure (CPAP) drop method), and by assessing its ability to detect the known reduction in loop gain with oxygen and acetazolamide.

Our method quantified loop gain from baseline polysomnography (correlation versus CPAP-estimated loop gain: n=28; r=0.63, p<0.001), detected the known reduction in loop gain with oxygen (n=11; mean±sem change in loop gain (LG) –0.23±0.08, p=0.02) and acetazolamide (n=11; LG –0.20±0.06, p=0.005), and predicted the OSA response to loop gain-lowering therapy.

We validated a means to quantify the ventilatory control contribution to OSA pathogenesis using clinical polysomnography, enabling identification of likely responders to therapies targeting ventilatory control.