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The association of latent tuberculosis infection (LTBI) with subsequent cancer remains unclear. We investigated the risk of future cancer among tuberculosis (TB) contacts with or without subsequent TB activation.

Using the Taiwan National Health Insurance Research Database, we conducted a nationwide population-based study. TB contacts during 1997 to 2012 were included as the study cohort. Patients with antecedent cancer and TB were excluded. Data from 11,522 TB contacts and 46,088 age-, sex-, and enrollment date-matched subjects during 1997 to 2012 were analyzed. The 2 cohorts were monitored until December 31, 2012 for incidence of cancer and TB infection. LTBI was defined as a TB contact with subsequent TB activation. The primary endpoint was occurrence of newly diagnosed cancer.

There was no difference in cancer development between the TB contact cohort and comparison cohort (log-rank test, P = 0.714). After multivariate adjustment, the hazard ratio (HR) for cancer among the LTBI patients was 2.29 [95% confidence interval (CI), 1.26-4.17; P = 0.007]. There was increase in cancer incidences for several specific cancer types, including multiple myeloma (HR 340.28), lung (HR 2.69), kidney and bladder (HR 6.16), hepatobiliary (HR 2.36), and gastrointestinal (HR 2.99) cancers. None of the 136 TB contacts who received isoniazid prophylaxis developed cancer.

LTBI patients had a higher risk of future cancer.

Chronic thromboembolic pulmonary hypertension (CTEPH), a rare complication of acute pulmonary embolism, is characterized by fibro-thrombotic obstructions of large pulmonary arteries combined with small vessel arteriopathy. It can be cured by pulmonary endarterectomy, and can be clinically improved by medical therapy in inoperable patients. A European registry was set up in 27 centers to evaluate long-term outcome and outcome correlates in 2 distinct populations of operated and not-operated CTEPH patients.

METHODS AND RESULTS: -A total of 679 newly diagnosed CTEPH patients were prospectively included over a 24-month period. Estimated survival at 1, 2, and 3 years was 93% (95% CI, 90-95), 91% (95% CI, 87-93), and 89% (95% CI, 86-92) in operated patients (n=404), and only 88% (95% CI, 83-91), 79% (95% CI, 74-83), and 70% (95% CI, 64-76) in not-operated patients (n=275). In both operated and not-operated patients, PAH-targeted therapy did not affect survival estimates significantly. Mortality was associated with NYHA functional class IV (HR 4.16, CI 1.49-11.62, p=0.0065 and HR 4.76, CI 1.76-12.88, p=0.0021), increased right atrial pressure (HR 1.34, CI 0.95 -1.90, p=0.0992 and HR 1.50, CI 1.20-1.88, p=0.0004), and a history of cancer (HR 3.02, CI 1.36-6.69, p=0.0065 and HR 2.15, CI 1.18-3.94, p=0.0129) in operated and not-operated patients, respectively. Additional correlates of mortality were bridging therapy with PAH-targeted drugs, postoperative PH, surgical complications, and additional cardiac procedures in operated patients, and comorbidities such as coronary disease, left heart failure, and COPD in not-operated patients.

CONCLUSIONS: -The long-term prognosis of operated patients is nowadays excellent and better than the outcome of not-operated patients.

We investigated the effects of indacaterol on cough and phlegm in patients with stable chronic obstructive pulmonary disease (COPD). We performed a meta-analysis with five randomized controlled trials (RCTs) of indacaterol in stable COPD patients.

The symptom severity was defined using the St. George's Respiratory Questionnaire (SGRQ). We analyzed patients treated with 150 µg (n = 945) and 300 µg (n = 832) out of 3,325 patients who completed the SGRQ from five RCTs. After a 12-week treatment of 150 µg indacaterol, cough improvement was reported in 36.5% (316/866) of patients treated with indacaterol vs. 32.2% (259/804) patients treated with placebo (Relative Ratio [RR], 1.13; 95% confidence interval [CI], 0.99-1.29). Phlegm improvement was reported in 31.0% (247/798) of patients treated with indacaterol vs. 30.6% (225/736) of patients treated with placebo (RR, 1.01; 95% CI, 0.87-1.18). Dyspnea improvement was reported in 39.5% (324/820) of patients treated with indacaterol vs. 31.5% (237/753) patients treated with placebo (RR, 1.33; 95% CI, 1.03-1.71; P = 0.001, I(2) = 55.1%). Only dyspnea improvement was significant compared to placebo even at the 300 µg indacaterol dose.

Compared to placebo, a 12-week treatment of the long-acting beta-agonist, indacaterol might not have a significant effect on cough or phlegm in stable COPD.

Suissa [1] provides the event-based number needed to treat (NNT) for a reduction in exacerbations with fluticasone/salmeterol compared with placebo for the TORCH (Towards a Revolution in COPD Health) trial by period of follow-up (0–1 years after treatment, 1–2 years after treatment and 2–3 years after treatment) [2]. These NNT data are misleading as they fail to recognise that in chronic obstructive pulmonary disease (COPD) trials, patients who exacerbate are more likely to withdraw from the trial than patients with no exacerbations. Keene et al. [3] show that for the TRISTAN (TRial of Inhaled STeroids ANd long-acting β₂ agonists) trial, the exacerbation rate is more than three per year among placebo patients withdrawing prior to 1 year compared with an exacerbation rate of one per year for patients completing a year of placebo treatment. In the TORCH trial, 25% of the placebo group withdrew compared with 15% of the fluticasone/salmeterol arm during the first year of follow-up; therefore, patients entering the second year of the trial on placebo and on fluticasone/salmeterol were no longer directly comparable. This is not accounted for in the calculation of exacerbation rates or NNT during years 2 and 3, as presented in table 2 of the study by Suissa [1].