New evidence of increased risk of rhinitis in subjects with COPD: a longitudinal population study.

Int J Chron Obstruct Pulmon Dis. 2016;11:2617-2623

Authors: Bergqvist J, Andersson A, Olin AC, Murgia N, Schiöler L, Bove M, Hellgren J

Abstract
BACKGROUND: The aim of this population-based study was to investigate the risk of developing noninfectious rhinitis (NIR) in subjects with chronic obstructive pulmonary disease (COPD).
MATERIALS AND METHODS: This is a longitudinal population-based study comprising 3,612 randomly selected subjects from Gothenburg, Sweden, aged 25-75 years. Lung function was measured at baseline with spirometry and the included subjects answered a questionnaire on respiratory symptoms. At follow-up, the subjects answered a questionnaire with a response rate of 87%. NIR was defined as symptoms of nasal obstruction, nasal secretion, and/or sneezing attacks without having a cold, during the last 5 years. COPD was defined as a spirometry ratio of forced expiratory volume in 1 second divided by forced vital capacity (FEV1/FVC) <0.7. Subjects who reported asthma and NIR at baseline were excluded from the study. The odds ratios for developing NIR (ie, new-onset NIR) in relation to age, gender, body mass index, COPD, smoking, and atopy were calculated.
RESULTS: In subjects with COPD, the 5-year incidence of NIR was significantly increased (10.8% vs 7.4%, P=0.005) and was higher among subjects aged >40 years. Smoking, atopy, and occupational exposure to gas, fumes, or dust were also associated with new-onset NIR. COPD, smoking, and atopy remained individual risk factors for new-onset NIR in the logistic regression analysis.
CONCLUSIONS: This longitudinal population-based study of a large cohort showed that COPD is a risk factor for developing NIR. Smoking and atopy are also risk factors for NIR. The results indicate that there is a link present between upper and lower respiratory inflammation in NIR and COPD.

PMID: 27799760 [PubMed - in process]

OBJECTIVES: Pulmonary hypertension (PH) has been linked to preterm birth explained by congenital heart defects and pulmonary diseases.
WORKING HYPOTHESIS: Other factors may influence the risk of PH among adolescences and children born premature.
STUDY DESIGN: This national registry-based study assess risk of PH following premature birth adjusted for known risk factors.

PATIENT-SUBJECT SELECTION AND METHODOLOGY: All cases born 1993-2010, identified by diagnostic codes applicable to PH and retrieved from the Swedish Registry of Congenital Heart Disease (N = 67). Six controls were randomly selected and matched to each case by year of birth and hospital by the Swedish Medical Birth Register (N = 402). Maternal and infant data related to preterm birth, pulmonary diseases, and congenital defects were retrieved. The association between preterm birth and pulmonary hypertension was calculated by conditional logistic regression taking into account potential confounding factors.

RESULTS: One third of the cases and seven percent of the controls were born preterm in our study. Preterm birth was associated with PH, OR = 8.46 (95%CI 2.97-24.10) (P < 0.0001) even after adjusting for confounding factors. Other factors, such as acute pulmonary diseases, congenital heart defects, congenital diaphragm herniation, and chromosomal disorders were also associated with PH in the multivariate analysis.

CONCLUSIONS: Children and young adults born preterm are known to have an increased risk of PH, previously explained by congenital heart defects and pulmonary diseases. By adjusting for such factors, our study indicates that new factors may play a role in the risk of developing PH among children born preterm. Pediatr Pulmonol. © 2016 Wiley Periodicals, Inc.

In the UK, chronic respiratory diseases cause 13% of adult disability. The major chronic respiratory disease is chronic obstructive pulmonary disease (COPD), a condition involving chronic airway inflammation that causes airflow obstruction and destruction of lung tissue. This leads to a progressive loss of respiratory membrane, which accounts for the clinical manifestation of COPD, which is difficulty maintaining sufficient gas exchange to meet metabolic demands.

The primary cause is smoking, with the vast majority of COPD patients having a past or present history of smoking. However exposure to industrial pollutants is also a contributing factor, as is a rare genetic predisposition to developing COPD.

In order to clarify the risk of hematotoxicity of carboplatin, we inspected 19901 case reports of non-small cell lung cancer patients that were submitted to the FDA Adverse Event Reporting System (FAERS) between January 2004 and December 2015.

These comprised 3907 cases which were treated with carboplatin and 15994 cases which were treated with other therapies in the absence of carboplatin. By comparison, carboplatin cases were significantly more likely to report anemia (OR = 2.27, 95% CI 1.85-2.78, P = 5.04×10-15), neutropenia (OR = 2.27, 95% CI 1.76-2.92, P = 2.39×10-10), and thrombocytopenia (OR = 2.38, 95% CI 1.84-3.08, P = 5.60×10-11). We further explored published evidences and found 205 human genes interacting with carboplatin. Functional analysis corroborated that these genes were significantly enriched in the biochemical pathway of hematopoietic cell lineage (adjusted P = 6.02×10-11).

This indicated that carboplatin could profoundly affect the development of blood cells. Given the early awareness of the hematologic risks, great caution should be exercised in prescribing carboplatin to non-small cell lung cancer patients. And functional enrichment analysis on carboplatin-related genes warranted subsequent research with regard to the underlying toxicological mechanisms.