Related Articles

Cost of hospitalization for non-communicable diseases in India: are we pro-poor?

Trop Med Int Health. 2016 Jun 2;

Authors: Tripathy JP, Prasad BM, Shewade HD, Kumar AM, Zachariah R, Chadha S, Tonsing J, Harries AD

Abstract
OBJECTIVES: To estimate out-of-pocket (OOP) expenditure due to hospitalization from NCDs and its impact on households in India.
METHODS: The study analysed nationwide representative data collected by the National Sample Survey Organization in 2014 that reported health service utilization and health care related OOP expenditure by income quintiles and by type of health facility (public or private). The recall period for inpatient hospitalization expenditure was 365 days. Consumption expenditure was collected for a recall period of one month. OOP expenditure amounting to >10% of annual consumption expenditure was termed as catastrophic. Weighted analysis was performed.
RESULTS: The median expenditure per episode of hospitalisation due to NCDs was USD 149 - this was ~3 times higher among the richest quintile compared to poorest quintile. There was a significantly higher prevalence of catastrophic expenditure among the poorest quintile, more so for cancers (85%), psychiatric and neurological disorders (63%) and injuries (63%). Mean private sector OOP hospitalization expenditure was nearly five times higher than in the public sector. Medicines accounted for 40% and 27% of public and private sector OOP hospitalization expenditure respectively.
CONCLUSION: Strengthening of public health facilities is required at community level for the prevention, control and management of NCDs. Promotion of generic medicines, better availability of essential drugs and possible subsidization for the poorest quintile will be measures to consider to reduce OOP expenditure in public sector facilities. This article is protected by copyright. All rights reserved.

PMID: 27253634 [PubMed - as supplied by publisher]

Related Articles

Pharmacogenetics and interstitial lung disease.

Curr Opin Pulm Med. 2016 May 31;

Authors: Oldham JM, Noth I, Martinez FJ

Abstract
PURPOSE OF REVIEW: Interstitial lung disease (ILD) is comprised of a heterogeneous group of disorders with highly variable natural histories and response to therapies. Pharmacogenetics focuses on the variability in drug response because of the presence of genetic factors that influence drug metabolism or disease activity. In this article, we review relevant drug-specific and disease-specific polymorphisms that may influence therapeutic response, and then highlight a recently identified drug-gene interaction in patients with idiopathic pulmonary fibrosis (IPF).
RECENT FINDINGS: The emergence of high-throughput genomic technology has allowed for identification of gene polymorphisms associated with susceptibility to specific disease states, including IPF and several connective tissue diseases known to cause ILD. IPF risk loci span a diverse group of genes, while most associated with connective tissue disease are critical to immune signaling. A recent pharmacogenetic analysis of patients enrolled in an IPF clinical trial identified a variant within TOLLIP to be associated with differential response to N-acetylcysteine therapy.
SUMMARY: Though few pharmacogenetic investigations have been conducted in patients with ILD to date, ample opportunities for pharmacogenetic exploration exist in this patient population. Such exploration will advance our understanding of specific ILDs and help usher in an era of personalized medicine.

PMID: 27253772 [PubMed - as supplied by publisher]

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Exposure to common respiratory bacteria alters the airway epithelial response to subsequent viral infection.

Respir Res. 2016;17(1):68

Authors: Bellinghausen C, Gulraiz F, Heinzmann AC, Dentener MA, Savelkoul PH, Wouters EF, Rohde GG, Stassen FR

Abstract
BACKGROUND: Colonization of the airways with potential pathogenic bacteria is observed in a number of chronic respiratory diseases, such as COPD or cystic fibrosis. Infections with respiratory viruses are known triggers of exacerbations of these diseases. We here investigated if pre-exposure to bacteria alters the response of lung epithelial cells to subsequent viral infection.
METHODS: Bronchial epithelial cells (BEAS-2B cells and primary bronchial epithelial cells) were exposed to heat-inactivated Haemophilus influenzae, Pseudomonas aeruginosa or Streptococcus pneumoniae and subsequently infected with respiratory syncytial virus (RSV), type 2 human adenovirus or influenza B. Levels of pro-inflammatory cytokines, viral replication and expression of pattern recognition receptors were determined in culture supernatants and/or cell lysates.
RESULTS: Exposure of BEAS-2B cells to H. influenzae before and during RSV-infection synergistically increased the release of IL-6 (increase above calculated additive effect at 72 h: 56 % ± 3 %, mean ± SEM) and IL-8 (53 % ± 12 %). This effect was sustained even when bacteria were washed away before viral infection and was neither associated with enhanced viral replication, nor linked to increased expression of key pattern recognition receptors. P. aeruginosa enhanced the release of inflammatory cytokines to a similar extent, yet only if bacteria were also present during viral infection. S. pneumoniae did not enhance RSV-induced cytokine release. Surprisingly, adenovirus infection significantly reduced IL-6 release in cells exposed to either of the three tested bacterial strains by on average more than 50 %. Infection with influenza B on the other hand did not affect cytokine production in BEAS-2B cells exposed to the different bacterial strains.
CONCLUSION: Pre-exposure of epithelial cells to bacteria alters the response to subsequent viral infection depending on the types of pathogen involved. These findings highlight the complexity of microbiome interactions in the airways, possibly contributing to the susceptibility to exacerbations and the natural course of airway diseases.

PMID: 27259950 [PubMed - as supplied by publisher]

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Understanding the feasibility and implications of implementing early peanut introduction for prevention of peanut allergy.

J Allergy Clin Immunol. 2016 May 2;

Authors: Koplin JJ, Peters RL, Dharmage SC, Gurrin L, Tang ML, Ponsonby AL, Matheson M, Togias A, Lack G, Allen KJ, HealthNuts study investigators

Abstract
BACKGROUND: A recent randomized trial (the Learning Early About Peanut Allergy [LEAP] study) provided evidence that earlier dietary peanut introduction reduces peanut allergy prevalence in high-risk infants. However, questions remain as to how to identify and target the "at-risk" population to facilitate timely introduction of peanut.
OBJECTIVE: We sought to use population-based infant peanut allergy data to understand feasibility and implications of implementing the LEAP trial intervention.
METHODS: Using the HealthNuts study cohort (n = 5276) of 1-year-old infants, we explored the impact of using various criteria to identify infants at high risk of developing peanut allergy, and the implications of skin prick test (SPT) screening before peanut introduction.
RESULTS: Screening all infants with early onset eczema and/or egg allergy could require testing 16% of the population and would still miss 23% of peanut allergy cases; 29% of screened infants would require clinical follow-up because of being SPT-positive. Around 11% of high-risk infants were excluded from the LEAP study because of an SPT wheal size of more than 4 mm to peanut at baseline; data from the HealthNuts study suggest that 80% of these would be peanut allergic on food challenge. There were no life-threatening events among either low- or high-risk infants whose parents chose to introduce peanut at home in the first year of life, or in 150 peanut-allergic infants during hospital-based challenges.
CONCLUSIONS: Based on this large epidemiological study, a population program aiming to identify and screen all infants at risk of peanut allergy would pose major cost and logistic challenges that need to be carefully considered. Further research might be required to provide data for low-risk infants.

PMID: 27260320 [PubMed - as supplied by publisher]