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These pubmed results were generated on 2018/07/13

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Next-generation sequencing for identifying genetic mutations in adults with bronchiectasis.

J Thorac Dis. 2018 May;10(5):2618-2630

Authors: Guan WJ, Li JC, Liu F, Zhou J, Liu YP, Ling C, Gao YH, Li HM, Yuan JJ, Huang Y, Chen CL, Chen RC, Zhang X, Zhong NS

Abstract
Background: Defective airway host-defense (e.g., altered mucus properties, ciliary defects) contributes to the pathogenesis of bronchiectasis. This study aims to determine whether genetic mutations associated with defective airway host-defense are implicated in the pathogenesis of bronchiectasis.
Methods: Based on the systematic screening of 32 frequently reported bronchiectasis-associated genes, we performed next-generation sequencing (NGS) on peripheral blood samples from 192 bronchiectasis patients and 100 healthy subjects. The variant distribution frequency and pathogenicity of mutations were analyzed.
Results: We identified 162 rare variants in 192 bronchiectasis patients, and 85 rare variants among 100 healthy subjects. Among bronchiectasis patients, 25 (15.4%), 117 (72.2%) and 18 (11.1%) rare variants were associated with cystic fibrosis transmembrane receptor (CFTR), epithelial sodium channel, and primary ciliary dyskinesia genes, respectively. Biallelic CFTR variants were detected in four bronchiectasis patients but none of the healthy subjects. Carriers of homozygous p.M470 plus at least one CFTR rare variant were detected in 6.3% of bronchiectasis patients (n=12) and in 1.0% of healthy subjects (n=1, P=0.039). Twenty-six patients (16 with idiopathic and 6 with post-infectious bronchiectasis) harbored biallelic variants. Bronchiectasis patients with biallelic DNAH5 variants, or biallelic CFTR variants plus an epithelial sodium channel variant, tended to have greater disease severity.
Conclusions: Genetic mutations leading to impaired host-defense might have implicated in the pathogenesis of bronchiectasis. Genetic screening may be a useful tool for unraveling the underlying causes of bronchiectasis, and offers molecular information which is complementary to conventional etiologic assessment for bronchiectasis.

PMID: 29997923 [PubMed]

The Effects of PCSO-524®, a Patented Marine Oil Lipid derived from the New Zealand Green Lipped Mussel (Perna canaliculus), on Pulmonary and Respiratory Muscle Function in Non-asthmatic Elite Runners.

Int J Exerc Sci. 2018;11(3):669-680

Authors: Shei RJ, Adamic EM, Chapman RF, Mickleborough TD

Abstract
Habitual endurance training may be associated with mild airway inflammation and subsequent deterioration in lung function. PCSO-524™ (Lyprinol®/Omega-XL®), a supplement extracted from the New Zealand green-lipped mussel (Perna canaliculus), has been shown to moderate airway inflammation in asthmatic subjects. The purpose of this study was to determine whether supplementation with PCSO-524™ improves pulmonary and respiratory muscle function in non-asthmatic elite runners. Sixteen male, non-asthmatic elite runners were randomly assigned to either a treatment (PCSO-524™; 1 capsule contains 50 mg n-3 polyunsaturated fatty acids and 100 mg olive oil, n=8) or placebo (1 capsule contains 150 mg olive oil; n=8) group. During the supplementation period, subjects ingested 8 capsules of either treatment or placebo per day for 12 weeks. Resting pulmonary and respiratory muscle function testing were assessed at baseline and every two weeks throughout the 12 week supplementation period. No significant between-or within-subjects main effects were observed in forced vital capacity, forced expiratory volume in 1-second, forced expiratory flow from 25-75% of lung volume (FEF25-75), peak expiratory flow, maximal voluntary ventilation, maximal inspiratory mouth pressure, and closing volume (p>0.05). A significant within-subjects main effect was observed in maximal expiratory mouth pressure (PEmax) (p=0.024) and lung diffusion capacity (DLCO) (p<0.0001), but no significant between-subjects main effects were observed for PEmax and DLCO (p>0.05). A significant treatment by time interaction was observed in FEF25-75 (p=0.026) and DLCO (p=0.024), but no other significant interactions were observed (all p>0.05). Supplementation with PCSO-524™ (Lyprinol®/Omega-XL®) does not improve pulmonary or respiratory muscle function in non-asthmatic elite runners.

PMID: 29997731 [PubMed]

CDG: An Online Server for Detecting Biologically Closest Disease-Causing Genes and its Application to Primary Immunodeficiency.

Front Immunol. 2018;9:1340

Authors: Requena D, Maffucci P, Bigio B, Shang L, Abhyankar A, Boisson B, Stenson PD, Cooper DN, Cunningham-Rundles C, Casanova JL, Abel L, Itan Y

Abstract
High-throughput genomic technologies yield about 20,000 variants in the protein-coding exome of each individual. A commonly used approach to select candidate disease-causing variants is to test whether the associated gene has been previously reported to be disease-causing. In the absence of known disease-causing genes, it can be challenging to associate candidate genes with specific genetic diseases. To facilitate the discovery of novel gene-disease associations, we determined the putative biologically closest known genes and their associated diseases for 13,005 human genes not currently reported to be disease-associated. We used these data to construct the closest disease-causing genes (CDG) server, which can be used to infer the closest genes with an associated disease for a user-defined list of genes or diseases. We demonstrate the utility of the CDG server in five immunodeficiency patient exomes across different diseases and modes of inheritance, where CDG dramatically reduced the number of candidate genes to be evaluated. This resource will be a considerable asset for ascertaining the potential relevance of genetic variants found in patient exomes to specific diseases of interest. The CDG database and online server are freely available to non-commercial users at: http://lab.rockefeller.edu/casanova/CDG.

PMID: 29997612 [PubMed]

Drug repurposing using deep embeddings of gene expression profiles.

Mol Pharm. 2018 Jul 12;:

Authors: Donner Y, Kazmierczak S, Fortney K

Abstract
Computational drug repositioning requires assessment of the functional similarities among compounds. Here, we report a new method for measuring compound functional similarity based on gene expression data. This approach takes advantage of deep neural networks to learn an embedding that substantially denoises expression data, making replicates of the same compound more similar. Our method uses unlabeled data in the sense that it only requires compounds to be labeled by identity rather than detailed pharmacological information, which is often unavailable and costly to obtain. Similarity in the learned embedding space accurately predicted pharmacological similarities despite the lack of any such labels during training, and achieved substantially improved performance in comparison with previous similarity measures applied directly to gene expression measurements. Our method could identify drugs with shared therapeutic and biological targets even when the compounds were structurally dissimilar, thereby revealing previously unreported functional relationships between compounds. Thus, our approach provides an improved engine for drug repurposing based on expression data.

PMID: 30001141 [PubMed - as supplied by publisher]

Sequence Analysis of Drug Target Genes with Suicidal Behavior in Bipolar Disorder Patients.

Mol Neuropsychiatry. 2018 Jun;4(1):1-6

Authors: Zai CC, Tiwari AK, Zai GC, de Luca V, Shaikh SA, King N, Strauss J, Kennedy JL, Vincent JB

Abstract
Background: A number of genes have been implicated in recent genome-wide association studies of suicide attempt in bipolar disorder. More focused investigation of genes coding for protein targets of existing drugs may lead to drug repurposing for the treatment and/or prevention of suicide.
Methods: We analyzed 2,457 DNA variants across 197 genes of interest to GlaxoSmithKline across the pipeline in our sample of European patients suffering from bipolar disorder (N = 219). We analyzed these variants for a possible association with the suicide severity score (ranging from suicidal ideation/plan to serious suicide attempt) from the Schedule for Clinical Assessment in Neuropsychiatry. We conducted tests of individual variants and gene-based tests.
Results: We found a number of DNA variants in the transforming growth factor beta receptor 1 gene (TGFBR1) to be suggestively associated with suicide severity scores (p < 0.005). The gene-based tests also pointed to TGFBR1 to be associated with suicide severity (p = 0.0001). However, these findings were not replicated in an independent bipolar disorder sample.
Conclusions: We report no significant association between DNA sequences of drug target genes and suicidal behavior. Additional larger sequencing studies could further interrogate associations between variants in drug target genes and suicidal behavior.

PMID: 29998113 [PubMed]

Mental Health and Well-Being in Mothers of Children With Rare Genetic Syndromes Showing Chronic Challenging Behavior: A Cross-Sectional and Longitudinal Study.

Am J Intellect Dev Disabil. 2018 05;123(3):241-253

Authors: Adams D, Clarke S, Griffith G, Howlin P, Moss J, Petty J, Tunnicliffe P, Oliver C

Abstract
It is well documented that mothers of children with challenging behavior (CB) experience elevated levels of stress and that this persists over time, but less is known about the experience of mothers of children with rare genetic syndromes. This article describes 2 studies, 1 cross-sectional and 1 longitudinal, comparing well-being in mothers of children with Angelman, Cornelia de Lange and Cri du Chat syndrome who have either shown chronic CB ( n = 18) or low/no CB ( n = 26) in the preceding 7 years. The presence of chronic, long-term CB increased maternal stress but not depression or anxiety, and did not influence positive well-being. Stress relating specifically to their child's genetic syndrome reduced with age, highlighting the need for further exploration in this area.

PMID: 29671635 [PubMed - indexed for MEDLINE]

OpenPVSignal: Advancing Information Search, Sharing and Reuse on Pharmacovigilance Signals via FAIR Principles and Semantic Web Technologies.

Front Pharmacol. 2018;9:609

Authors: Natsiavas P, Boyce RD, Jaulent MC, Koutkias V

Abstract
Signal detection and management is a key activity in pharmacovigilance (PV). When a new PV signal is identified, the respective information is publicly communicated in the form of periodic newsletters or reports by organizations that monitor and investigate PV-related information (such as the World Health Organization and national PV centers). However, this type of communication does not allow for systematic access, discovery and explicit data interlinking and, therefore, does not facilitate automated data sharing and reuse. In this paper, we present OpenPVSignal, a novel ontology aiming to support the semantic enrichment and rigorous communication of PV signal information in a systematic way, focusing on two key aspects: (a) publishing signal information according to the FAIR (Findable, Accessible, Interoperable, and Re-usable) data principles, and (b) exploiting automatic reasoning capabilities upon the interlinked PV signal report data. OpenPVSignal is developed as a reusable, extendable and machine-understandable model based on Semantic Web standards/recommendations. In particular, it can be used to model PV signal report data focusing on: (a) heterogeneous data interlinking, (b) semantic and syntactic interoperability, (c) provenance tracking and (d) knowledge expressiveness. OpenPVSignal is built upon widely-accepted semantic models, namely, the provenance ontology (PROV-O), the Micropublications semantic model, the Web Annotation Data Model (WADM), the Ontology of Adverse Events (OAE) and the Time ontology. To this end, we describe the design of OpenPVSignal and demonstrate its applicability as well as the reasoning capabilities enabled by its use. We also provide an evaluation of the model against the FAIR data principles. The applicability of OpenPVSignal is demonstrated by using PV signal information published in: (a) the World Health Organization's Pharmaceuticals Newsletter, (b) the Netherlands Pharmacovigilance Centre Lareb Web site and (c) the U.S. Food and Drug Administration (FDA) Drug Safety Communications, also available on the FDA Web site.

PMID: 29997499 [PubMed]

Pharmacogenomics of vincristine-induced peripheral neuropathy implicates pharmacokinetic and inherited neuropathy genes.

Clin Pharmacol Ther. 2018 Jul 12;:

Authors: Wright GEB, Amstutz U, Drögemöller BI, Shih J, Rassekh SR, Hayden MR, Carleton BC, Ross CJD, Canadian Pharmacogenomics Network for Drug Safety Consortium

Abstract
Vincristine is an effective chemotherapeutic drug for various cancers, including acute lymphoblastic leukemia (ALL). Unfortunately, clinical utility is restricted by dose-limiting vincristine-induced peripheral neuropathies (VIPN). We sought to determine the association of VIPN with a recently-identified risk variant, CEP72 rs924607 and drug absorption, distribution, metabolism, and excretion (ADME) gene variants in pediatric ALL. This was followed by a meta-analysis of pharmacogenomic data from over 500 patients. CEP72 rs924607 was significantly associated with VIPN (P=0.02, OR 3.4). ADME analyses identified associations between VIPN and ABCC1 rs3784867 (P=5.34 x 10-5 , OR 4.9), and SLC5A7 rs1013940 (P=9.00 x 10-4 , OR 8.6); genes involved in vincristine transport and inherited neuropathies respectively. Meta-analysis identified an association with a variant related to TTPA (rs10504361: P=6.85 x 10-4 , OR 2.0), a heritable neuropathy-related gene. This study provides essential corroboratory evidence for CEP72 rs924607 and highlights the importance of drug transporter and inherited neuropathy genes in VIPN. This article is protected by copyright. All rights reserved.

PMID: 29999516 [PubMed - as supplied by publisher]

CYP3A4*22 impairs the elimination of ticagrelor, but has no significant effect on the bioactivation of clopidogrel or prasugrel.

Clin Pharmacol Ther. 2018 Jul 11;:

Authors: Holmberg MT, Tornio A, Paile-Hyvärinen M, Tarkiainen EK, Neuvonen M, Neuvonen PJ, Backman JT, Niemi M

Abstract
CYP3A enzymes participate in the elimination of ticagrelor and the bioactivation of clopidogrel and prasugrel. We studied the effects of functional CYP3A genetic variants (CYP3A4*22; rs35599367 and CYP3A5*3; rs776746) on the pharmacokinetics and pharmacodynamics of ticagrelor, clopidogrel, and prasugrel. Six healthy volunteers with the CYP3A4*1/*22 and CYP3A5*3/*3 genotype (CYP3A4*22 carriers), eight with the CYP3A4*1/*1 and CYP3A5*1/*3 genotype (CYP3A5 expressors), and 11 to 13 with the CYP3A4*1/*1 and CYP3A5*3/*3 genotypes (controls) ingested single doses of ticagrelor, clopidogrel, and prasugrel on separate occasions. Ticagrelor area under the plasma concentration-time curve was 89% (P=0.004) higher in CYP3A4*22 carriers than in controls. CYP3A4*22 carriers also showed more pronounced platelet inhibition at 24 h after ticagrelor ingestion than the controls (43% vs. 21%; P=0.029). CYP3A5 genotype did not affect ticagrelor pharmacokinetics. Neither CYP3A5 nor CYP3A4 genotypes significantly affected prasugrel or clopidogrel. In conclusion, the CYP3A4*22 allele markedly impairs ticagrelor elimination enhancing its antiplatelet effect. This article is protected by copyright. All rights reserved.

PMID: 29998574 [PubMed - as supplied by publisher]

ETV4 transcription factor and MMP13 metalloprotease are interplaying actors of breast tumorigenesis.

Breast Cancer Res. 2018 Jul 11;20(1):73

Authors: Dumortier M, Ladam F, Damour I, Vacher S, Bièche I, Marchand N, de Launoit Y, Tulasne D, Chotteau-Lelièvre A

Abstract
BACKGROUND: The ETS transcription factor ETV4 is involved in the main steps of organogenesis and is also a significant mediator of tumorigenesis and metastasis, such as in breast cancer. Indeed, ETV4 is overexpressed in breast tumors and is associated with distant metastasis and poor prognosis. However, the cellular and molecular events regulated by this factor are still misunderstood. In mammary epithelial cells, ETV4 controls the expression of many genes, MMP13 among them. The aim of this study was to understand the function of MMP13 during ETV4-driven tumorigenesis.
METHODS: Different constructs of the MMP13 gene promoter were used to study the direct regulation of MMP13 by ETV4. Moreover, cell proliferation, migration, invasion, anchorage-independent growth, and in vivo tumorigenicity were assayed using models of mammary epithelial and cancer cells in which the expression of MMP13 and/or ETV4 is modulated. Importantly, the expression of MMP13 and ETV4 messenger RNA was characterized in 456 breast cancer samples.
RESULTS: Our results revealed that ETV4 promotes proliferation, migration, invasion, and anchorage-independent growth of the MMT mouse mammary tumorigenic cell line. By investigating molecular events downstream of ETV4, we found that MMP13, an extracellular metalloprotease, was an ETV4 target gene. By overexpressing or repressing MMP13, we showed that this metalloprotease contributes to proliferation, migration, and anchorage-independent clonogenicity. Furthermore, we demonstrated that MMP13 inhibition disturbs proliferation, migration, and invasion induced by ETV4 and participates to ETV4-induced tumor formation in immunodeficient mice. Finally, ETV4 and MMP13 co-overexpression is associated with poor prognosis in breast cancer.
CONCLUSION: MMP13 potentiates the effects of the ETV4 oncogene during breast cancer genesis and progression.

PMID: 29996935 [PubMed - in process]

Triple-negative breast cancer and the potential for targeted therapy.

Pharmacogenomics. 2017 Nov;18(17):1595-1609

Authors: Jhan JR, Andrechek ER

Abstract
Breast cancer is composed of several well-recognized subtypes including estrogen receptor, progesterone receptor and HER2 triple-negative breast cancer (TNBC). Without available targeted therapy options, standard of care for TNBC remains chemotherapy. It is of interest to note that TNBC tumors generally have better responses to chemotherapy compared with other subtypes. However, patients without complete response account for approximately 80% of TNBC. Mounting evidence suggests significant heterogeneity within the TNBC subtype, and studies have focused on genetic targets with high rates of altered expression. Recent studies suggest clear possibilities for benefits from targeted therapy in TNBC. In this review, we summarize studies of targeted therapy, including within mouse models, and discuss their applications in the development of combinatorial treatments to treat TNBC.

PMID: 29095114 [PubMed - indexed for MEDLINE]

SLCO1B1 rs4149056 genetic polymorphism predicting methotrexate toxicity in Chinese patients with non-Hodgkin lymphoma.

Pharmacogenomics. 2017 Nov;18(17):1557-1562

Authors: Yang L, Wu H, Gelder TV, Matic M, Ruan JS, Han Y, Xie RX

Abstract
AIM: To investigate the impact of polymorphisms in the FPGS, GGH and SLCO1B1 genes on high dose methotrexate (HD-MTX) related toxicity in Chinese patients with non-Hodgkin lymphoma (NHL).
MATERIALS & METHODS: We analyzed FPGS (rs10106), GGH (rs719235, rs10464903, rs12681874), SLCO1B1 (rs4149056) genetic polymorphisms in 105 Chinese patients with NHL treated with HD-MTX.
RESULTS: There was a statistically significant impact of the SLCO1B1 rs4149056 polymorphism on hepatotoxicity. Patients with TC and CC genotype had more hepatotoxicity than TT genotype (60 vs 32.94%, p = 0.025). After adjusting for disease stage, dosage, infusion time and therapy method, SLCO1B1 rs4149056 genotype remained significantly associated with hepatotoxicity (p = 0.028).
CONCLUSION: SLCO1B1 rs4149056 genetic variants can affect the HD-MTX-related toxicity in Chinese patients with NHL.

PMID: 29095107 [PubMed - indexed for MEDLINE]

Rethinking ovarian cancer genomics: where genome-wide association studies stand?

Pharmacogenomics. 2017 Nov;18(17):1611-1625

Authors: Pinto R, Assis J, Nogueira A, Pereira C, Pereira D, Medeiros R

Abstract
Genome-wide association studies (GWAS) allow the finding of genetic variants associated with several traits. Regarding ovarian cancer (OC), 15 GWAS have been conducted since 2009, with the discovery of 49 SNPs associated with disease susceptibility and 46 with impact in the clinical outcome of patients (p < 5.00 × 10-2). Among them, 14 variants reached the genome-wide significance (p < 5.00 × 10-8). Despite the results obtained, they should be validated in independent sets. So far, five validation studies have been conducted which could confirm the association of 12 OC susceptibility SNPs. Consequently, post-GWAS studies are crucial unravel the biological plausibility of GWAS' findings and the allelic spectrum of OC.

PMID: 29095100 [PubMed - indexed for MEDLINE]

Introducing personalized health for the family: the experience of a single hospital system.

Pharmacogenomics. 2017 Nov;18(17):1589-1594

Authors: Huddleston KL, Klein E, Fuller A, Jo G, Lawrence G, Haga SB

Abstract
Pharmacogenetic testing is leading the personalized health movement, gradually being implemented in a variety of healthcare settings. To inform the efforts of other hospital and clinical practices implementing personalized health or medicine applications, we describe the implementation of a newborn pharmacogenetic testing program at Inova Health System (VA, USA). In particular, we describe the efforts to gather patient feedback through focus groups, the training and program staff, the pilot program and our experiences to date. In our experience, a multidisciplinary team was essential to address the myriad facets of program development and implementation as well as an in-person approach to introduce testing and patient education.

PMID: 29061078 [PubMed - indexed for MEDLINE]

The Value of Evidence in the Decision-Making Process for Reimbursement of Pharmacogenetic Dosing of Warfarin.

Am J Cardiovasc Drugs. 2017 Oct;17(5):399-408

Authors: Janzic A, Locatelli I, Kos M

Abstract
BACKGROUND: After early clinical trials that evaluated pharmacogenetic (PG) algorithms, many healthcare payers were reluctant to cover this technology and, consequently, PG dosing of warfarin could not be translated into clinical practice.
OBJECTIVE: The aim of this study was to estimate the value of upgrading evidence relating to PG dosing of warfarin from the healthcare payer perspective.
METHODS: Randomized controlled trials (RCTs) that evaluated PG dosing of warfarin were identified through a systematic literature search, and their findings were combined by a cumulative meta-analysis. A health economic model was used to estimate economic outcomes and to calculate the expected value of perfect information (EVPI) as a measure of the value of clinical trials for decision makers.
RESULTS: Nine RCTs were identified and included in our analysis. The estimated difference in the percentage of time in the therapeutic range was 5.6 percentage points in 2007, decreasing to 4.3 percentage points when all studies were included. At a reimbursement price of €160 per PG testing, the EVPI for the clinical benefit was estimated at €80 and €90 per patient in 2007 and 2014, respectively. A reduction in the price of PG testing to €40, which was observed in this period, resulted in an EVPI of €3 per patient.
CONCLUSIONS: The estimated cumulative effect of PG dosing has remained similar since 2007, but additional evidence has contributed to a more precise estimation. While these variations should not affect the reimbursement decision, a large decline in the cost of PG testing in recent years calls for reconsideration.

PMID: 28528365 [PubMed - indexed for MEDLINE]

Are patients willing to incur out-of-pocket costs for pharmacogenomic testing?

Pharmacogenomics J. 2017 01;17(1):1-3

Authors: Bielinski SJ, St Sauver JL, Olson JE, Wieland ML, Vitek CR, Bell EJ, Mc Gree ME, Jacobson DJ, McCormick JB, Takahashi PY, Black JL, Caraballo PJ, Sharp RR, Beebe TJ, Weinshilboum RM, Wang L, Roger VL

PMID: 27779246 [PubMed - indexed for MEDLINE]

The CYP2D6 VCF Translator.

Pharmacogenomics J. 2017 07;17(4):301-303

Authors: Qiao W, Wang J, Pullman BS, Chen R, Yang Y, Scott SA

PMID: 26975230 [PubMed - indexed for MEDLINE]

Inflammation in cystic fibrosis: An update.

Pediatr Pulmonol. 2018 Jul 12;:

Authors: Roesch EA, Nichols DP, Chmiel JF

Abstract
Inflammation plays a critical role in cystic fibrosis (CF) lung pathology and disease progression making it an active area of research and important therapeutic target. In this review, we explore the most recent research on the major contributors to the exuberant inflammatory response seen in CF as well as potential therapeutics to combat this response. Absence of functional cystic fibrosis transmembrane conductance regulator (CFTR) alters anion transport across CF airway epithelial cells and ultimately results in dehydration of the airway surface liquid. The dehydrated airway surface liquid in combination with abnormal mucin secretion contributes to airway obstruction and subsequent infection that may serve as a trigger point for inflammation. There is also evidence to suggest that airway inflammation may be excessive and sustained relative to the infectious stimuli. Studies have shown dysregulation of both pro-inflammatory mediators such as IL-17 and pro-resolution mediators including metabolites of the eicosanoid pathway. Recently, CFTR potentiators and correctors have garnered much attention in the CF community. Although these modulators address the underlying defect in CF, their impact on downstream consequences such as inflammation are not known. Here, we review pre-clinical and clinical data on the impact of CFTR modulators on inflammation. In addition, we examine other cell types including neutrophils, macrophages, and T-lymphocytes that express CFTR and contribute to the CF inflammatory response. Finally, we address challenges in developing anti-inflammatory therapies and highlight some of the most promising anti-inflammatory drugs under development for CF.

PMID: 29999593 [PubMed - as supplied by publisher]

Bullying and mental health amongst Australian children and young people with cystic fibrosis.

Am J Orthopsychiatry. 2018;88(4):402-412

Authors: Branch-Smith C, Shaw T, Lin A, Runions K, Payne D, Nguyen R, Hugo H, Balding L, Cross D

Abstract
Currently, there is little research investigating how schools can support the mental health and social development of young people with cystic fibrosis (CF), given their heightened risk of mental illness. Few studies have examined the relationship between bullying and mental health in populations of children with CF. This study describes the peer bullying experiences of young people with CF, and examines associations between school bullying and the psychological well-being of these young people. A sequential mixed-methods approach was used to collect data from 26 young people with CF (10-16 years of age). These data were compared with large samples of healthy children. Following an online survey, 11 young people, through online focus groups, expanded on the survey findings, describing their experiences within the school environment. Young people with CF reported lower involvement in bullying victimization and perpetration relative to the comparison population. For older adolescents with CF, victimization was associated with less connectedness to school and less peer support, and more school loneliness, anxiety, and depression. Young people with CF reported they generally liked the school environment, and were happy with their friendships, whereas some older adolescents reported that bullying evoked anxiety and mood problems. Reported bullying was primarily verbal and targeted characteristics of their CF, including their coughing, noninvolvement in certain activities because of shortness of breath, use of medication, and being underweight (for boys only). The findings provide some recommendations for interventions to promote mental health and school engagement among young people with CF. (PsycINFO Database Record

PMID: 29999388 [PubMed - in process]