There are an increasing number of mobile apps available for adolescents with mental health problems and an increasing interest in assimilating mobile health (mHealth) into mental health services. ...Despite the growing number of apps available, the evidence base for their efficacy is unclear.
This review aimed to systematically appraise the available research evidence on the efficacy and acceptability of mobile apps for mental health in children and adolescents younger than 18 years.
The following were systematically searched for relevant publications between January 2008 and July 2016: APA PsychNet, ACM Digital Library, Cochrane Library, Community Care Inform-Children, EMBASE, Google Scholar, PubMed, Scopus, Social Policy and Practice, Web of Science, Journal of Medical Internet Research, Cyberpsychology, Behavior and Social Networking, and OpenGrey. Abstracts were included if they described mental health apps (targeting depression, bipolar disorder, anxiety disorders, self-harm, suicide prevention, conduct disorder, eating disorders and body image issues, schizophrenia, psychosis, and insomnia) for mobile devices and for use by adolescents younger than 18 years.
A total of 24 publications met the inclusion criteria. These described 15 apps, two of which were available to download. Two small randomized trials and one case study failed to demonstrate a significant effect of three apps on intended mental health outcomes. Articles that analyzed the content of six apps for children and adolescents that were available to download established that none had undergone any research evaluation. Feasibility outcomes suggest acceptability of apps was good and app usage was moderate.
Overall, there is currently insufficient research evidence to support the effectiveness of apps for children, preadolescents, and adolescents with mental health problems. Given the number and pace at which mHealth apps are being released on app stores, methodologically robust research studies evaluating their safety, efficacy, and effectiveness is promptly needed.
Abstract
Objectives
Lung involvement in RA has several manifestations and is a major cause of morbidity and mortality. The aim of this study was to characterize the different types of lung disease ...and response to treatment in a UK cohort of RA patients.
Methods
RA patients who had undergone high resolution CT scans of the lung were identified and scans reviewed. Demographic data, RA features, complementary exams and treatments were recorded for those with radiological evidence of lung involvement. Descriptive analysis was performed, and Mann–Whitney U and χ2 tests were used for comparison between different radiological subtypes.
Results
Lung disease was reported in 87 (7.7%) of 1129 RA patients, usually (97.7%) post-dating articular symptoms. Most patients had positive RF (74/84; 88.1%) and ACPA (72/82; 87.7%). Interstitial lung disease (ILD) was the most common pattern, reported in 45 (51.7%) patients. Drug-induced lung disease was reported in 2 of 64 (3.1%) patients treated with MTX. Rituximab was used in 26 (57.8%) patients with ILD, with evidence of disease improvement or stabilization in patients with non-specific interstitial pneumonia and organizing pneumonia. During lung disease follow-up (6.7 ± 4.1 years), 22 (25.3%) patients were admitted to hospital with respiratory infections, with 14 (63.6%) of them having underlying bronchiectasis. Lung disease-related mortality was estimated at 8%.
Conclusion
ILD was the most prevalent manifestation of lung involvement in RA and was associated with higher mortality. Immunosuppressive drugs used in RA were rarely associated with lung toxicity, and rituximab demonstrated promising results for the treatment of RA-ILD.
Large numbers of people are being discharged from hospital following COVID-19 without assessment of recovery. In 384 patients (mean age 59.9 years; 62% male) followed a median 54 days post discharge, ...53% reported persistent breathlessness, 34% cough and 69% fatigue. 14.6% had depression. In those discharged with elevated biomarkers, 30.1% and 9.5% had persistently elevated d-dimer and C reactive protein, respectively. 38% of chest radiographs remained abnormal with 9% deteriorating. Systematic follow-up after hospitalisation with COVID-19 identifies the trajectory of physical and psychological symptom burden, recovery of blood biomarkers and imaging which could be used to inform the need for rehabilitation and/or further investigation.
Pulmonary cavities, the hallmark of tuberculosis (TB), are characterized by high mycobacterial load and perpetuate the spread of M. tuberculosis. The mechanism of matrix destruction resulting in ...cavitation is not well defined. Neutrophils are emerging as key mediators of TB immunopathology and their influx are associated with poor outcomes. We investigated neutrophil-dependent mechanisms involved in TB-associated matrix destruction using a cellular model, a cohort of 108 patients, and in separate patient lung biopsies. Neutrophil-derived NF-kB-dependent matrix metalloproteinase-8 (MMP-8) secretion was up-regulated in TB and caused matrix destruction both in vitro and in respiratory samples of TB patients. Collagen destruction induced by TB infection was abolished by doxycycline, a licensed MMP inhibitor. Neutrophil extracellular traps (NETs) contain MMP-8 and are increased in samples from TB patients. Neutrophils lined the circumference of human pulmonary TB cavities and sputum MMP-8 concentrations reflected TB radiological and clinical disease severity. AMPK, a central regulator of catabolism, drove neutrophil MMP-8 secretion and neutrophils from AMPK-deficient patients secrete lower MMP-8 concentrations. AMPK-expressing neutrophils are present in human TB lung biopsies with phospho-AMPK detected in nuclei. These data demonstrate that neutrophil-derived MMP-8 has a key role in the immunopathology of TB and is a potential target for host-directed therapy in this infectious disease.
Mycobacterium tuberculosis (M.tb) infection causes marked tissue inflammation leading to lung destruction and morbidity. The inflammatory extracellular microenvironment is acidic, however the effect ...of this acidosis on the immune response to M.tb is unknown. Using RNA-seq we show that acidosis produces system level transcriptional change in M.tb infected human macrophages regulating almost 4000 genes. Acidosis specifically upregulated extracellular matrix (ECM) degradation pathways with increased expression of Matrix metalloproteinases (MMPs) which mediate lung destruction in Tuberculosis. Macrophage MMP-1 and -3 secretion was increased by acidosis in a cellular model. Acidosis markedly suppresses several cytokines central to control of M.tb infection including TNF-α and IFN-γ. Murine studies demonstrated expression of known acidosis signaling G-protein coupled receptors OGR-1 and TDAG-8 in Tuberculosis which are shown to mediate the immune effects of decreased pH. Receptors were then demonstrated to be expressed in patients with TB lymphadenitis. Collectively, our findings show that an acidic microenvironment modulates immune function to reduce protective inflammatory responses and increase extracellular matrix degradation in Tuberculosis. Acidosis receptors are therefore potential targets for host directed therapy in patients.
The COVID-19 pandemic is a global public health crisis, with considerable mortality and morbidity exerting pressure on health-care resources, including critical care. An excessive host inflammatory ...response in a subgroup of patients with severe COVID-19 might contribute to the development of acute respiratory distress syndrome (ARDS) and multiorgan failure. Timely therapeutic intervention with immunomodulation in patients with hyperinflammation could prevent disease progression to ARDS and obviate the need for invasive ventilation. Granulocyte macrophage colony-stimulating factor (GM-CSF) is an immunoregulatory cytokine with a pivotal role in initiation and perpetuation of inflammatory diseases. GM-CSF could link T-cell-driven acute pulmonary inflammation with an autocrine, self-amplifying cytokine loop leading to monocyte and macrophage activation. This axis has been targeted in cytokine storm syndromes and chronic inflammatory disorders. Here, we consider the scientific rationale for therapeutic targeting of GM-CSF in COVID-19-associated hyperinflammation. Since GM-CSF also has a key role in homoeostasis and host defence, we discuss potential risks associated with inhibition of GM-CSF in the context of viral infection and the challenges of doing clinical trials in this setting, highlighting in particular the need for a patient risk-stratification algorithm.
Correspondence to Professor Joanna C Porter, Centre for Inflammation and Tissue Repair, UCL Respiratory, University College London Division of Medicine, WC1E 6JF London, UK; joanna.porter@ucl.ac.uk ...Drug-induced interstitial lung disease (DILD) with an estimated incidence of approximately 4.1–12.4 cases/million/year is implicated in ~5% of ILD cases.1 Data vary by country, with DILD more commonly diagnosed in Japan, perhaps due to higher reporting.2 The Common Terminology Criteria for Adverse Events (CTCAE) scale3 (table 1) helps quantify severity and treatment includes cessation of the drug and, in more severe cases, corticosteroid use. At least 350 drugs have been implicated in causing lung toxicity, or pneumonitis, across a spectrum from mild radiological infiltrates to life-threatening respiratory failure.4 This heterogeneity of presentation and lack of diagnostic standards, with rechallenge to confirm toxicity rarely justified, makes DILD difficult to identify, even at individual patient level.4 The result is a heavy reliance on databases such as pneumotox5 that collate evidence from the literature, often case reports or small series, but with no large-scale assessment.Table 1 Common Terminology Criteria for Adverse Events (CTCAE), V.5.0 Adverse event Grade 1 Grade 2 Grade 3 Grade 4 Grade 5 Pneumonitis* Asymptomatic; clinical or diagnostic observations only; intervention not indicated Symptomatic; medical intervention indicated; limiting instrumental ADL† Severe symptoms; limiting self-care ADL†; oxygen indicated Life-threatening respiratory compromise: urgent intervention indicated (eg, tracheostomy or intubation) Death *Pneumonitis: a disorder characterised by inflammation focally or diffusely affecting the lung parenchyma. †Instrumental activities of daily living (ADLs) include preparing meals, shopping, using the telephone, managing money. ...it remains unclear how representative this highly select population is of the whole DILD spectrum (figure 1).
We thank P-S. Bellaye and co-workers for their considered and insightful response. Given their finding of
18
Ffluoromisonidazole (
18
FF-MISO) uptake in the bleomycin mouse model of fibrosis 1, we ...too were surprised not to demonstrate a similar signal in patients with idiopathic pulmonary fibrosis (IPF). However, as acknowledged, there are other examples of positron emission tomography (PET) tracers, such as cis-4-
18
F-fluoro-
l
-proline, yielding PET signals in animal lung fibrosis models that have not been replicated in humans with fibrotic lung disease 2, 3.
In vivo
PET imaging in IPF patients shows no significant evidence of lung tissue hypoxia
https://bit.ly/3fywY7K
Background 18Fluorine-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) CT imaging has been used in many inflammatory and infectious conditions to differentiate areas of increased ...metabolic activity. FDG uptake differs between areas of normal lung parenchyma and interstitial lung disease (ILD).ObjectivesIn this study, we investigated whether FDG-PET/CT parameters were associated with a change in the quality of life (QoL) in patients with ILD over 4 years of follow-up.MethodsPatients underwent PET-CT imaging at diagnosis and were followed up with annual QoL assessment using the St George’s Respiratory Questionnaire (SGRQ) until death or 4 years of follow-up. Maximum standard uptake value (SUVmax) and Tissue-to-Background Ratio (TBR) were assessed against SGRQ overall and subscale scores.Results193 patients (94 patients in the idiopathic pulmonary fibrosis (IPF) subgroup and 99 patients in the non-IPF subgroup) underwent baseline FDG-PET/CT imaging and QoL assessment. Weak-to-moderate correlation was observed between baseline SUVmax and SGRQ scores in both ILD subgroups. No relationship was observed between baseline SUVmax or TBR and change in SGRQ scores over 4 years of follow-up. In the IPF subgroup, surviving patients reported a decline in QoL at 4 years post diagnosis whereas an improvement in QoL was seen in surviving patients with non-IPF ILD.ConclusionsWeak-to-moderate positive correlation between baseline SUVmax and SGRQ scores was observed in both ILD subgroups (IPF:rs=0.187, p=0.047, non-IPF: rs=0.320, p=0.001). However, baseline SUVmax and TBR were not associated with change in QoL in patients with IPF and non-IPF ILD over 4 years of follow-up. At 4 years post diagnosis, surviving patients with IPF reported declining QoL whereas improvement was seen in patients with ILD who did not have IPF.
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