Airborne occupational exposures associated with pulmonary sarcoidosis: a systematic review and meta-analysis.

The aetiology and pathophysiology of sarcoidosis is ill defined-current hypotheses centre on complex genetic-immune-environmental interactions in an individual, triggering a granulomatous process. The aim of this systematic review is to define and describe which airborne occupational exposures (aOE) are associated with and precede a diagnosis of pulmonary sarcoidosis. The methodology adopted for the purpose was systematic review and meta-analyses of ORs for specified aOE associated with pulmonary sarcoidosis (DerSimonian Laird random effects model (pooled log estimate of OR)). Standard search terms and dual review at each stage occurred. A compendium of aOE associated with pulmonary sarcoidosis was assembled, including mineralogical studies of sarcoidosis granulomas. N=81 aOE were associated with pulmonary sarcoidosis across all study designs. Occupational silica, pesticide and mould or mildew exposures were associated with increased odds of pulmonary sarcoidosis. Occupational nickel and aluminium exposure were associated with a non-statistically significant increase in the odds of pulmonary sarcoidosis. Silica exposure associated with pulmonary sarcoidosis was reported most frequently in the compendium (n=33 studies) and was the most common mineral identified in granulomas. It was concluded that aOE to silica, pesticides and mould or mildew are associated with increased odds of pulmonary sarcoidosis. Equipoise remains concerning the association and relationship of metal dusts with pulmonary sarcoidosis.

A multicentre observational study of the prevalence, management, and outcomes of subsegmental pulmonary embolism.

BACKGROUND: The incidence of subsegmental pulmonary embolism (SSPE) has increased with improvements in imaging technology. There is clinical equipoise for SSPE treatment, with conflicting evidence of improved mortality or reduced venous thromboembolism recurrence with anticoagulation. SSPE studies have significant heterogeneity and often lack adequately matched disease comparator groups. OBJECTIVES: To determine the prevalence, management, and outcomes of SSPE and compare them to patients with main, lobar, segmental, and no pulmonary embolism (PE). PATIENTS/METHODS: All adult patients undergoing CT pulmonary angiography (CTPA) between 2013 and 2019, at 3 UK hospitals were included in the study. CTPA reports were text mined for language relating to PE, and then further manually screened for the presence and anatomical location of PE. Patient groups were propensity matched by age, sex, and year of CTPA prior to analysis. 3-month outcomes of major bleeding, VTE recurrence, and death were recorded. RESULTS: 79 (3.8%) SSPEs were identified from 2,055 diagnoses of PE, and 14,300 CTPA reports. 44 (56%) of SSPEs were single artery emboli, 25 (32%) were multiple unilateral emboli, and 10 (13%) were multiple bilateral emboli. Mortality, VTE recurrence and major bleeding were similar at 3 months across all groups. 87.3% of SSPE imaging reports had an additional radiological diagnosis, with pleural effusion (30%), consolidation (19%), and cardiomegaly (19%) being the most common. CONCLUSION: The prevalence of SSPE was 3.8% of all PEs and there were a substantial number of additional radiological findings in the SSPE group that may have accounted for their symptoms.

An update on hypersensitivity pneumonitis: what a clinician wants to know.

PURPOSE OF REVIEW: A recent international collaboration has updated the clinical definition and diagnostic recommendations for hypersensitivity pneumonitis, focusing on fibrotic and non-fibrotic phenotypes. However, how these transfer to clinical practice and their impact upon clinical management and prognosis of hypersensitivity pneumonitis is unclear. This review will focus on recent advances in the understanding of the clinical aspects of hypersensitivity pneumonitis, predominantly its epidemiology, diagnosis, classification and treatment. RECENT FINDINGS: Hypersensitivity pneumonitis is a rare disease within the general population, with variable geographical incidence because of environmental, cultural and occupational factors. Confidence in diagnosis relies upon the presence of clinical features with a temporal relationship to an associated exposure, radiological and histopathological features, bronchiolo-alveolar lavage lymphocytosis and precipitating antibodies/specific immunoglobulin G to antigens. Although emerging evidence regarding nintedanib use in progressive fibrotic interstitial lung disease is promising, the majority of therapies (corticosteroids and immunosuppressive agents) used traditionally in hypersensitivity pneumonitis lack a robust evidence base. SUMMARY: With a clear definition of fibrotic and nonfibrotic hypersensitivity pneumonitis phenotypes now established, clinical research trials (predominantly randomized controlled trials) should clarify and resolve the discussion regarding antigen avoidance, corticosteroid therapy, immunosuppressive therapy and antifibrotic therapy in fibrotic and nonfibrotic subtypes of hypersensitivity pneumonitis.

Exploring the causes of COPD misdiagnosis in primary care: A mixed methods study.

BACKGROUND: Within primary care there exists a cohort of patients misdiagnosed with Chronic Obstructive Pulmonary Disease (COPD). Misdiagnosis can have a detrimental impact on healthcare finances and patient health and so understanding the factors leading to misdiagnosis is crucial in order to reduce misdiagnosis in the future. The objective of this study is to understand and explore the perceived causes of COPD misdiagnosis in primary care. METHODS: A sequential mixed methods study, quantifying prevalence and features of patients misdiagnosed with COPD in primary care followed by a qualitative analysis to explore perceived causes of misdiagnosis. Quantitative data was collected for 206 patients identified as misdiagnosed with COPD within the INTEGR COPD study (NCT03482700). Qualitative data collected from 21 healthcare professionals involved in providing COPD care and 8 misdiagnosed patients who were recruited using a maximum variation purposive sampling. RESULTS: Misinterpretation of spirometry results was the prevailing factor leading to patients initially being misdiagnosed with COPD, affecting 59% of misdiagnosed patients in this cohort. Of the 99 patients who were investigated for their underlying diagnosis; 41% had normal spirometry and 40% had asthma. Further investigation through qualitative methodology uncovered reluctance to challenge historical misdiagnoses and challenges in differential diagnosis as the underlying explanations for COPD misdiagnosis in this cohort. CONCLUSIONS: Patients historically diagnosed with COPD without spirometric evidence are at risk of remaining labelled and treated for COPD despite non-obstructive respiratory physiology, leading to a persistent cohort of patients misdiagnosed with COPD in primary care. The lack of spirometry services during and after the COVID19 pandemic in primary care risks adding to the cohort of misdiagnosed patients. Support from respiratory specialists can potentially help to reduce the prevalence of COPD misdiagnosis in primary care. TRIAL REGISTRATION: NCT03482700.

Novel occupational causes of hypersensitivity pneumonitis.

PURPOSE OF REVIEW: Hypersensitivity pneumonitis (HP) remains a challenging diagnosis, and a cause is not established in up to 50% of cases. This paper aims to update clinicians on traditional and novel occupational causes of HP, and clinical tools for identifying of causative exposures and antigens. RECENT FINDINGS: Metalworking fluid has become the most frequently cited occupational cause of HP, though geographical variations in exposures exist. Occupational HP is usually associated with work-related symptoms. Systematically derived questionnaires and compendia for HP have been developed for use in cryptogenic disease, though have previously lacked validation; these may help identify inciting antigens or relevant occupational exposures. SUMMARY: Clinicians should enquire about job roles and work-relatedness of symptoms when considering a diagnosis of HP. Outbreaks of metalworking fluid associated HP from around the world are well described, so clinicians should remain vigilant. The usual classification for causative antigen includes animal and plant proteins, fungi, bacteria, low-molecular weight chemicals and metals; however novel occupational exposures and work processes are frequently reported.

Occupational lung disease: when should I think of it and why is it important?

Exposure to toxic inhalants in the workplace has the potential to cause (in susceptible individuals) almost any major type of lung disease, such as asthma, COPD and interstitial lung diseases. Patients with occupational lung disease will often present to or will be managed by respiratory specialists without training in occupational respiratory medicine, and patients (or their clinicians) may not identify a link between their disease and their current or a past job. Without an awareness of the range of different occupational lung diseases that exist, their similarity to their non-occupational counterparts, and without directed questioning, these conditions may go unidentified. Patients with occupational lung diseases are often in lower paid work and are disproportionally affected by health inequality. Both clinical and socioeconomic outcomes generally improve if cases are identified early. This allows appropriate advice to be given about the risks of ongoing exposure, clinical management, occupational mobility and, in some cases, eligibility for legal compensation. As respiratory professionals, it is important that these cases are not missed, and if needed, are discussed with a physician with specialised expertise. Here we describe some of the most common occupational lung diseases and outline the diagnostic and treatment approach.

Pulmonary function test and computed tomography features during follow-up after SARS, MERS and COVID-19: a systematic review and meta-analysis.

Background: The COVID-19 pandemic follows severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) coronavirus epidemics. Some survivors of COVID-19 infection experience persistent respiratory symptoms, yet their cause and natural history remain unclear. Follow-up after SARS and MERS may provide a model for predicting the long-term pulmonary consequences of COVID-19. Methods: This systematic review and meta-analysis aims to describe and compare the longitudinal pulmonary function test (PFT) and computed tomography (CT) features of patients recovering from SARS, MERS and COVID-19. Meta-analysis of PFT parameters (DerSimonian and Laird random-effects model) and proportion of CT features (Freeman-Tukey transformation random-effects model) were performed. Findings: Persistent reduction in the diffusing capacity for carbon monoxide following SARS and COVID-19 infection is seen at 6 months follow-up, and 12 months after MERS. Other PFT parameters recover in this time. 6 months after SARS and COVID-19, ground-glass opacity, linear opacities and reticulation persist in over 30% of patients; honeycombing and traction dilatation are reported less often. Severe/critical COVID-19 infection leads to greater CT and PFT abnormality compared to mild/moderate infection. Interpretation: Persistent diffusion defects suggestive of parenchymal lung injury occur after SARS, MERS and COVID-19 infection, but improve over time. After COVID-19 infection, CT features are suggestive of persistent parenchymal lung injury, in keeping with a post-COVID-19 interstitial lung syndrome. It is yet to be determined if this is a regressive or progressive disease.