Atherosclerosis is an inflammatory disease. Because high plasma concentrations of cholesterol, in particular those of low-density lipoprotein (LDL) cholesterol, are one of the principal risk factors for atherosclerosis,1 the process of atherogenesis has been considered by many to consist largely of the accumulation of lipids within the artery wall; however, it is much more than that. Despite changes in lifestyle and the use of new pharmacologic approaches to lower plasma cholesterol concentrations,2,3 cardiovascular disease continues to be the principal cause of death in the United States, Europe, and much of Asia.4,5 In fact, the lesions of atherosclerosis represent . . .

https://www.nejm.org/doi/pdf/10.1056/NEJM199901143400207

Atherosclerosis — An Inflammatory Disease

Atherosclerosis is an Inflammatory Disease

This document is an international evidence-based guideline on the diagnosis and management of idiopathic pulmonary fibrosis, and is a collaborative effort of the American Thoracic Society, the European Respiratory Society, the Japanese Respiratory Society, and the Latin American Thoracic Association. It represents the current state of knowledge regarding idiopathic pulmonary fibrosis (IPF), and contains sections on definition and epidemiology, risk factors, diagnosis, natural history, staging and prognosis, treatment, and monitoring disease course. For the diagnosis and treatment sections, pragmatic GRADE evidence-based methodology was applied in a question-based format. For each diagnosis and treatment question, the committee graded the quality of the evidence available (high, moderate, low, or very low), and made a recommendation (yes or no, strong or weak). Recommendations were based on majority vote. It is emphasized that clinicians must spend adequate time with patients to discuss patients' values and preferences and decide on the appropriate course of action.

An Official ATS/ERS/JRS/ALAT Statement: Idiopathic Pulmonary Fibrosis: Evidence-Based Guidelines for Diagnosis and Management

SERIES “ATS/ERS TASK FORCE: STANDARDISATION OF LUNG FUNCTION TESTING” 

Edited by V. Brusasco, R. Crapo and G. Viegi 

Number 5 in this Series 







This section is written to provide guidance in interpreting pulmonary function tests (PFTs) to medical directors of hospital-based laboratories that perform PFTs, and physicians who are responsible for interpreting the results of PFTs most commonly ordered for clinical purposes. Specifically, this section addresses the interpretation of spirometry, bronchodilator response, carbon monoxide diffusing capacity ( D L,CO) and lung volumes.

The sources of variation in lung function testing and technical aspects of spirometry, lung volume measurements and D L,CO measurement have been considered in other documents published in this series of Task Force reports 1–4 and in the American Thoracic Society (ATS) interpretative strategies document 5.

An interpretation begins with a review and comment on test quality. Tests that are less than optimal may still contain useful information, but interpreters should identify the problems and the direction and magnitude of the potential errors. Omitting the quality review and relying only on numerical results for clinical decision making is a common mistake, which is more easily made by those who are dependent upon computer interpretations.

Once quality has been assured, the next steps involve a series of comparisons 6 that include comparisons of test results with reference values based on healthy subjects 5, comparisons with known disease or abnormal physiological patterns ( i.e. obstruction and restriction), and comparisons with self, a rather formal term for evaluating change in an individual patient. A final step in the lung function report is to answer the clinical question that prompted the test.

Poor choices made during these preparatory steps increase the risk of misclassification, i.e. a falsely negative or falsely positive interpretation for a lung function abnormality or a change …

https://erj.ersjournals.com/content/erj/26/5/948.full.pdf

Interpretative strategies for lung function tests

Executive Summary Objectives Participants Evidence Validation Key Messages Introduction Rationale for a Change in the Approach to Classification of Idiopathic Interstitial Pneumonias Development of a New Classification of Idiopathic Interstitial Pneumonia Current Classification of IIP New ATS/ERS Classification Principles Guiding the Assessment of Patients with Idiopathic Interstitial Pneumonias The Diagnostic Process Is Dynamic Clinical Evaluation Radiological Evaluation Role of Surgical Lung Biopsy Unclassifiable Interstitial Pneumonia Bronchoalveolar Lavage Fluid Evaluation Idiopathic Pulmonary Fibrosis Clinical Features Radiologic Features Histologic Features IPF: Areas of Uncertainty Nonspecific Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features NSIP: Areas of Uncertainty Cryptogenic Organizing Pneumonia Clinical Features Radiologic Features Histologic Features COP: Areas of Uncertainty Acute Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features AIP: Areas of Uncertainty Respiratory Bronchiolitis-Associated Interstitial Lung Disease Clinical Features Radiologic Features Histologic Features RB-ILD: Areas of Uncertainty Desquamative Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features DIP: Areas of Uncertainty Lymphoid Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features LIP: Areas of Uncertainty References Appendix

American thoracic society/European respiratory society international multidisciplinary consensus classification of the idiopathic interstitial pneumonias

Hemolytically active C4, C3, C5, and C6, and trace amounts of C1, were present in bronchoalveolar lavage fluid from healthy adult rabbits. Both the alternative and classical pathways were functionally intact through C5. Complement depletion by intravascularly administered cobra venom factor caused a parallel decrease in lavageable C5 from the rabbit's lungs. Whereas BALF C5 had specific activity comparable to serum C5, that of BALF C3 was lower than predicted. This was found to be due to the action of a substance that selectively blocked C3 activation. The inhibitor did not cause irreversible inactivation of C3, and it had no effect on C5 activity. It blocked the formation of EAC423 from EAC42 + C3, but not the lysis of preformed EAC423 + C5-9 or EAC423 rosetting with rabbit neutrophils. Hydrophobic chromatography of BALF separated the activity of the inhibitor from that of C3. Further chromatography showed that it had a net negative charge at physiologic pH, and molecular weight between 14 and 30 kilodaltons. The presence of an inhibitor of C3 activation in the airways would provide control of complement activation in an environment that is constantly exposed to bacteria, dust, and other potential inflammatory stimuli.

Complement activity in normal rabbit bronchoalveolar fluid. Description of an inhibitor of C3 activation.

To study the prevalence of beryllium sensitization (BeS) and chronic beryllium disease (CBD) in a cohort of workers from a nuclear weapons research and development facility. We evaluated 50 workers with BeS with medical and occupational histories, physical examination, chest imaging with HRCT (N=49), and pulmonary function testing. Forty of these workers also underwent bronchoscopy for bronchoalveolar lavage (BAL) and transbronchial biopsies. The mean duration of employment at the facility was 18 yrs and the mean latency (from first possible exposure) to time of evaluation was 32 yrs. Five of the workers had CBD at the time of evaluation (based on histology or HRCT); three others had evidence of probable CBD. These workers with BeS, characterized by a long duration of potential Be exposure and a long latency, had a low prevalence of CBD.

/pdf/low-prevalence-of-chronic-beryllium-disease-among-workers-at-40w0rolodc.pdf

Low prevalence of chronic beryllium disease among workers at a nuclear weapons research and development facility.

The accumulation of inflammatory and immune effector cells in the lungs of patients at early stages of Interstitial lung disease has been well documented, but little is known about the functional activity of these cells, particularly alveolar macrophages. The purpose of the experiments described here was to determine whether alveolar macrophages from patients with idiopathic pulmonary fibrosis (IPF) differed from alveolar macrophages of normal subjects using a model system that assesses a component of cell-mediated immunity. Alveolar macrophages were tested for their ability to phagocytose and kill the facultative intracellular bacterium Listeria monocytogenes. Because this system requires the stimulation of macrophages by antigen-specific T-cells, it allows the assessment of effector functions of macrophages found in the lower respiratory tract of patients with IPF. Data showed that alveolar macrophages from normal subjects both phagocytosed and killed those bacteria. However, alveolar macrophages from p...

Bronchoalveolar Macrophages from Patients with Idiopathic Pulmonary Fibrosis Are Unable To Kill Facultative Intracellular Bacteria

Update in Pulmonary Medicine

Aspergillus terreus is an uncommon cause of human disease. A patient with acute myelomonocytic leukemia is described who developed an invasive pulmonary infection with A terreus characterized by an air-crescent sign on chest roentgenogram. Previous reports of A terreus infections and the pathogenesis and significance of an air-crescent sign in invasive pulmonary aspergillosis are reviewed.

Talmadge E. King

Papers

Complement activity in normal rabbit bronchoalveolar fluid. Description of an inhibitor of C3 activation.

Low prevalence of chronic beryllium disease among workers at a nuclear weapons research and development facility.

Bronchoalveolar Macrophages from Patients with Idiopathic Pulmonary Fibrosis Are Unable To Kill Facultative Intracellular Bacteria

Update in Pulmonary Medicine

Aspergillus terreus causing invasive pulmonary aspergillosis with air-crescent sign.