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Molecular Imaging of Activated Platelets Allows the Detection of Pulmonary Embolism with Magnetic Resonance Imaging.

Sci Rep. 2016;6:25044

Authors: Heidt T, Ehrismann S, Hövener JB, Neudorfer I, Hilgendorf I, Reisert M, Hagemeyer CE, Zirlik A, Reinöhl J, Bode C, Peter K, von Elverfeldt D, von Zur Muhlen C

Abstract
Early and reliable detection of pulmonary embolism (PE) is critical for improving patient morbidity and mortality. The desire for low-threshold screening for pulmonary embolism is contradicted by unfavorable radiation of currently used computed tomography or nuclear techniques, while standard magnetic resonance imaging still struggles to provide sufficient diagnostic sensitivity in the lung. In this study we evaluate a molecular-targeted contrast agent against activated platelets for non-invasive detection of murine pulmonary thromboembolism using magnetic resonance imaging. By intravenous injection of human thrombin, pulmonary thromboembolism were consistently induced as confirmed by immunohistochemistry of the lung. Magnetic resonance imaging after thrombin injection showed local tissue edema in weighted images which co-localized with the histological presence of pulmonary thromboembolism. Furthermore, injection of a functionalized contrast agent targeting activated platelets provided sensitive evidence of focal accumulation of activated platelets within the edematous area, which, ex vivo, correlated well with the size of the pulmonary embolism. In summary, we here show delivery and specific binding of a functionalized molecular contrast agent against activated platelets for targeting pulmonary thromboembolism. Going forward, molecular imaging may provide new opportunities to increase sensitivity of magnetic resonance imaging for detection of pulmonary embolism.

PMID: 27138487 [PubMed - as supplied by publisher]

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Pharmacological Management of Elderly Patients with Asthma-Chronic Obstructive Pulmonary Disease Overlap Syndrome: Room for Speculation?

Drugs Aging. 2016 Apr 30;

Authors: Castiglia D, Battaglia S, Benfante A, Sorino C, Scichilone N

Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are two distinct diseases that share a condition of chronic inflammation of the airways and bronchial obstruction. In clinical settings, it is not rare to come across patients who present with clinical and functional features of both diseases, posing a diagnostic dilemma. The overlap condition has been termed asthma-COPD overlap syndrome (ACOS), and mainly occurs in individuals with long-standing asthma, especially if they are also current or former smokers. Patients with ACOS have poorer health-related quality of life and a higher exacerbation rate than subjects with asthma or COPD alone. Whether ACOS is a distinct nosological entity with genetic variants or rather a condition of concomitant diseases that overlap is still a matter of debate. However, there is no doubt that extended life expectancy has increased the prevalence of asthma and COPD in older ages, and thus the probability that overlap conditions occur in clinical settings. In addition, age-associated changes of the lung create the basis for the two entities to converge on the same subject. ACOS patients may benefit from a stepwise treatment similar to that of asthma and COPD; however, the proposed therapeutic algorithms are only speculative and extrapolated from studies that are not representative of the ACOS population. Inhaled corticosteroids are the mainstay of therapy, and always in conjunction with long-acting bronchodilators. The potential heterogeneity of the overlap syndrome in terms of inflammatory features (T helper-1 vs. T helper-2 pathways) may be responsible for the different responses to treatments. The interaction between respiratory drugs and concomitant diseases should be carefully evaluated. Similarly, the effect of non-respiratory drugs, such as aspirin, statins, and β-blockers, on lung function needs to be properly assessed.

PMID: 27138954 [PubMed - as supplied by publisher]

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Serum Procalcitonin for Differential Diagnosis of Acute Exacerbation and Bacterial Pneumonia in Patients With Interstitial Lung Disease.

Am J Med Sci. 2016 May;351(5):499-505

Authors: Sim JK, Oh JY, Lee EJ, Hur GY, Lee SH, Lee SY, Lee SY, Kim JH, Shin C, Shim JJ, In KH, Kang KH, Min KH

Abstract
BACKGROUND: Acute exacerbation and bacterial pneumonia are major life-threatening conditions in patients with interstitial lung disease (ILD). The rapid recognition of these 2 different conditions is important for their proper treatment. An elevated procalcitonin (PCT) level is commonly detected in patients with bacterial infections. This study assessed the usefulness of the serum PCT level as a biomarker for the differential diagnosis of acute exacerbation and bacterial pneumonia in patients with ILD.
MATERIALS AND METHODS: In this prospective observational study, we enrolled patients with ILD who had experienced recently progressive dyspnea and exhibited new infiltrations on chest radiographs. We classified these patients into an acute exacerbation group and a bacterial pneumonia group and compared their baseline characteristics and laboratory parameters, including the PCT level.
RESULTS: Of 21 patients with ILD, 9 patients had bacterial pneumonia. Both the groups showed similar baseline characteristics. The bacterial pneumonia group demonstrated a high PCT level. The PCT level in the acute exacerbation group was significantly lower than that in the bacterial pneumonia group (0.05 versus 0.91ng/mL, respectively; P < 0.001). Other parameters, such as the C-reactive protein level, leukocyte count and body temperature, were also lower in the acute exacerbation group. At a cutoff value of 0.1ng/mL, the sensitivity, specificity and negative predictive values of the serum PCT level were 88.9%, 100.0% and 92.3%, respectively.
CONCLUSIONS: These findings suggest that the serum PCT level is useful in the differential diagnosis of acute exacerbation and bacterial pneumonia in patients with ILD.

PMID: 27140709 [PubMed - as supplied by publisher]

The aim of this document was to provide a critical review of the current knowledge on hypersensitivity pneumonitis caused by the occupational environment and to propose practical guidance for the diagnosis and management of this condition. Occupational hypersensitivity pneumonitis (OHP) is an immunologic lung disease resulting from lymphocytic and frequently granulomatous inflammation of the peripheral airways, alveoli, and surrounding interstitial tissue which develops as the result of a non-IgE-mediated allergic reaction to a variety of organic materials or low molecular weight agents that are present in the workplace. The offending agents can be classified into six broad categories that include bacteria, fungi, animal proteins, plant proteins, low molecular weight chemicals, and metals. The diagnosis of OHP requires a multidisciplinary approach and relies on a combination of diagnostic tests to ascertain the work relatedness of the disease. Both the clinical and the occupational history are keys to the diagnosis and often will lead to the initial suspicion. Diagnostic criteria adapted to OHP are proposed. The cornerstone of treatment is early removal from exposure to the eliciting antigen, although the disease may show an adverse outcome even after avoidance of exposure to the causal agent.