Bronchiectasis is a chronic lung disease characterized by an abnormal dilation of the bronchial lumen caused by weakening or destruction of the muscle or elastic components of the bronchial wall, decreased mucous clearance and frequent infections of the respiratory tract. The golden standard for bronchiectasis diagnosis is high-resolution computed tomography (HRCT) of the chest. Inflammation holds a central role in the development of structural lung changes, as well as airway and lung parenchyma damage. Infection and colonization of the respiratory tract contribute to increased inflammation and further damage to the lung. Upon entry into the respiratory tract, the pathogens activate epithelial cells, macrophages and dendritic cells. Activated inflammatory cells secrete chemical mediators which activate the immune response and thus allow the phagocytosis of pathogens. Early diagnosis, appropriate treatment and interruption of the vicious circle between infection and inflammation in patients suffering from bronchiectasis, prevent the development of structural changes to the airways.

Neurosarcoidosis is a relatively common extrapulmonary form of sarcoidosis. It is characterized by variable clinical presentation, low probability of spontaneous remission, and significant impact on the quality of life, as well as potential increase in mortality. In addition to corticosteroids, other drugs are used in the treatment of neurosarcoidosis, such as methotrexate, azathioprine, mycophenolate mofetil, tumor necrosis factor a (TNF-a) inhibitors, infliximab and adalimumab. In this paper, by reviewing the available literature, we have attempted to consolidate the current knowledge and novelties in the treatment of neurosarcoidosis, for the purpose of assisting physicians in their day-to-day clinical work. Previous studies still favor pulsed doses of corticosteroids, while other forms of therapy have proven beneficial only in individual cases. However, it should be noted that additional research is needed in order to successfully develop individual therapy.

Interstitial lung disease alone can have a poor prognosis, and when associated with pulmonary hypertension there is a significant reduction in survival rates. Since the incidence of pulmonary hypertension in patients with interstitial lung diseases is very high and the symptoms are similar and often unrecognized, our aim is to point out the significance of both coexisting diseases and to prompt clinicians to suspect pulmonary hypertension. Through a brief review of the pathohistological changes, diagnostic methods, and the clinical presentation of these diseases, the similarities and differences that can help in the management of these patients, are shown. The latest treatment guidelines, with a special focus on the impact of antifibrotic treatment (nintedanib and pirfenidone) on pulmonary hypertension, are presented.

Introduction/aim Clinical signs and symptoms of pulmonary embolism (PE) are non-specific, which is why it is commonly not diagnosed on time or sometimes not diagnosed at all. We are presenting a case of pulmonary embolism manifesting with syncope as a dominant symptom. Case report A 74-year-old female patient was hospitalized at the Clinic for Pulmonary Diseases with PE manifested with syncope. At admission, she was afebrile, tachypneic, with normal cardiac function and normal blood tension. Upon auscultation, breathing was muffled with late inspiration crackles above the base of the left lung. There were no other significant findings. The chest X-ray recorded at admission showed a non-homogenous shadow towards the base of the left lung and minimal pleural effusion. The ECG and echocardiography findings were normal. Partial respiratory insufficiency was verified by the acid-base balance analysis. Inflammatory markers were significantly elevated, with erythrocyte sedimentation rate of 30mm/h, fibrinogen of 8.62g/l and D-dimer of 18.6mg/l. Anticardiolipin IgG and IgM antibodies were negative, as well as beta-2 GPI IgG and IgM antibodies. An MDCT lung angiography was performed because of the elevated values of D-dimer and tachypnea, which showed multiple emboli of various sizes in the distal part of the right pulmonary artery and all lobar branches, as well as an embolus in the lobar branch for the lower lobe of the left lung. After a neurology consult, a head CT was ordered because the patient had suffered from loss of consciousness, but there were no pathological densities in the brain. Colour Doppler Ultrasonography of the blood vessels in the lower extremities showed organized thrombosis of the left femoral vein. A vascular surgeon was consulted and he prescribed anticoagulant therapy and an elastic compressive stocking, with control Colour Doppler Ultrasonography to be performed in six months. Conclusion Although syncope is an easily detectable symptom, it is still an unregulated crossroad of many an internal and neurological disease.

Tuberculous pleuritis (TP) is one of the most common extra-pulmonary tuberculosis form. Because of tuberculous pleurisy is hard to diagnose due to slow course of disease and lack of specificity in symptoms and diagnostic methods. In that reason, we need multidisciplinary approach and efficient biomarkers. Acid-fast bacilli (AFB) staining, cultures and pathophysiological biopsy finding from the majority of patients are positive only in less than 10%. Löwenstein culture results need time about 6-8 weeks what delays diagnosis. Adenosine deaminase (ADA) is biomarker with high sensitivity and specificity (more than 90%) and considered as gold standard of biomarkers in the diagnosis of TP. It is very hard to distinguish malignant from TP with lymphocyte predomination, but in patient with malignant pleural effusion the level of ADA is decreased, opposite from TP. ADA in pleural punctate is a fast, simple, efficient and economical way for clarification the etiology of the pleural effusion as tuberculous pleurisy. Also, many studies have proved the role of ADA in the response to treatment for tuberculosis at follow up period