Numerous biomarkers have been evaluated for the diagnosis, assessment of disease activity, prognosis, and response to treatment in sarcoidosis. In this report, we discuss the clinical and research utility of several biomarkers used to evaluate sarcoidosis. Areas covered: The sarcoidosis biomarkers discussed include serologic tests, imaging studies, identification of inflammatory cells and genetic analyses. Literature was obtained from medical databases including PubMed and Web of Science. Expert commentary: Most of the biomarkers examined in sarcoidosis are not adequately specific or sensitive to be used in isolation to make clinical decisions. However, several sarcoidosis biomarkers have an important role in the clinical management of sarcoidosis when they are coupled with clinical data including the results of other biomarkers.

Lung cancer is considered one of the most fatal malignant neoplasms because of its late detection. Detecting molecular markers in samples from routine bronchoscopy, including many liquid-based cytology procedures, such as bronchoalveolar lavage fluid (BALF), could serve as a favorable technique to enhance the efficiency of a lung cancer diagnosis. BALF analysis is a promising approach to evaluating the tumor progression microenvironment. BALF’s cellular and non-cellular components dictate the inflammatory response in a cancer-proliferating microenvironment. Furthermore, it is an essential material for detecting clinically significant predictive and prognostic biomarkers that may aid in guiding treatment choices and evaluating therapy-induced toxicities in lung cancer. In the present article, we have reviewed recent literature about the utility of BALF analysis for detecting markers in different stages of tumor cell metabolism, employing either specific biomarker assays or broader omics approaches.

Background. Because pulmonary sarcoidosis often affects the airway, it is commonly confused with asthma. Methods. This article reviews the mechanisms of airflow obstruction in sarcoidosis, the symptoms associated with this phenomenon, and the approach to distinguish sarcoidosis from asthma. Discussion. Because asthma is highly likely in a patient with wheeze, cough, and chest tightness, sarcoidosis is usually not considered unless the patient has extrapulmonary manifestations of sarcoidosis or a family history of the disease. When pulmonary sarcoidosis is a consideration, a chest radiograph should be performed. A chest radiograph should also be performed in an asthmatic patient when the presentation is atypical, or fails to respond to standard asthma treatment; chest radiography should be performed in this situation to consider not only pulmonary sarcoidosis but also other possible cardiopulmonary disorders. In a patient with confirmed pulmonary sarcoidosis, the diagnosis of concomitant asthma is problematic. The symptoms associated with the two disorders are often identical. Airflow obstruction is common in sarcoidosis so that pulmonary function testing is unlikely to differentiate these two diseases. Demonstration of airway hyperreactivity may fail to distinguish these disorders as this is common in sarcoidosis. Serum IgE, serum angiotensin-converting enzyme levels, sputum eosinophilia, and exhaled nitric oxide measurements show promise as distinguishing tests, although they have not been studied specifically. Pulmonary imaging is probably of limited value unless baseline studies are available for comparison. We suspect that historical information will be more useful in distinguishing these two diseases. Not infrequently, it may be impossible to exclude or confirm an asthmatic component in a confirmed pulmonary sarcoidosis patient. Fortunately, exacerbations of both these diseases are often treated with systemic corticosteroids initially. Significant variability in pulmonary symptoms and airflow obstruction suggest that an asthma component is present, and inhaled corticosteroids and bronchodilators should be considered in these cases, Conclusions. Asthma and sarcoidosis share many of the same symptoms, as sarcoidosis commonly affects the airways. Therefore, it is problematic to distinguish these two diseases. In this article, we have outlined an approach to assess the presence of each of these diseases and an approach to therapy.

Obstructive sleep apnea (OSA) is a sleeping disorder caused by complete or partial disturbance of breathing during the night. Existing screening methods include questionnaire-based evaluations which are time-consuming, vary in specificity, and are not globally adopted. Point-of-care ultrasound (PoCUS), on the other hand, is a painless, inexpensive, portable, and useful tool that has already been introduced for the evaluation of upper airways by anesthetists. PoCUS could also serve as a potential screening tool for the diagnosis of OSA by measuring different airway parameters, including retropalatal pharynx transverse diameter, tongue base thickness, distance between lingual arteries, lateral parapharyngeal wall thickness, palatine tonsil volume, and some non-airway parameters like carotid intima–media thickness, mesenteric fat thickness, and diaphragm characteristics. This study reviewed previously reported studies to highlight the importance of PoCUS as a potential screening tool for OSA.

Background The objective of our study was to assess the possible relationship between splenic F-18-fluorodeoxyglucose (¹⁸F-FDG) uptake and other established biochemical markers of sarcoidosis activity. Patients and methods Thirty treatment-naive sarcoidosis patients were prospectively enrolled in this study. They underwent biochemical laboratory tests, including serum interleukin-2 receptor (sIL-2R), serum C-reactive protein, serum angiotensin-I converting enzyme, and 24-h urine calcium levels, and a whole-body combined ¹⁸F-FDG PET/computed tomography (PET/CT) scan as a part of an ongoing study at our institute. These biomarkers were statistically compared in these patients. Results A statistically significant linear dependence was detected between sIL-2R and log-transformed spleen-average standard uptake value (SUV_avg) (R²=0.488, P<0.0001) and log-transformed spleen-maximum standard uptake value (SUV_max) (R²=0.490, P<0.0001). sIL-2R levels and splenic size correlated linearly (Pearson’s r=0.373, P=0.042). Multivariate linear regression analysis revealed that this correlation remained significant after age and sex adjustment (β=0.001, SE=0.001, P=0.024). No statistically significant associations were detected between (a) any two serum biomarkers or (b) between spleen-SUV measurements and any serum biomarker other than sIL-2R. Conclusion Our analysis revealed an association between sIL-2R levels and spleen ¹⁸F-FDG uptake and size, whereas all other serum biomarkers were not significantly associated with each other or with PET ¹⁸F-FDG uptake. Our results suggest that splenic inflammation may be related to the systemic inflammatory response in sarcoidosis that may be associated with elevated sIL-2R levels.