Search

Background: Remodeling is a crucial feature of severe asthma and may be associated with activation of the allergic cascade by immunoglobulin E (IgE). Omalizumab, an anti-IgE monoclonal antibody, effectively targets the severe allergic asthma phenotype. Pregnancy-associated plasma protein-A (PAPP-A) is an insulin-like growth factor binding protein-4 (IGFBP-4) protease, increasing local insulin-like growth factor (IGF)-1 concentrations, which in turn initiating a cascade involved in the regulation of cell growth, differentiation, and proliferation in various tissues. In the present study, we evaluated the effects of omalizumab on serum PAPP-A, IGFBP-4, and IGF-1 levels in subjects with severe allergic asthma. Methods: We studied 36 asthmatic subjects and 36 healthy controls. An ultrasensitive enzyme-linked immunosorbent assay (ELISA) kit was used to measure serum PAPP-A levels, and routine commercial ELISA kits were employed to assess serum levels of IGF-1, IGFBP-4 in control subjects and asthmatic subjects before therapy (baseline) and after six months of omalizumab therapy in patients with severe asthma. Results: Compared to control subjects, serum PAPP-A and IGFB-4 levels were significantly higher in asthmatic subjects (both p values < 0.001). However, the serum IGF-I levels of asthmatic subjects were similar to those of control subjects (p > 0.05). In asthma subjects, 6-month omalizumab treatment significantly decreased the serum PAPP-A (p < 0.001), IGF-I (p = 0.031), and IGFB4 (p = 0.025) levels. Conclusion: PAPP-A level may be a useful biomarker for predicting airway remodeling in patients with severe asthma receiving omalizumab, and may also reflect the response to treatment. [ABSTRACT FROM AUTHOR]

Background: Obstructive sleep apnea (OSA) is the most common sleep disorder affecting 2-4 % of the adult population. In addition to several potential mechanisms, inflammation is one of the suggested etiological factors in OSA. Fractalkine/CX3CL1 which is detected in activated or stressed endothelium, smooth muscle cells, skeletal muscle cells, macrophages, neurons, and hepatocytes is an inflammatory marker and attracts attention of sleep specialists in OSA pathogenesis. In this study, we had two goals. The first one was to investigate the role of fractalkine in OSA pathogenesis while the second one was to detect the impact of OSA treatment with positive airway pressure (PAP) on serum fractalkine levels. Method: This study included 34 patients (6 females, 28 males) diagnosed as OSA and 20 healthy controls (4 females, 16 males). Initial serum fractalkine levels of both groups were first evaluated in order to demonstrate any potential relation of OSA with fractalkine. Subsequently, serum fractalkine levels of the OSA patients were evaluated following 1 week of PAP treatment to demonstrate the impact of PAP treatment on serum fractalkine levels. Results: Although there was no significant difference between OSA patients and healthy controls by means of plasma fractalkine levels ( p, 0.67) statistically, plasma fractalkine levels significantly decreased in OSA patients after 1 week of PAP treatment ( p, 0.001). Conclusion: This study showed that fractalkine, a potential mediator of chronic inflammation, was not sensitive in diagnosing OSA but might be an indicator of the success of OSA treatment. [ABSTRACT FROM AUTHOR]

Copyright of Turkiye Klinikleri Archives of Lung is the property of Turkiye Klinikleri and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background. Asthma is characterized by inflammation and airway hyperesponsiveness, which results in episodic airflow obstruction. A relationship between inflammation and insulin resistance (IR) has been previously characterized, and asthma is known to correlate with increasing IR. Thus, we tested whether patients with asthma bronchiale exhibited abnormally low glucose tolerance. The aim of this study was to compare the occurrence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), two precursors of type 2 diabetes mellitus (DM), in patients with asthma bronchiale and paired control patients. Patients and Methods. We examined patients diagnosed with asthma bronchiale. We excluded patients taking any medications other than inhaler broncodilators, patients with a history of other systemic illness, and patients with any diabetic risk factors. Age- and sex-matched healthy volunteers were included as the control group in this study. History, physical examination, and laboratory analyses were performed for both study and control groups. Results. Mean age of the study group was 40.3 ± 7.8 (F/M: 32/19), and mean BMI of the study group was 26.7 ± 2.2. Mean age of the control group was 39.5 ± 6.7 (F/M: 25/15) and mean BMI of the control group was 26.0 ± 2.1. Fasting blood glucose (FBG), Pg2hBG, Plasma insulin, Homeostasis Model Assessment-Insulin Resistance (HOMA IR), IFG, IGT, both IFG and IGT and (LDL) C levels were significantly higher in the asthmatic group, while HDL C levels were significantly higher in the control group. Conclusion. Our results suggest that disturbance of the glucose metabolism caused by inflammation-induced insulin resistance may occur in asthmatic patients and that this phenomenon may increase the risk of diabetes mellitus in these individuals. [ABSTRACT FROM AUTHOR]