Glycated Hemoglobin (HbA1c) as a Predictor of Outcomes during Acute Exacerbations of Chronic Obstructive Pulmonary Disease.

Systemic inflammation may be the common denominator between COPD and type 2 diabetes and may explain the correlation in both diseases' development and progress. The aim of this prospective observational study is to examine the prognostic value of glycated hemoglobin levels (HbA1c) and HbA1c-adjusted glycemic variables (glycemic gap, stress hyperglycemia ratio και modified stress hyperglycemia ratio) in an acute exacerbation of COPD (AECOPD) as well as in COPD disease's morbidity and mortality during the following year. We evaluated patients hospitalized only for COPD exacerbations. Levels of HbA1c and HbA1c-adjusted glycemic variables were recorded upon admission. The study outcomes included duration of hospital stay, need for mechanical ventilation and exacerbation outcome. All subjects were followed up for one year. A total of 156 patients were included in the study (74.4% men, age [mean ± SD] 72 ± 7 years). Patients (21.8%) had type 2 diabetes and 67.9% of patients were receiving ICS treatment. The median value of HbA1c was 5.9 (IQR: 5.4, 6.5). Necessity for mechanical ventilation was significantly higher for patients with lower values of HbA1c [median: 5.3 (IQR 5.02, 6.3) vs. 5.9 (IQR 5.5, 6.5), p = .038]. However, duration of hospitalization, death during hospitalization as well as the number of new exacerbation events, time to next exacerbation and mortality during the following year did not differ significantly. Moreover, none of the HbA1c-adjusted glycemic variables examined, demonstrated any statistical significance. In conclusion neither the preceding nor the present glycemic state exhibit a predictive value regarding short- or long-term outcomes of an AECOPD.

Sirtuin 1: Endocan and Sestrin 2 in Different Biological Samples in Patients with Asthma. Does Severity Make the Difference?

BACKGROUND: Sestrin 2, Endocan, and Sirtuin 1 are distinct molecules with some biologic actions associated with asthma pathophysiology. The aim of the present study was to determine the molecular level differences attributable to underlying asthma severity. METHODS: We initially recruited 85 asthmatics with a wide spectrum of severity. All of the patients were optimally treated according to current guidelines. Demographics, test results of lung function, and treatment regimes of all patients were recorded. Sestrin 2, Endocan, and Sirtuin 1 were measured in different biological samples (sputum with two processing methods and serum). RESULTS: A total of 60 patients (35 with severe asthma) were analyzed, since 25 patients failed to produce an adequate sample of sputum. Patients with severe asthma showed significantly higher values for Sestrin 2 [pg/mL], measured in both sputum supernatant and cell pellet, compared to those with mild to moderate asthma [9524 (5696, 12,373) vs. 7476 (4265, 9273) p = 0.029, and 23,748 (15,280, 32,742) vs. 10,084 (3349, 21,784), p = 0.008, respectively]. No other significant differences were observed. No significant associations were observed between biomarkers, inflammatory cells, and lung function. CONCLUSION: Sestrin 2 is increased in patients with severe asthma as part of a mechanism that may modify structural alterations through the imbalance between oxidative stress and antioxidant activity.