دورية أكاديمية

Serum lactate dehydrogenase and its isoenzymes as predictors of clinical outcomes in acute exacerbation of chronic obstructive pulmonary disease: a retrospective analysis of a hospitalized cohort

التفاصيل البيبلوغرافية
العنوان: Serum lactate dehydrogenase and its isoenzymes as predictors of clinical outcomes in acute exacerbation of chronic obstructive pulmonary disease: a retrospective analysis of a hospitalized cohort
المؤلفون: Dimitrios Papadopoulos, Vlasios Skopas, Nikolaos Trakas, Eleni Papaefstathiou, Nikolaos Tzogas, Demosthenes Makris, Zoe Daniil, Konstantinos Gourgoulianis
المصدر: Monaldi Archives for Chest Disease (2023)
بيانات النشر: PAGEPress Publications, 2023.
سنة النشر: 2023
المجموعة: LCC:Medicine
مصطلحات موضوعية: Lactate dehydrogenase, LDH isoenzymes, COPD acute exacerbation, COPD outcomes, Medicine
الوصف: We aimed to test the association between serum lactate dehydrogenase (LDH) and its isoenzymes and treatment outcomes during hospitalization for acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Thirty-eight AECOPD patients were recruited from a tertiary hospital from December 2017 to June 2018. Serum LDH and LDH isoenzymes were measured on venous blood collected at admission. Treatment outcomes included duration of hospital stay, initiation of non-invasive (NIV) or mechanical ventilation, initiation of antipseudomonal antibiotics, change in empirical antibiotic treatment, need for intravenous corticosteroids or methylxanthines, and percentage of change in C-reactive protein from admission to the third day. Multivariate linear and binary logistic regression analyses were used to test the study’s objectives. We found that, after adjusting for age, gender, comorbidities, COPD severity, level of hypoxemia, and inflammation markers, each 10 U/L increase in serum LDH was associated with prolongation of the hospital stay by 0.25 (0.03, 0.46) days, 42% higher odds (odds ratio [OR] 1.42 [1.00, 2.03]) for need of NIV, and 25% higher odds (OR 1.25 [1.04, 1.49]) for initiation of antipseudomonal treatment. LDH1 and LDH2 were the LDH isoenzymes that mainly drove these relationships. LDH release in the context of an AECOPD could originate from lung, muscle, or heart tissue damage due to airway inflammation, respiratory muscle recruitment, and myocardial stress. Myocardial injury and aerobic adaptation in respiratory muscles may explain the predominance of LDH1 and LDH2 isoenzymes in these associations.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1122-0643
2532-5264
Relation: https://www.monaldi-archives.org/index.php/macd/article/view/2543; https://doaj.org/toc/1122-0643; https://doaj.org/toc/2532-5264
DOI: 10.4081/monaldi.2023.2543
URL الوصول: https://doaj.org/article/ea73e7e7b18f48558cc7b0c0ba66830d
رقم الأكسشن: edsdoj.73e7e7b18f48558cc7b0c0ba66830d
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:11220643
25325264
DOI:10.4081/monaldi.2023.2543