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(IRMS – Nicolae Testemițanu SUMPh)

Community-acquired pneumonia in chronic heart failure: approach through the oxidative stress and systemic inflammation

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dc.contributor.author Cascaval, Virginia
dc.contributor.author Dumitras, Tatiana
dc.contributor.author Fetco-Mereuta, Diana
dc.contributor.author Matcovschi, Sergiu
dc.contributor.author Grib, Livi
dc.date.accessioned 2025-11-04T17:36:54Z
dc.date.available 2025-11-04T17:36:54Z
dc.date.issued 2025
dc.identifier.citation CASCAVAL, Virginia; Tatiana DUMITRAS; Diana FETCO-MEREUTA; Sergiu MATCOVSCHI și Livi GRIB. Community-acquired pneumonia in chronic heart failure: approach through the oxidative stress and systemic inflammation. In: Revista de Ştiinţe ale Sănătăţii din Moldova = Moldovan Journal of Health Sciences. 2025, vol. 12, nr. 3, p. 53-59. ISSN 2345-1467. https://doi.org/10.52645/MJHS.2025.3.08 en_US
dc.identifier.issn 2345-1467
dc.identifier.uri https://mjhs.md/article/community-acquired-pneumonia-chronic-heart-failure-approach-through-oxidative-stress-and
dc.identifier.uri https://doi.org/10.52645/MJHS.2025.3.08
dc.identifier.uri https://repository.usmf.md/handle/20.500.12710/31410
dc.description.abstract Introduction. Diagnosing community-acquired pneumonia in patients with chronic heart failure can be challenging. Oxidative stress and inflammatory response play an important role in the development and diagnosis of community-acquired pneumonia and are also involved in many cardiovascular diseases, including chronic heart failure. Materials and methods. A total of 210 patients were enrolled and divided into two groups: group 1 (n = 105) – patients with community-acquired pneumonia associated with chronic heart failure, and group 2 (n = 105) – patients with community- acquired pneumonia without chronic heart failure. Several biomarkers were measured. For oxidative stress, we assessed prooxidant markers (ischemic modified albumin, advanced glycation end-products, advanced oxidation protein products, malonic dialdehyde) and antioxidant markers (total antioxidant activity with CUPRAC and ABTS methods, superoxide dismutase and catalase). Inflammatory status was assessed by determining leukocyte count, erythrocyte sedimentation rate, lactate dehydrogenase, fibrinogen and C-reactive protein. In all patients, N-terminal pro b-type natriuretic peptide values were determined. Results. The age of patients in the study group ranged from 50 to 92 years, with an overall mean of 70.6 ± 8.89 years (95% CI [68.8-72.3]), (F = 18.109; p = 0.205). Ischemic modified albumin values were higher in patients in Group 1 compared to Group 2: 236.60 ± 57.23 μM/L and 229.77 ± 64.35 μM/L, respectively (F = 0.660; p = 0.045). Serum lactate dehydrogenase had higher values in Group 1, compared to the control group: 232.65 ± 109.80 units/L and 192.40 ± 44.98 units/L, respectively (p = 0.001). The mean fibrinogen values were also higher in Group 1 (5.24 ± 1.60 g/L), compared to Group 2 (4.51 ± 1.78 g/L), p = 0.002. Total antioxidant activity by CUPRAC method, had higher values in Group 1 (6.70 ± 4.62) versus Group 2 (4.99 ± 2.29), p = 0.006. Conclusions. The coexistence of community-acquired pneumonia and chronic heart failure resulted in a higher inflammatory response and greater accumulation of pro-oxidative reaction products. This condition was characterized by increased serum lactate dehydrogenase, erythrocyte sedimentation rate and fibrinogen levels. Furthermore, the state of heightened oxidative stress was marked by increased ischemic modified albumin and total antioxidant activity detected with CUPRAC method. en_US
dc.language.iso en en_US
dc.publisher Instituţia Publică Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu” din Republica Moldova en_US
dc.relation.ispartof Revista de Științe ale Sănătății din Moldova = Moldovan Journal of Health Sciences en_US
dc.subject community-acquired pneumonia en_US
dc.subject heart failure en_US
dc.subject oxidative stress en_US
dc.subject inflammatory response en_US
dc.title Community-acquired pneumonia in chronic heart failure: approach through the oxidative stress and systemic inflammation en_US
dc.type Article en_US


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