2University of Health Sciences, Regional Training and Research Hospital, Department of Immunology and Allergic Diseases, Erzurum, Turkey
3University of Health Sciences, Trabzon Kanuni Training and Research Hospital, Department of Infectious Disease and Clinical Microbiology, Trabzon, Turkey
Abstract
Objective: C1-inhibitor (C1-INH), an acute-phase protein, regulates the activation of the complement cascade and acts as a down-regulator of the inflammatory process. In experimental models, it was shown that pneumonia with mechanical ventilation is associated with an increase of complement activation in the lungs. The primary aim of this study was to evaluate the serial changes of C1-INH levels in patients with ventilator-associated pneumonia (VAP).
Methods: Twelve patients were included in this prospective and observational study conducted between June 2018 and February 2019. Blood samples for C1-INH levels were obtained at the time of VAP diagnosis and on the 2nd, 4th, and 6th days following diagnosis (total of 48 samplings). At the time of C1-INH sampling, patients were screened for clinical pulmonary infection score, arterial blood gas analysis, mechanical ventilation parameters, complete blood count, C-reactive protein, procalcitonin levels, and other routine laboratory tests.
Results: No differences were found between surviving (n=7) and non-surviving (n=5) patients in terms of C1-INH levels at any measurement time (days 0, 2, 4 and 6) (p=0.982, p=0.677, p=0.790, p=0.930, respectively). VAP patients with septic shock had higher C1-INH levels than patients without shock, on the days following the diagnosis. C1-INH levels significantly correlated with concurrently measured white blood cell (R2= 0.095, p=0.030), lactate (R2=0.109, p=0.012), procalcitonin (R2=0.120, p=0.009), alanine aminotransferase (R2=0.179, p=0.002) levels, and PaO2 / FiO2 ratio (R2=0.091, p=0.022).
Conclusion: Serial monitoring of C1-INH levels may aid in prediction of prognosis in the early phase of VAP patients, especially those accompanied by septic shock.