Table 6.
Patients | Participants | Role of complement/References |
---|---|---|
ARDS | 124 | BALF levels of sCR1 were significantly increased in ARDS patients (281) |
ARDS | 36 | BALF levels of C proteins were differentially expressed between survivors and non-survivors (282) |
ARDS | 26 | Blood C activation was associated with ARDS pathological mechanism (283) |
ARDS | 15 | Plasma C3a and C4a were helpful in predicting ADRS 16hrs post-injury (4) |
ARDS | 8 | Elevated plasma C3a had better predictive value than WBC counts for ARDS during the first 24hrs (284) |
ARDS | 10 | Plasma and BALF C3 and PFB activation and C5a were increased in ARDS patients (47) |
RDS | 53 | Poor responders to surfactant had lower plasma C4 and C3c at admission and 24hrs after birth (285) |
RDS | 48 | Poor responders to surfactant showed lower plasma C1q and C4 and higher plasma C3a and C5a 24hrs after birth (71) |
RDS | 35 | There was no evidence of significant C activation in RDS (286) |
ALI (allograft) | 32/8 | Pulmonary subendothelial C4d deposition was associated with HLA-Ab-induced ALI; elevated the plasma levels of C4d, Bb, iC3b, and C5b-9 after OKT3 administration in kidney and lung transplant recipients (287, 288) |
Trauma-induced ARDS | 208 | Increased plasma C5b-9 was associated with ARDS development (94) |
Trauma-induced ARDS | 108 | C activation was associated with ARDS development (5) |
Trauma-induced ARDS | 38 | Increased plasma C3a was associated with ARDS development; C3a/C3 ratio discriminated ARDS and non-ARDS (53) |
Trauma-induced ALI | 54 | Complement activation after traumatic injury, and complement activation is correlated with clinical outcomes in trauma patients (256) |
Trauma/sepsis-induced ARDS | 48 | Plasma C3a was associated with ARDS development (289) |
Trauma/sepsis-induced ARDS | 26 | Plasma C3a correlated with alveolar-capillary permeability (113) |
Trauma/sepsis-induced ARDS | N/A | Plasma C1 inhibitor activity was significantly reduced in ARDS patients (290) |
Sepsis-induced ARDS | 87 | Increased plasma C5b-9, C1rC1s-C1 inhibitor and C3bbP preceded ARDS development and resolution; plasma C5b-9 was more sensitive than C3a, C4a, C5a and CH50 (241, 291) |
Sepsis-induced ARDS | 48 | Increased plasma C3a was useful for prognosis and diagnosis of sepsis and septic shock but not for ARDS (292) |
Sepsis-induced ALI | 40 | Plasma C3a and C5a were increased in patients but did not predict the development of ALI (293) |
H1N1-induced ARDS (H1N1) | 97 | Elevated baseline blood levels of MBL were associated with high mortality (NCT03641690) |
COVID-19-induced ARDS | 276 | Complement consumption was associated with the severity of COVID-19 patients (165) |
COVID-19-induced ARDS | 100 | Show an overexpression of C5a receptor in patients with ARDS secondary to COVID-19 compared to control patients (NCT04369820) |
COVID-19-induced ARDS | Increased plasma levels of C3a, C3c and C5b-9 were related to disease severity in COVID-19 patients (48) | |
COVID-19-induced ALI | 19 | Elevated plasma levels of C3a, C3d/g, C4d, and C5b-9 were associated lung damage in COVID-19 patients (190) |
COVID-19-induced ARDS/ALI | High expression levels of C3a, C3bc, C4bc, C5a and factor P were positively correlated with IL-8, CCL5, and the fatality rate in COVID-19 patients (294, 295) | |
COVID-19-induced ALI/ARDS | Significant deposits of C4d, C5b-9 and MASP-2, and colocalization of COVID-19 spike glycoproteins with C4d and C5b-9 in the interalveolar septa microvasculature in COVID-19 patients (57) | |
ECMO | 2 | Rapid activation of the complement alternative pathway by ECMO (296) |
Ab, antibody; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; BALF, bronchoalveolar lavage fluid; CCL5, C-C motif chemokine ligand 5; ECMO, extracorporeal membrane oxygenation; HLA, human leukocyte antigen; MASP-2, mannan-biding lectin serine protease 2; PFB, properdin factor B; RDS, respiratory distress syndrome; sCR1, soluble complement receptor 1; WBC, white blood cell; N/A, not available.