Prognostic predictive values of serum cytochrome c, cytokines, and other laboratory measurements in acute encephalopathy with multiple organ failure

Abstract

Aims: To evaluate the prognostic predictive values of cytochrome c, cytokines, and other laboratory measurements in serum collected during neurological onset in acute encephalopathy with multiple organ failure. Methods: In addition to general laboratory examinations, the concentrations of cytochrome c (apoptosis marker) and cytokines (inflammatory markers) were measured in serum samples collected at the initial phase in 29 patients with acute encephalopathy. The obtained values were evaluated as predictors for the development of severe encephalopathy. Results: Cytochrome c, tumour necrosis factor a (TNF-a), interleukin 6 (IL-6), soluble TNF-receptor 1 (sTNF-R1), and aspartate aminotransferase (AST) concentrations at the initial phase were high and correlated well with patient outcome. High concentrations of serum cytochrome c (.45 ng/ml), sTNF-R1 (.2000 pg/ml), AST (.58 IU/dl), IL-6 (.60 pg/ml), and TNF-a (.15 pg/ml) predicted an unfavourable prognosis (sequelae and death) at 93%, 79%, 82%, 77%, and 60%, respectively. The specificity of those markers was 100%, 89%, 83%, 100%, and 100%, respectively. Conclusions: Serum cytochrome c is the most sensitive and specific predictor for the development of severe encephalopathy at the initial phase. Results suggest that this marker might be used to guide decisions regarding the start of the initial treatment and further intensive care.

Analysis of the molecular mechanism underlying bone marrow necrosis with acute lymphoblastic leukemia

“…In order to clarify this hypothesis, we first examined the levels of cytochrome C in sera obtained at the time of BMN. However, elevation of these values was not recognized in our patients with BMN, who were previously reported to display systemic inflammatory response syndrome and multiorgan failure [16][17][18], which suggests that there is no intense relationship with the intrinsic pathway of apoptosis in patients with BMN. Second, we examined the expression levels of Fas-L, PRF1, GzmB, TRAIL, and TNF-α using the RQ-RT-PCR method in order to identify the relationship of the extrinsic pathway and cytotoxic granules.…”

Elevated serum levels of neutrophil elastase in patients with influenza virus-associated encephalopathy

“…Moreover, other cytokines and their receptors, cell adhesion molecules, and other factors are also related reportedly to the severity of IE. These include IL-10, sE-selectin, sCD163, sCD40L, cytochrome c in the serum [13][14][15][16][17], and d-ROM in the CSF [18]. These findings demonstrate that influenza virus-induced inflammation is a major contributor to IE.…”

“…Based on the evidence that proinflammatory cytokines and their receptors (such as TNF-α, IL-6, soluble TNF-receptor, and sE-selectin) as well as the mitochondrial respiratory chain enzyme cytochrome c oxidase are elevated in plasma, serum, or CSF in patients with IE [11][12][13]16], and that neuropathology showed no evidence of direct viral invasion in the CNS [5,19], it has been hypothesized that vascular inflammation caused by hypercytokinemia leads to apoptosis of endothelial cells and loss of vascular integrity, which result in increased permeability of the cerebral vessels and cerebral edema [2,16,20].…”

Circulating levels of cytochromecafter resuscitation from cardiac arrest: a marker of mitochondrial injury and predictor of survival

“…Recent studies in Jurkat leukemic T cells and mouse fibroblasts suggest that cytochrome c leaves the cell and is detected in the extracellular milieu through mechanisms apparently unrelated to cell necrosis (37,46). In patients, elevated levels of circulating cytochrome c have been reported in association with conditions that can injure mitochondria, such as chemotherapy (6,37), acute myocardial infarction (2), fulminant hepatitis (38), systemic inflammatory response syndrome (1), and influenza-associated encephalopathy (24,25).…”