scholarly journals Correction of redox metabolism and the relationship of markers of systemic chronic inflammation with a measure of overall survival in cancer patients with multiorgan resections

2021 ◽  
Vol 17 (4) ◽  
pp. 74-79
Author(s):  
Ye.V. Shulga

Background. According to the literature, multiorgan resections are carried out with the most radical removal of healthy tissue. Therefore, there is a need for the most favorable preparation of the patient with perioperative therapy to reduce further complications with obtaining improved clinical and pathological prognostic indicators to increase the overall survival. Purpose: correction of redox metabolism based on the data of the oxidative modification of proteins, degree of their catabolic reaction, and data on the enzymatic state and lipid peroxidation in cancer patients with multiorgan resections on the gastrointestinal tract under conditions of perioperative intensive care. Materials and methods. The study involved 117 cancer patients aged 67.6 ± 3.7 years with locally advanced tumor processes of the gastrointestinal tract. Studies have been conducted on the enzymatic state, lipid peroxidation and oxidative modification of proteins, both in terms of the degree of fragmentation of their products in spontaneous and iron-induced reactions, and the level of medium-weight protein molecules. Serum levels of circulating tumor necrosis factor alpha, interleukin-6 and -8 were determined. Survival analysis was performed using the Kaplan-Meier method. Results. The study of patients has shown an improvement in the indicators of oxidative modification of proteins and lipid peroxidation. Survival in cancer patients with multiorgan resections demonstrated dependence on the levels of tumor necrosis factor alpha, interleukin-6 and -8 in the blood serum. Conclusions. Conducting perioperative intensive care makes it possible to reliably restore indicators of the enzymatic state, lipid peroxidation and oxidative protein modification products (on the fourth day and second week, p < 0.05). This gives us grounds for recommending the determination of these parameters in the group of cancer patients and the implementation of metabolic intensive care. In the group of L-ornithine L-aspartate and quercetin combination with povidone, the lowest indicators of systemic chronic inflammation and the best overall survival were found.

2013 ◽  
Vol 94 (5) ◽  
pp. 723-726
Author(s):  
N N Mayanskaya ◽  
L D Hidirova ◽  
S D Mayanskaya

Aim. To study the features of inflammatory effector mechanisms variation in Wistar rats with metabolic non-coronary myocardial infarction. Methods. Metabolic myocardial infarction was reproduced in Wistar rats by adrenalin injection. Metabolic myocardial infarction was verified by electrocardiography and histological examination. Biocidal activity of blood neutrophils was determined by nitro blue tetrazolium test and chemiluminescence, cytokine serum levels (interleukin-1β, interleukin 6 and tumor necrosis factor alpha) were determined by ELISA. Lipid peroxidation was assessed by measuring malondialdehyde, diene conjugates and diketones blood concentrations. Catalase activity and reduced glutathione level were determined in erythrocyte hemolysate, serum activity of superoxide dismutase was also measured. Intact animals were examined as a control group. Results. In rats with metabolic myocardial infarction, oxygen-dependent leukocyte biocidity (determined by nitro blue tetrazolium test and chemiluminescence) increased dramatically from the first day of the adrenalin administration and continued to increase until the end of the experiment (day 14). Accordingly, the production of active oxygen metabolites, which intensified the lipid peroxidation, was increasing. Simultaneously an imbalance between pro-and antioxidant system parameters was detected. Serum concentration of pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin-1β, interleukin-6) increased. Conclusion. Long-term administration of adrenalin to experimental animals causes an increase in the neutrophils biocidal activity, accompanied by release of reactive oxygen species, pro-inflammatory cytokines, lipid peroxidation intensifying and decreased compensation by antioxidant defense system, which together can be a powerful trigger of myocardial damage.


1997 ◽  
Vol 20 (5) ◽  
pp. 387-398 ◽  
Author(s):  
Theodore F. Logan ◽  
William E. Gooding ◽  
Theresa L. Whiteside ◽  
Marc S. Ernstoff ◽  
Sandra S. Kaplan ◽  
...  

Metabolism ◽  
1999 ◽  
Vol 48 (3) ◽  
pp. 324-329 ◽  
Author(s):  
R.A. Feelders ◽  
A.J.G. Swaak ◽  
J.A. Romijn ◽  
A.M.M. Eggermont ◽  
E.T. Tielens ◽  
...  

2009 ◽  
Vol 24 (3) ◽  
pp. 142-146 ◽  
Author(s):  
Sezer Saglam ◽  
Rafi Suzme ◽  
Figen Gurdol

Aim Cytokines have been associated with symptoms and adverse outcomes in breast cancer. Overexpression of ERBB2 (c-erb-b2; formerly HER2/neu), which is a member of the epidermal growth receptor family, is associated with involvement of lymph nodes, large tumor size, high grade, steroid receptor negativity, aneuploidy, high proliferation rate, and low overall survival in breast cancer. The aim of the study was to examine whether ERBB2 amplification has any effect on circulating levels of tumor necrosis factor-alpha (TNF-α) and interleukin-2 (IL-2) in breast cancer patients. Material and methods Fifty patients with primary breast carcinoma, classified as either ERBB2 (+) or (-) by the fluorescence in situ hybridization (FISH) technique, were included in the study. Cytokines were studied by ELISA according to the procedure described in the commercial kit. Results IL-2 levels were found significantly higher in ERBB2+ patients than in controls (p<0.05). A significant negative correlation existed between ERBB2 positivity and estrogen receptor status (p=0.004). Plasma TNF-α and IL-2 levels were positively correlated in ERBB2+ breast cancer patients (p<0.01). Conclusion The increase in IL-2 concentrations observed in our study suggests an activation of T cells by ERBB2 peptides.


1996 ◽  
Vol 76 (06) ◽  
pp. 0897-0901 ◽  
Author(s):  
André B Mulder ◽  
Jan H Zwaveling ◽  
W Martin Smid ◽  
John K Maring ◽  
Robert J van Ginkel ◽  
...  

SummarySeveral investigators have reported that interferon-gamma (IFN³) can alter tumor necrosis factor alpha induced effects in vitro. We assessed in vivo effects of recombinant interferon-gamma (rIFN³) on recombinant tumor necrosis factor-alpha (rTNF±) induced activation of systemic blood coagulation in a non-randomized study in 20 consecutive cancer patients. Eight patients were treated with rIFN³ prior to and during hyperthermic isolated limb perfusion with rTNF± and melphalan (IFN³ group). They were compared with twelve patients who did not additionally receive rIFN³ (non-IFN³ group)Before start of perfusion, higher levels of TNFa, F1+2 and TAT levels were found in the IFN³ group. Fibrinogen and ATIII levels tended to be lower in this group. High TNF± levels, due to leakage during perfusion, were associated with activation of coagulation in all patients, that became obvious after the end of perfusion, when heparin treatment had been antagonized. Activation, measured by increased F1+2 and TAT levels, was significantly stronger in the IFN³y group. Monocytic TF remained low, possibly due to shedding of TF positive vesicles and/or sequestration of TF positive activated monocytes against the vessel wall. In both groups F1+2 and TAT levels declined 24 h after the perfusion, whereas monocytic TF increased to levels that were higher in the IFN³ group.In conclusion, our data confirm a strong activation of coagulation induced by rTNF± in cancer patients. They suggest that rIFN³ may lead to a slight activation of coagulation and augments TNFa induced procoagulant activity. These effects may be due to rIFN³ induced sustained monocytic TF activity.


Nephron ◽  
1997 ◽  
Vol 76 (2) ◽  
pp. 146-152 ◽  
Author(s):  
Jan H. Zwaveling ◽  
Harald J. Hoekstra ◽  
John K. Maring ◽  
Robert J.v. Ginkel ◽  
Heimen Schraffordt Koops ◽  
...  

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