scholarly journals Human Soluble Recombinant Thrombomodulin, ART-123, Resolved Early Phase Coagulopathies, but Did Not Significantly Alter the 28 Day Outcome in the Treatment of DIC Associated with Infectious Systemic Inflammatory Response Syndromes

2019 ◽  
Vol 8 (10) ◽  
pp. 1553 ◽  
Author(s):  
Shusuke Mori ◽  
Tomohiko Ai ◽  
Toshiki Sera ◽  
Kanae Ochiai ◽  
Yasuhiro Otomo
Keyword(s):  
Inflammatory Response ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Clinical Severity ◽  
Major Life ◽  
Severity Scores ◽  
Common Causes ◽  
Systemic Disorder ◽  
Life Threatening ◽  
Recombinant Thrombomodulin

Disseminated intravascular coagulation (DIC) is a catastrophic systemic disorder of coagulation, resulting in uncontrollable bleeding, multiple organ failure, and death. Sepsis is one of the common causes of DIC. Despite many attempts to correct these coagulation pathologies, no adjunctive treatments have been shown to improve the mortality of DIC associated with sepsis. Although some clinical studies showed a recently developed human recombinant thrombomodulin, ART-123, might be effective in the treatment of DIC, few randomized, placebo-controlled studies have been conducted. In this study, we treated 60 DIC patients associated with systemic inflammatory response syndrome (SIRS) using ART-123 (n = 29) or saline as a placebo (n = 31). The basal clinical characteristics were similar in both groups. We compared clinical severity scores and DIC score in acute phase, and 28 day mortality between the two groups. Our study demonstrated the DIC score improved a few days earlier in the ART-123 group than the placebo group, and there were no major life-threatening adverse events in both groups. The overall survival rate at day 28 was not significantly altered. In conclusion, ART-123 can be used safely in DIC associated with infectious SIRS patients; however, its true efficacy in the treatment of DIC needs to be further investigated.

Possible role of increased oxidant stress in multiple organ failure after systemic inflammatory response syndrome

2003 ◽  
Vol 31 (4) ◽  
pp. 1048-1052 ◽  
Author(s):  
Takeshi Motoyama ◽  
Kazufumi Okamoto ◽  
Ichirou Kukita ◽  
Masamichi Hamaguchi ◽  
Yoshihiro Kinoshita ◽  
...  
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Oxidant Stress ◽  
Multiple Organ ◽  
Systemic Inflammatory Response

scholarly journals Systemic inflammatory response syndrome and multiple-organ damage / dysfunction in complicated canine babesiosis

2001 ◽  
Vol 72 (3) ◽  
Author(s):  
C. Welzl ◽  
A.L. Leisewitz ◽  
L.S. Jacobson ◽  
T. Vaughan-Scott ◽  
E. Myburgh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Renal Involvement ◽  
Organ Damage ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
The Body ◽  
Increased Risk

This study was designed to document the systemic inflammatory response syndrome (SIRS) and multiple-organ dysfunction syndrome (MODS) in dogs with complicated babesiosis, and to assess their impact on outcome. Ninety-one cases were evaluated retro-spectively for SIRS and 56 for MODS. The liver, kidneys, lungs, central nervous system and musculature were assessed. Eighty-seven percent of cases were SIRS-positive. Fifty-two percent of the cases assessed for organ damage had single-organ damage and 48 % had MODS. Outcome was not significantly affected by either SIRS or MODS, but involvement of specific organs had a profound effect. Central nervous system involvement resulted in a 57 times greater chance of death and renal involvement in a 5-fold increased risk compared to all other complications. Lung involvement could not be statistically evaluated owing to co-linearity with other organs, but was associated with high mortality. Liver and muscle damage were common, but did not significantly affect outcome. There are manysimilarities between the observations in this study and previous human and animal studies in related fields, lending additional support to the body of evidence for shared underlying pathophysiological mechanisms in systemic inflammatory states.

scholarly journals Sepsis, mitochondrial failure and multiple organ dysfunction

2014 ◽  
Vol 37 (2) ◽  
pp. 58 ◽  
Author(s):  
Josefina Duran-Bedolla ◽  
Marco A Montes de Oca-Sandoval ◽  
Vianey Saldaña-Navor ◽  
José A Villalobos-Silva ◽  
Maria Carmen Rodriguez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Physiological State ◽  
Redox Balance ◽  
Multiple Organ ◽  
Reactive Species ◽  
Systemic Inflammatory Response ◽  
Antioxidant Systems ◽  
Multiple Organ Dysfunction

Purpose: The purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis. Principal findings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated inflammatory response. Involved in the pathogenesis of sepsis are the activation of inflammatory, immune, hormonal, metabolic and bioenergetic responses. One of the pivotal factors in these processes is the increase of reactive species accompanied by the failure of the antioxidant systems, leading to a state of irreversible oxidative stress and mitochondrial failure. In a physiological state, reactive species and antioxidant systems are in redox balance. The loss of this balance during both chronic and infectious diseases leads to a state of oxidative stress, which is considered to be the greatest promoter of a systemic inflammatory response. The loss of the redox balance, together with a systemic inflammatory response during sepsis, can lead to progressive and irreversible mitochondrial failure, energy depletion, hypoxia, septic shock, severe sepsis, multiple organ dysfunction and death of the patient. Conclusion: Knowledge of the molecular processes associated with the development of oxidative stress should facilitate the development of effective therapies and better prognosis for patients with sepsis and organ dysfunction.

Article Commentary: Sepsis, Systemic Inflammatory Response, and Multiple Organ Dysfunction: The Mystery Continues

2012 ◽  
Vol 78 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Donald E. Fry
Keyword(s):  
Clinical Trials ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Invasive Infection ◽  
Multiple Organ Dysfunction ◽  
Human Sepsis ◽  
Critical Organ

Human sepsis is thought to be systemic inflammatory response syndrome (SIRS) that is activated by invasive infection. The multiple organ dysfunction syndrome (MODS) is the identified failure of critical organ function in patients that have sustained SIRS. Because SIRS and MODS are consequences of the excessive activation of inflammation, extensive research and numerous clinical trials have pursued treatments that would modify the inflammatory response. This presentation reviews the normal local mechanisms of inflammation and provides a theoretical framework for the transition of the inflammatory process to a systemic level. Clinical trials with biomodulators to block or inhibit inflammation have generally failed to improve the outcomes in patients with severe sepsis, septic shock, and MODS. The role of counter-inflammatory signaling and the newer concept of the cholinergic anti-inflammatory pathway are being investigated, and newer hypotheses are focusing upon the balancing of proinflammatory and counter-inflammatory mechanisms as important directions for newer therapies. It is concluded that failure to define novel and effective treatments reflects fundamental gaps in our understanding of inflammation and its regulation.

The systemic inflammatory response syndrome following cardiac surgery: different expression of proinflammatory cytokines and procalcitonin in patients with and without multiorgan dysfunctions

Perfusion ◽  
2002 ◽  
Vol 17 (2) ◽  
pp. 103-109 ◽  
Author(s):  
Armin Sablotzki ◽  
Ivar Friedrich ◽  
Jörg Mühling ◽  
Marius G Dehne ◽  
Jan Spillner ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Apache Ii Score ◽  
Organ Dysfunctions

Cardiopulmonary bypass is associated with an injury that may cause pathophysiological changes in the form of systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS). In the present study, we investigated the inflammatory response of patients with multiple organ dysfunctions following open-heart surgery. Plasma levels of cytokines (IL-1β, IL-6, IL-8, IL-18) and procalcitonin (PCT) were measured on the first four postoperative days in 12 adult male patients with SIRS and two or more organ dysfunctions after myocar-dial revascularization (MODS group), and 15 patients without organ dysfunctions (SIRS group). All cytokines (except IL-1β) and PCT were significantly elevated in MODS patients, with peak values at the first two postoperative days. The results of our study show a different expression of members of the IL-1 family following extracorporeal circulation. For the first time, we can document that IL-18 is involved in the inflammatory response and the initiation of the MODS following cardiopulmonary bypass. In addition to APACHE-II score, PCT, IL-8, and IL-18 may be used as parameters for the prognosis of patients with organ dysfunctions after cardiac surgery. Furthermore, it must be noted that the duration of the surgical procedure is one of the most important factors for the initiation of the inflammatory response.

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