Disease relevance of Multiple Organ Failure

• Consequently, Mkp-1 knockout mice develop severe hypotension and multiple organ failure, and exhibit a remarkable increase in mortality [1].
• IL-2 mediates the regression of certain malignancies, but clinical use is limited because of associated toxicities, including parenchymal lymphocytic infiltration with multiple organ failure [2].
• Plasma fibronectin deficiency and opsonic dysfunction exist in critically ill septic surgical, trauma, and burn patients with multiple organ failure [3].
• In addition, GM-CSF therapy was not associated with worsened acute respiratory distress syndrome or the multiple organ dysfunction syndrome, suggesting a homeostatic role for GM-CSF in sepsis-related pulmonary dysfunction [4].
• Plasma AM and IL-8 levels correlated positively with Acute Physiology and Chronic Health Evaluation (APACHE) II score, peak multiple organ failure (MOF) score during the first month and prognosis in patients with septic shock, as did plasma IL-6 levels in patients with traumatic shock [5].

High impact information on Multiple Organ Failure

• Ablation of IKK-beta in enterocytes prevented the systemic inflammatory response, which culminates in multiple organ dysfunction syndrome (MODS) that is normally triggered by gut ischemia-reperfusion [6].
• CONCLUSIONS: In this study, prolonged administration of methylprednisolone in patients with unresolving ARDS was associated with improvement in lung injury and MODS scores and reduced mortality [7].
• Low levels of ATIII and PC are markers of and may be involved in the pathogenesis of MODS in BMT [8].
• Therefore, these studies demonstrate that C1INH, in addition to its role in suppression of LPS-mediated macrophage activation, may play an important role in the prevention of LPS-mediated increased vascular permeability, endothelial cell injury, and multiple organ failure [9].
• OBJECTIVE: To evaluate the prognostic significance of the activational status of p38, specifically progression to multiple organ dysfunction syndrome (MODS), in a group of severely injured trauma patients [10].

Chemical compound and disease context of Multiple Organ Failure

• Glutathione levels were reduced both in patients who developed MODS and those who did not at the onset of surgery [11].
• CONCLUSION: Treatment with GH for 5 days in patients with multiple organ failure stimulated muscle protein synthesis, increased muscle free glutamine, and increased intracellular muscle water [12].
• The regional production of cytokines and lactate in sepsis-related multiple organ failure [13].
• Aldehyde adducts well mark the progression of the disease towards multiple organ failure [14].
• A plasma LOS level of greater than 700 ng/L correlated with development of severe septic shock (P less than .0001), adult respiratory distress syndrome (P = .0035), a pathologically elevated serum creatinine level (P less than .0001), or death as a consequence of multiple organ failure (P = .0002) [15].

Biological context of Multiple Organ Failure

• We tested the hypothesis that activated neutrophil-endothelial cell interaction in DIC can cause endothelial injury contributing to multiple organ dysfunction syndrome (MODS) and a poor outcome after trauma [16].
• KEY WORDS: ceramide; tumor necrosis factor; outcome; apoptosis; multiple organ dysfunction syndrome; critical illness; mononuclear cells; intensive care unit (ICU); sphingomyelin pathway[17]
• High interleukin-10 producers were under-represented in the multiple organ dysfunction syndrome group: This genotype occurred in 30% of controls but in only 6% of patients ( <.001) [18].
• Chronic type IV phosphodiesterase inhibition protects glomerular filtration rate and renal and mesenteric blood flow in a zymosan-induced model of multiple organ dysfunction syndrome treated with norepinephrine [19].
• Tissue-specific gene expression of heme oxygenase-1 (HO-1) and non-specific delta-aminolevulinate synthase (ALAS-N) in a rat model of septic multiple organ dysfunction syndrome [20].

Anatomical context of Multiple Organ Failure

• The role of phagocyte proteinases and proteinase inhibitors in multiple organ failure [21].
• Sequential systemic platelet-activating factor and interleukin 8 primes neutrophils in patients with trauma at risk of multiple organ failure [22].
• MEASUREMENTS/MAIN RESULTS: T cells were considerably depleted in SIRS/MODS patients (p <.001), and Fas and FasL expression on PBMCs (flow cytometric analysis) was elevated significantly compared with controls (p <.001) [23].
• Relationship between neopterin and granulocyte elastase plasma levels and the severity of multiple organ failure [24].
• OBJECTIVE: To investigate the relationship between single-frequency bioimpedance at 50 kHz (both total body impedance and segmental impedance) and total body water, measured using tritiated water in the presence of the severe fluid retention seen in multiple organ failure [25].

Gene context of Multiple Organ Failure

• Genetic inactivation of MnSOD (Sod2) results in multiple organ failure and early neonatal death [26].
• By contrast, increased IL-6 values were observed in both septic and nonseptic, multiple organ failure patients [27].
• Circulating interleukin-8 concentrations in patients with multiple organ failure of septic and nonseptic origin [27].
• OBJECTIVE: To determine the precise relationship among tissue factor, tissue factor pathway inhibitor (TFPI), and neutrophil elastase in sepsis, as well as to test the hypothesis that low TFPI concentrations are not sufficient to prevent tissue factor-dependent intravascular coagulation, leading to multiple organ dysfunction syndrome and death [28].
• To determine whether or not changes in SLPI correlate with the severity of multiple organ dysfunction syndrome as measured by the maximal multiple organ dysfunction score [29].

Analytical, diagnostic and therapeutic context of Multiple Organ Failure

• METHODS: Plasma separation and bilirubin adsorption by an anion-exchange adsorbent column (BR-350) were performed in two patients with severe jaundice (total serum bilirubin > 55 mg/dl) and multiple organ failure that had developed after orthotopic liver transplantation [30].
• CONCLUSIONS: Soluble TNF receptor p55 can be employed as a predictive marker for cytokinemia and the development of SIRS/MODS that may arise from a major insult to the body such as cardiopulmonary bypass [31].
• Despite these high concentrations of TNF-alpha, no patient died in the ICU, although the patient with the highest TNF-alpha concentration developed multiple organ failure and required continuous venovenous hemofiltration for 16 days [32].
• Many of the serious, potentially fatal complications of hematopoietic stem cell transplantation have similarities to the multiple organ dysfunction syndrome (MODS) in critically ill nontransplant patients [33].
• Cortisol and catecholamine kinetics during continuous hemodiafiltration in patients with multiple organ dysfunction syndrome [34].

References