Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac troponin I (cTnI) is a specific marker of myocardial damage used in the diagnosis of acute coronary syndrome (ACS). Recent studies have shown that cTnI levels can also be elevated in patients without ACS, such as in sepsis and trauma patients, and that this is associated with an adverse prognosis. We have evaluated the clinical implications and prognostic significance of serum cTnI levels in noncardiac critically ill patients in a prospective observational study in a general medical intensive care unit at a tertiary-level hospital. A total of 108 consecutive patients without ACS or other cardiac disease was enrolled. Serum cTnI levels were measured on admission using enzyme-linked immunoabsorbant assay kits. Clinical laboratory parameters and outcome were compared between patients with elevated and normal cTnI levels. The prognostic significance of cTnI levels and the Acute Physiology And Chronic Health Evaluation (APACHE) II score was also analyzed. Forty-nine patients (45%) had elevated cTnI levels and 59 (55%) had normal levels. Compared with patients with normal cTnI levels, patients with elevated levels had a higher incidence of new failure of two or more organs, had a lower left ventricular ejection fraction during admission, were more likely to be associated with bacteremia, and had a higher intensive care unit mortality; they also had a significantly shorter survival over a 180-day follow up, before and after stratification by the APACHE II score. Multiple organ failure was the leading cause of mortality in patients with elevated cTnI levels. By multivariate analysis, elevated cTnI levels, a high APACHE II score, and underlying cancer were the three most important independent predictors for a shorter survival. Combination analysis showed a shorter survival in patients with a high APACHE II score plus elevated cTnI levels than in patients with a high APACHE II score or elevated cTnI levels alone. In conclusion, elevated serum cTnI levels is a risk factor for multiple organ failure and mortality in noncardiac critically ill patients, and the cTnI levels and APACHE II score have an additive effect in outcome prediction.
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PMID:Cardiac troponin I levels are a risk factor for mortality and multiple organ failure in noncardiac critically ill patients and have an additive effect to the APACHE II score in outcome prediction. 1525 80

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are valuable heart markers in patients presenting with symptoms of ischaemic heart disease. A number of categories of patients frequently have raised concentrations of cardiac troponin (cTn) without having ischaemic heart disease. These include patients with heart diseases such as heart failure, myocarditis and valvular disease but also those with lung emboli, renal failure and sepsis. Possible underlying mechanisms are diffuse necrosis, cTn proteolysis or leakage of cytoplasmatic cTn with no irreversible damage to the contraction complex of heart-muscle cells. It is possible that cTn-measurement in patients with non-cardiac conditions is of prognostic value but so far this has only been demonstrated in dialysis patients and patients with pulmonary embolism.
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PMID:[The significance of elevated troponin levels in the absence of acute cardiac ischaemia]. 1661 May 13

Sepsis aggregates undesirable immune response causing depression of ventricular myocardium and diastolic dysfunction. This present study examined the effect of a plant-derived flavone tangeretin (TG) on autophagy and reduction in myocardial dysfunction. The sepsis was induced by cecum ligation and puncture (CLP) in male Sprague-Dawley rats. Abnormal changes were seen in the heart after the sepsis induction. These abnormalities were analyzed based on the cardiac markers, namely Cardiac myosin light chain-1 (cMLC1) and Cardiac troponin I (cTnl), echocardiography, and plasma parameters, like Lactate dehydrogenase (LDH) and Creatinine kinase (CK). Microanatomy of the heart was studied using hematoxylin and eosin stained histopathological samples of cardiac tissue. Western blot technique was used to detect the nature and extent of protein with the amount of a specific RNA (gene expression) in the cardiac homogenate. Oxidative damage was analyzed using redox marker, reduced glutathione. This study successfully showed that TG attenuated sepsis-induced myocardial dysfunction by inhibiting myocardial autophagy via silencing the Phosphatase and tensin homolog (PTEN) expression and acting on the AKT/mTOR pathway. The present findings supported that TG is a novel cardioprotective therapeutic target for sepsis induced myocardial dysfunction.
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PMID:Cardioprotective Effect of Tangeretin by Inhibiting PTEN/AKT/mTOR Axis in Experimental Sepsis-Induced Myocardial Dysfunction. 3326 Apr 22