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)

Although amino-terminal pro-B-type natriuretic peptides (NT-proBNP) are useful for the diagnosis or exclusion of heart failure (HF), this marker may identify a wide range of disease processes other than HF. Indeed, elevation of NT-proBNP may occur in a number of heart diseases (including heart muscle disease, valve disease, rhythm abnormalities, pulmonary hypertension, and cytotoxic injury to the heart) and in disease processes other than primary cardiac illnesses, including gram-negative sepsis. Importantly, although NT-proBNP may increase in settings other than HF, the presence and severity of such NT-proBNP release is often significantly associated with risk for adverse outcome. Accordingly, elevation of NT-proBNP in the context of non-HF situations should not be regarded as a "false-positive" finding, and elevated NT-proBNP values should not be discarded without consideration of the serious adverse outcomes associated with the elevation. Future studies will be necessary to further understand the utility of NT-proBNP testing in states other than cardiovascular disease.
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PMID:The differential diagnosis of an elevated amino-terminal pro-B-type natriuretic peptide level. 1824 58

Respiratory care centers (RCCs) provide effective care for patients who have been in intensive care and have undergone prolonged mechanical ventilation. Between February 2002 and December 2005, 891 patients who met the admission criteria of RCCs were referred to our RCC at Kaohsiung Medical University Hospital in southern Taiwan for attempted weaning. We recorded demographic and clinical data, including variables identified previously as predictive of weaning success among highly selected populations. The common causes of respiratory failure at RCC admission were neuromuscular disease (29.2%), pneumonia (27.5%), cancer (18.0%), cardiovascular disease (10.1%), sepsis (5.7%) and post-surgery (1.6%). The percentage of patients successfully weaned was 40.2%, while 59.8% remained dependent on ventilators. In a stepwise multivariate logistic regression analysis, significant predictors of weaning success included neuromuscular disease (odds ratio [OR], 2.64), APACHE II score (OR, 0.93) and blood urea nitrogen level at RCC admission (OR, 0.99). The results could be helpful in the accreditation of medical care quality and may provide guidelines for future research and education programs.
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PMID:Successful weaning predictors in a respiratory care center in Taiwan. 1828 Dec 25

Inflammation is a physiologic response to irritants, injury, and infection. Inflammatory dysregulation is believed to contribute to mortality and morbidity in illnesses common to critical care units, such as burns, trauma, sepsis, and cardiovascular disease. This article reviews the approaches used to investigate the molecular basis of inflammatory function. Genomic findings are providing insight into clinical diagnosis and treatment of inflammatory derangements in critically ill patients.
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PMID:Inflammation and genomics in the critical care unit. 1842 50

The incidence of type 2 diabetes (T2D) is rapidly expanding. Some of the more obvious pathologies associated with it include: defective glucose metabolism, obesity, cardiovascular disease and an inability to mount an effective immune response to infection by certain pathogenic organisms, leading to sepsis and death. A common tie linking these seemingly disparate complications is chronic inflammation. Today we know that inflammation is regulated locally and systemically by numerous biochemical signals. One of the most important of these signals is a class of molecules called cytokines. Cytokines can be generally classified as proinflammatory or anti-inflammatory and allow an organism to respond rapidly to an immune challenge by coordinating an appropriate immune response. In T2D, the balance between proinflammatory and anti-inflammatory cytokines is shifted toward proinflammation, potentially causing or exacerbating the health complications found in T2D. Over-nutrition has been shown to trigger the innate immune system but activation of the innate immune system, itself, induces hyperglycemia and insulin resistance. In all likelihood, diabetes and chronic inflammation are inseparable and act as a reciprocal feed-forward loop.
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PMID:The implication of proinflammatory cytokines in type 2 diabetes. 1850 80

The mortality rate for end-stage renal disease patients is six times higher than in the general population. Hemodialysis central venous catheter (CVC) utilization has increased by 50% between 1998 and 2004 and data from the United States Renal Data System suggest that 81% of the patients initiate hemodialysis through a CVC. There is evidence that the two observations are linked in both an obvious way (catheter-related sepsis) as well as in a less obvious manner-chronic inflammation. Inflammation is highly prevalent in chronic hemodialysis (CHD) patients and is consistently associated with poor outcomes. Some of the most important consequences of inflammation in CHD include, but are not limited to, cardiovascular disease, uremic protein-energy wasting, erythropoietin hyporesponsiveness, and increased hospitalization and death rates. Use of CVC has been long suspected to play a role in the inflammatory response in CHD patients. Recent studies have shown that the presence of CVCs is associated with higher levels of C-reactive protein (CRP), lower serum albumin values, and lower hemoglobin values. Furthermore, there are data showing that CRP levels decrease following CVC removal. Accordingly, avoidance of CVC represents an effective strategy to limit the inflammatory response in CHD patients and potentially prevent its devastating consequences.
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PMID:Hemodialysis central venous catheters as a source of inflammation and its implications. 1857 35

Chronic kidney disease (CKD) carries an increased risk of cardiovascular disease (CVD). Macrophage migration inhibiting factor (MIF) is a proinflammatory cytokine implicated in the pathogenesis of sepsis, autoimmune disease, atherogenesis, and plaque instability, and is a known cardiac depressant. This post-hoc, cross-sectional study examined whether MIF serum concentrations are elevated in CKD patients. Our study included CKD 3-5 patients with moderate to severe renal dysfunction (n = 257) (mean age SD; 55 +/- 12 years) and 53 controls (60 +/- 12 years). Serum MIF concentrations, measured by enzyme-linked immunosorbent assay (ELISA), were studied in relation to glomerular filtration rate (GFR), presence of CVD, outcome and inflammatory and oxidative stress markers. MIF was significantly elevated in CKD patients compared with controls (CKD: median 676 [range 118-8275 pg/mL] controls: 433 [142-4707] pg/mL; P = 0.008). MIF was also associated with 8-hydroxy-2-deoxyguanosine (8-OH-dG) levels (rho = 0.26; P = 0.001), a marker of oxidative stress, and ICAM-1 levels (rho = 0.14; P = 0.02), a marker of endothelial activation. However, the elevated MIF concentrations were neither correlated with glomerular filtration rate (GFR) nor inflammatory markers such as CRP, IL-6, and TNF. When combining MIF and IL-6 as a marker of inflammation, a significant increase in risk for CVD was found, but when analyzing all-cause mortality, this did not differ significantly with regard to mortality from inflamed patients with low MIF levels. The data suggest that increased serum MIF levels found in CKD is not caused primarily by poor renal function, but is associated with markers of oxidative stress and endothelial activation and may play a role in vascular disease associated with CKD.
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PMID:Elevated serum macrophage migration inhibitory factor (MIF) concentrations in chronic kidney disease (CKD) are associated with markers of oxidative stress and endothelial activation. 1908 68

Elevated plasma concentrations of plasminogen activator inhibitor type 1 (PAI-1), also named serpin E1, are encountered in patients with thrombophilia, atherosclerosis, septicemia and the metabolic syndrome and may be associated with an increased risk of complications. Expression of PAI-1 is increased by inflammatory stimuli and decreased by statins, drugs widely used in patients with cardiovascular disease. Increased expression of PAI-1 by inflammatory stimuli is mediated by a large variety of signal transduction pathways, which include the NF-kappaB and MAP kinase pathways. The downregulating effect of statins on PAI-1 expression is dependent on the inhibition of Rho family proteins and may involve an activation of PI-3 kinase/Akt signaling pathways. In this review we summarize the findings on the effect of inflammation and statins on PAI-1 expression.
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PMID:Regulation of plasminogen activator inhibitor type 1 gene expression by inflammatory mediators and statins. 1913 19

Little attention has been paid to the function of lipoproteins as part of a nonspecific immune defense system that binds and inactivates microbes and their toxins effectively by complex formation. Because of high extra-capillary tissue pressure, aggregates of such complexes may be trapped in vasa vasorum of the major arteries. This complex formation and aggregation may be enhanced by hyperhomocysteinemia, because homocysteine thiolactone reacts with the free amino groups of apo-B to form homocysteinylated low-density lipoprotein (LDL), which is subject to spontaneous precipitation in vitro. Obstruction of the circulation in vasa vasorum, caused by the aggregated complexes, may result in local ischemia in the arterial wall, intramural cell death, bursting of the capillary, and escape of microorganisms into the intima, all of which lead to inflammation and creation of vulnerable plaques. The presence of homocysteinylated LDL and oxidized LDL stimulates production of LDL autoantibodies, which may start a vicious circle by increasing the complex formation and aggregation of lipoproteins. The content of necrotic debris and leukocytes and the higher temperature than its surroundings give the vulnerable plaque some characteristics of a micro-abscess that by rupturing may initiate an occluding thrombosis. This suggested chain of events explains why many of the clinical symptoms and laboratory findings in acute myocardial infarction are similar to those seen in infectious diseases. It explains the presence of microorganisms in atherosclerotic plaques and why bacteriemia and sepsis are often seen in myocardial infarction complicated with cardiogenic shock. It explains the many associations between infections and cardiovascular disease. And it explains why cholesterol accumulates in the arterial wall. Some risk factors may not cause vascular disease directly, but they may impair the immune system, promote microbial growth, or cause hyperhomocysteinemia, leading to vulnerable plaques.
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PMID:Review and Hypothesis: Vulnerable plaque formation from obstruction of Vasa vasorum by homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL autoantibodies. 1920 35

Inflammation is the host's defense mechanism to infection or trauma including surgical procedures. In the clinic, non-infectious inflammation plays an important part in cardiology (e.g. Percutaneous transluminal coronary angioplasty, PTCA), intensive care medicine (e.g. polytrauma), cardiac (e.g. extracorporeal circulation) and vascular surgery (e.g. reperfusion injury). An imbalance of the inflammatory response can cause an acute condition like sepsis or long-term Cardiovascular disease (CVD), both of which are leading killers in the Western world. Alterations in coagulation, innate immunity and endothelial function represent key aspects in the mechanism of inflammation and are the link between the pathogenesis of these two diseases. Studying inflammatory pathways or targeting specific mediators during inflammation may help to develop strategies to improve the clinical outcome of patients undergoing major surgery, where postoperative inflammation plays a crucial role.
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PMID:Innate immunity, coagulation and surgery. 1927 49

In severe untreated rheumatoid arthritis (RA), reductions in high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol and total cholesterol have been noted; this is in line with findings in other pathologies/conditions associated with inflammation or infection, such as sepsis, cancer, trauma or the postoperative period. Although the precise mechanisms remain to be established, cytokine-induced activation of the reticuloendothelial system is potentially critical to such changes. Consequently, dampening of inflammation in severe RA-as occurs with several biologics-may lead to increases, not only in high-density lipoprotein-cholesterol, but also with other lipid moieties, including total and low-density lipoprotein-cholesterol and, perhaps, triglycerides. This concept is consistent with findings following antitumour necrosis factor treatment and interleukin-6 receptor inhibition in patients with RA. At the same time, it is increasingly apparent that potent dampening of inflammation, however achieved, broadly reduces the risk of cardiovascular disease in RA. Therefore, changes in lipid profiles, particularly increases in cholesterol and triglycerides that occur with treatments for severe inflammation, may not represent increased cardiovascular risk as in the usual understanding of lipid-level elevations in individuals without significant inflammation. Rather, changes in lipid levels, in part or largely, may represent a predictable response to attenuation of inflammation. These observations are increasingly important clinically and should aid in the understanding and interpretation of lipid changes under inflammatory conditions, as well as in the context of potent anti-inflammatory interventions.
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PMID:Interpreting lipid levels in the context of high-grade inflammatory states with a focus on rheumatoid arthritis: a challenge to conventional cardiovascular risk actions. 1928 5


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