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)

The diagnosis of heart failure in the outpatient setting can be difficult. A rapid assay for B-type natriuretic peptide (BNP) has been advocated for the diagnosis of heart failure, using a single cutoff of 100 pg/mL. BNP is produced by both the right and left cardiac ventricles and is elevated in a variety of conditions, including heart failure, pulmonary hypertension, cor pulmonale, pulmonary embolism, left ventricular hypertrophy, renal failure, circulatory overload, acute coronary syndromes, atrial fibrillation, lung cancer, and sepsis. This multitude of causes of BNP elevation imposes limits on its diagnostic use for heart failure. The literature on the use of BNP testing for diagnosis of heart failure is reviewed, and improved guidelines for its interpretation are suggested.
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PMID:B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. 1593 Apr 11

Brain natriuretic peptide (BNP) is a diagnostic marker for left ventricular dysfunction. Sepsis and septic shock are increasing in incidence and mortality. Myocardial dysfunction frequently accompanies severe sepsis and septic shock. Although previously described as a preterminal event, ventricular dysfunction with reduced ejection fraction and biventricular dilatation is present in most patients with severe sepsis and septic shock. In survivors, this depression in cardiac function is reversible over the course of seven to ten days. Even though some prognostic factors have been identified in patients with sepsis-induced myocardial dysfunction, their measurement often includes costly and cumbersome techniques. Thus, there is a need for an inexpensive, simple, rapid and readily available marker to predict mortality in septic shock. At present, a relationship between BNP with myocardial dysfunction in septic shock has not been evaluated. However, growing evidence supports the hypothesis that BNP could be an early predictor of mortality in septic shock. If proven, the hypothesis would have important clinical and public health implications.
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PMID:Brain natriuretic peptide: a potential marker for mortality in septic shock. 1532 95

The present review will cover the mechanisms of release and the potential pathophysiological role of different natriuretic peptides in critically ill patients. By focusing on the cardiovascular system, possible implications of natriuretic peptides for diagnosis and treatment will be presented. In critical illness such as sepsis, trauma or major surgery, systemic hypotension and an intrinsic myocardial dysfunction occur. Impairment of the cardiovascular system contributes to poor prognosis in severe human sepsis. Natriuretic peptides have emerged as valuable marker substances to detect left ventricular dysfunction in congestive heart failure of different origins. Increased plasma levels of circulating natriuretic peptides, atrial natriuretic peptide, N-terminal pro-atrial natriuretic peptide, brain natriuretic peptide and its N-terminal moiety N-terminal pro-brain natriuretic peptide have also been found in critically ill patients. All of these peptides have been reported to reflect left ventricular dysfunction in these patients. The increased wall stress of the cardiac atria and ventricles is followed by the release of these natriuretic peptides. Furthermore, the release of atrial natriuretic peptide and brain natriuretic peptide might be triggered by members of the IL-6-related family and endotoxin in the critically ill. Apart from the vasoactive actions of circulating natriuretic peptides and their broad effects on the renal system, anti-ischemic properties and immunological functions have been reported for atrial natriuretic peptide. The early onset and rapid reversibility of left ventricular impairment in patients with good prognosis associated with a remarkably augmented plasma concentration of circulating natriuretic peptides suggest a possible role of these hormones in the monitoring of therapy success and the estimation of prognosis in the critically ill.
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PMID:Science review: natriuretic peptides in critical illness. 1546 96

B-type natriuretic peptide is known to predict outcome in congestive cardiac failure and myocardial infarction. We aimed to determine whether measurement of B-type natriuretic peptide would predict hospital mortality in patients admitted to an intensive care unit. We conducted a prospective observational cohort study in 78 consecutive patients. Demographics, clinical details and clinical outcomes were recorded. Admission and 24 h B-type natriuretic peptide and cardiac troponin I levels were measured. B-type natriuretic peptide and cardiac troponin I levels taken on intensive care admission and 24 h after admission did not accurately predict hospital mortality for all patients, including patients with severe sepsis or septic shock (all p > 0.05). B-type natriuretic peptide levels were higher in patients with severe sepsis and septic shock (p = 0.02), in patients > or = 65 years (p = 0.04) and in patients with raised creatinine > or = 110 micromol.l(-1) (p = 0.02). We concluded that B-type natriuretic peptide, measured soon after admission to intensive care, does not usefully predict outcome after intensive care.
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PMID:B-type natriuretic peptide and the prediction of outcome in patients admitted to intensive care. 1560 Dec 67

B-type natriuretic peptide (BNP), is a cardiac neurohormone, and is released as prepro BNP and then enzymatically cleaved to the N-terminal-proBNP and BNP upon ventricular myocyte stretch. Blood measurements of BNP have been used to identify patients with heart failure (HF). The BNP assay is currently used in diagnosis, prognosis, screening, and response to treatment for patients with HF. In general, a BNP level below 100 pg/mL excludes acutely decompensated HF and levels > 500 pg/ml indicate decompensation. There are supportive data for using BNP to guide both inpatient and outpatient HF diagnosis and treatment. When BNP is elevated in acute coronary syndromes, pulmonary embolism, and sepsis, it implies that subclinical left ventricular dysfunction is present and a higher mortality rate can be expected. Elevated BNP levels before cardiac surgery are associated with higher rates of atrial fibrillation and death. After bypass surgery, as left ventricular function improves, the BNP level can be expected to fall. Lastly, in patients with aortic stenosis, aortic regurgitation, and mitral regurgitation, BNP elevates and is associated or may precede the development of symptoms and possibly can serve as a trigger for additional evaluation or intervention.
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PMID:Clinical applications of B-type natriuretic peptide levels in the care of cardiovascular patients. 1572 9

Reactive oxygen species (ROS) cause damage to the structure and function of tissues. Therefore tissues have systems that eliminate ROS. Bilirubin is one antioxidant that reacts with ROS to produce oxidative metabolites. Biopyrrins are one of the metabolites, the level of which in urine reflects oxidative stress. They are measured by non-competitive inhibition ELISA that employs anti-bilirubin antibody (24G7) and the results are corrected for the urinary concentration of cereatinine. Some reports suggested that psychological stress increased oxidative stress markers. Urinary biopyrrins were also elevated by speech stress, and the subjective stress score recorded by the speakers correlated with the level. The result suggests that bilirubin might eliminate ROS generated by psychological stress. From the beginning of the study of biopyrrins, their urinary level has been known to be increased by surgical stress. Furthermore, it was significantly higher in a major operation patient group than in a minor one, and correlated with operation duration. Sepsis increased the level in surgical patients. Ischemia-reperfusion elevates ROS and, as a result, biopyrrin production. An increase in urinary biopyrrins was observed in a coronary spastic angina group after a spasm provocation test, and the level in myocardial infarction patients with NYHA (New York Heart Association) classification became higher. Correlation between urinary biopyrrins and plasma B-type natriuretic peptide (BNP) was also reported. Research that determines the structures of biopyrrins and their clinical application are in progress.
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PMID:[Oxidative stress related diseases and biopyrrins]. 1579 50

The imbalance of Starling's forces was investigated in 25 elderly patients hospitalized for acute diastolic heart failure. Tissue Doppler evidence of elevated left ventricular filling pressures was present on admission in 17 patients with high B-type natriuretic peptide (BNP) levels. Serum proteins concentrations and colloid osmotic pressure, related to malnutrition and severe sepsis, were significantly less in the 8 patients without tissue Doppler evidence of elevated filling pressures, and a high level of BNP was consistent with paroxysmal elevation in filling pressures in this setting.
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PMID:B-type natriuretic peptide and tissue Doppler study findings in elderly patients hospitalized for acute diastolic heart failure. 1597 45

A 64-year-old female patient was admitted to a general intensive care unit with sustained hypotension resulting from severe sepsis. Her admission plasma B-type natriuretic peptide was elevated (407 pg/ml), and echocardiogram displayed normal ventricular dimensions and function. The right ventricular end-diastolic diameter increased with acute fluid loading, and this coincided with a parallel increase in B-type natriuretic peptide. Subsequent fluid depletion was accompanied by a reduction in both right ventricular end-diastolic diameter and B-type natriuretic peptide. The present case indicates that acute fluid loading may alter plasma B-type natriuretic peptide levels, and highlights the importance of taking the clinical context into account when interpreting these levels.
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PMID:The effects of acute fluid loading on plasma B-type natriuretic peptide levels in a septic shock patient. 1611 99

The family of natriuretic peptides comprises several structurally related 22-53-amino acid peptides, such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which are vasoactive peptides with vasodilator and diuretic properties and play an important role in cardiovascular homeostasis. The salutary cardiovascular effects of natriuretic peptides suggest that ANP and BNP may have a pathophysiological significance in the cardiac dysfunction of septic patients. We determined plasma levels of the stable N-terminal prohormone forms of ANP (NT-proANP) and BNP (NT-proBNP) as well as troponin I (TNI) as a marker of myocardial cell injury by ELISA methods in 19 septic patients and 19 healthy controls at day one of severe sepsis. Left ventricular ejection fraction (LVEF) was determined on day 1 of severe sepsis by echocardiography. Significantly higher concentrations of NT-proANP were measured in non-survivors (mean = 13415 pmol/l +/- SEM = 4295) and survivors (mean = 7386 pmol/l +/- SEM = 1807) as compared to controls (mean = 1404 pmol/l +/- SEM = 181; p<0.001). Levels of NT-proBNP were also significantly higher in non-survivors (mean = 3439 pmol/l +/- SEM = 1246; p<0.05) and survivors (mean = 1009 pmol/l +/- SEM = 263; p<0.001) as compared to controls (mean = 200 pmol/l +/- SEM = 24) and correlated well with an increase in TNI-levels (r = 0.71; p<0.001). NT-proANP and NT-proBNP may serve as useful laboratory markers to indicate myocardial dysfunction and may help to differentiate between survivors and non-survivors of severe sepsis.
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PMID:Increased plasma levels of NT-proANP and NT-proBNP as markers of cardiac dysfunction in septic patients. 1612 47

A term (39-wk-old) male neonate exhibited respiratory distress and anuria within 2 days of birth. The patient was diagnosed with pulmonary hypertension, polycystic kidney disease, and heart failure; his initial B-type natriuretic peptide concentration was 2460 pg/ml. After minimal response to loop diuretics, the patient was given an infusion of nesiritide 0.01 microg/kg/minute, with no loading dose. Urine output increased over 400%, and cardiac function improved. Nesiritide was titrated to 0.03 microg/kg/minute with no hypotension, decreased renal function, or adverse cardiac sequelae over the next 6 days. No subsequent changes in cardiac function occurred during the infant's stay in a progressive care unit, but he died at age 5.5 months due to sepsis. This case report demonstrates the successful first use of nesiritide therapy in a neonate with renal disease. Further studies are warranted to evaluate the safety and administration of this agent in the neonatal patient population.
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PMID:Nesiritide therapy in a term neonate with renal disease. 1646 34


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