Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous clinical results of left ventricular assist system (LVAS) therapy for cardiogenic shock due to acute myocardial infarction (AMI) are still unacceptable. Japanese LVAS was designed for left atrial inflow cannulation. However, to obtain higher initial LVAS flow and more decompression of left ventricular (LV) cavity and to avoid thromboembolic event, LV inflow cannulation is a preferable procedure. Therefore, LV inflow cannula for Japanese LVAS (Toyobo) was developed. We treated three AMI cases with Toyobo-LVAS using the new LV inflow cannula. All patients were in cardiogenic shock status since broad antero-septal AMI and treated with percutaneous cardio-pulmonary support before the LVAS installation. The LVAS was effective for recovery from cardiogenic shock status and multiple organ failure. Two patients died because of serious LVAS associated complications such as bleeding (case 1, 8 days) and cerebral thromboembolism (case 2, 45 days). One of them was assisted for 202 days and underwent second operation. Sixty days after removal of LVAS, the patient died due to sepsis. The technique of LV inflow cannulation is improved through our experiences. However, our result suggests that renovation of the regimen for anti-coagulation and anti-septic therapy are necessary.
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PMID:[A report of initial clinical use of left ventricular assist system with left ventricular inflow cannula for acute myocardial infarction]. 1184 53

Ischemic coronary syndrome is still the most frequent cause of mortality in the United States. Despite extensive investigation into the diagnosis of acute myocardial infarction (MI), this process remains quite complex because the majority of patients with chest pain have atypical symptoms and nonspecific electrocardiogram (ECG) changes and fall in the low or medium risk category. The biochemical cardiac markers play an important role in helping physicians make the diagnosis of acute MI and stratify patients for risk modifications. The use of cardiac markers in the diagnosis of acute MI is discussed extensively on pages 36-44 of this issue. This article focuses on reviewing other clinical applications. This field is large and rapidly expanding, making it impossible to cover every single clinical application of cardiac markers. Several research efforts are underway to find better cardiac markers and develop new applications for them. We review the literature on the use of cardiac markers, particularly troponin, with the risk stratification of acute coronary syndromes, the detection of reperfusion, perioperative MI, periprocedural MI, myocarditis, cardiac contusion, and MI associated with sepsis.
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PMID:Evolving clinical applications of cardiac markers: a review of the literature. 1210 2

A 29-year-old female was admitted with fever, purpura and hemiparesis. She was treated for meningococcal sepsis after a Gram stain of a purpuric lesion showed Gram-negative diplococci. CT scan of the brain revealed multiple haemorrhagic lesions with obliteration of the sulci and basal cisterns. In the course of the disease she developed an acute myocardial infarction. Besides wall motion abnormalities, echocardiography revealed a bicuspid aortic valve with a vegetation on one of its cusps. Despite these findings, both the doctors who were involved in the treatment of this patient and the consulted physician in this article failed to reject the diagnosis 'meningococcal sepsis' and to replace it with a more likely diagnosis, namely Staphylococcus aureus endocarditis. The patient died one day after admission due to transtentorial herniation. Although purpuric lesions are common in meningococcal sepsis, they are not specific for this disease. The false-positive result of the Gram stain resulted in a process known as 'premature closure': the diagnosis of meningococcal sepsis was accepted before it was fully verified. In this case, the consequence was that other diagnostic tests and symptoms were misinterpreted with the result that inappropriate antibiotic therapy was instituted.
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PMID:[Clinical reasoning and decision making in practice. Fever, purpura and hemiparesis in a 29-year old female]. 1247 58

There is a lack of consensus among cardiologists regarding the length of time patients should be hospitalized after an uncomplicated acute myocardial infarction (AMI) and successful direct percutaneous coronary intervention (d-PCI). The purpose of this study was to evaluate the feasibility and safety of early discharge (discharge <4 days after the procedure) for low risk patients with AMI who underwent successful d-PCI. From May 1996 through December 2001, d-PCI was performed in 898 consecutive patients with AMI. Of these 898 patients, 463 (51.6%) were stratified to be at low risk. Lower risk was defined as: (1) Killip classification < or = 2 on admission; (2) the infarct-related artery achieved normal blood flow without recurrent ischemia or reinfarction in the first 24 hours; (3) no mechanical or electrical complications after d-PCI. (4) no acute renal failure, acute stroke, or major bleeding complication; (5) no advanced congestive heart failure (defined as > or = New York Heart Association functional class 3); and (6) no sepsis. Patients who were discharged <4 days after undergoing the procedure were enrolled in group 1 (n = 266). Patients who were discharged > or = 4 days after undergoing the procedure were enrolled in group 2 (n = 197). Univariate analysis demonstrated that group 2 patients had a significantly longer hospital stay (P = 0.0001) than group 1 patients. At the first 30-day follow-up examination, there were no significant differences in the combined major cardiac events (death, recurrent isehemia, reinfarction, revascularization. or advanced congestive heart failure) between the group 1 and group 2 patients (1.50% vs 1.52%, P = 0.92). There were also no significant differences in the combined major noncardiac complications (acute stroke, acute renal failure, bleeding complications requiring blood transfusion, vascular sequelae, or sepsis) between the group 1 and group 2 patients (1.13% vs 0.51%. P = 0.89). Early discharge was feasible in a majority of the patients who experienced AMI and were at lower risk 24 hours after successful d-PCI. Thus, the patients had a shortened hospital stay and no increased risk.
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PMID:The feasibility and safety of early discharge for low risk patients with acute myocardial infarction after successful direct percutaneous coronary intervention. 1262 36

Therapeutic application of the serpin C1-inhibitor (C1-Inh) in inflammatory diseases like sepsis, acute myocardial infarction and vascular leakage syndrome seems promising, but large doses may be required. Therefore, a high-yield recombinant expression system for C1-Inh is very interesting. Earlier attempts to produce high levels of C1-Inh resulted in predominantly inactive C1-Inh. We describe the high yield expression of rhC1-Inh in Pichia pastoris, with 180 mg/l active C1-Inh at maximum. On average, 30 mg/l of 80-100% active C1-Inh was obtained. Progress curves were used to study the interaction with C1s, kallikrein, coagulation factor XIIa and XIa, and demonstrated that rhC1-Inh had the same inhibitory capacity as plasma C1-Inh. Structural integrity, as monitored via heat stability, was comparable despite differences in extent and nature of glycosylation. We conclude that the P. pastoris system is capable of high-level production of functionally and structurally intact human C1 inhibitor.
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PMID:Recombinant human C1-inhibitor produced in Pichia pastoris has the same inhibitory capacity as plasma C1-inhibitor. 1275 49

This review discusses the myocardial protective property of the insulin/glucose-insulin-potassium regimen and the mechanisms involved in this beneficial action. Several recent studies suggest that insulin not only is useful to control hyperglycemia and maintain glucose homeostasis but also may have the unique property to protect the myocardium from reperfusion injury and ischemia and prevent apoptosis of myocardial cells. The insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha, interleukin-6, macrophage migration inhibitory factor and other pro-inflammatory cytokines, and free radicals; and enhances the synthesis of endothelial nitric oxide and anti-inflammatory cytokines interleukin-4 and interleukin-10. Thus, the insulin/GIK regimen brings about its cardioprotective action. This may also explain why the insulin/GIK regimen is useful in sepsis and septic shock, myocardial recovery in acute myocardial infarction, and critical illness. It is suggested that the infusion of adequate amounts of insulin to patients with acute myocardial infarction, congestive heart failure, cardiogenic shock, and critical illness preserves myocardial integrity and function and ensures rapid recovery. In view of the suppressive action of insulin on the synthesis of proinflammatory cytokines and free radicals, it is possible that the insulin/GIK regimen, when used in a timely and appropriate fashion, may also protect other tissues and organs and facilitate in the recovery of patients who are critically ill.
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PMID:Insulin: an endogenous cardioprotector. 1450 50

NF-kappaB activation, and elevated concentrations of macrophage migration inhibitory factor (MIF), tumor necrosis factor-alpha (TNF-alpha), interleukin-1(IL-1), IL-6, free radicals, inducible nitric oxide (iNO), and stress hyperglycemia occurs in sepsis and this leads to systemic inflammatory response and myocardial depression seen in sepsis and septic shock. Conversely, insulin suppresses production of MIF, TNF-alpha, IL-1, IL-6, and free radicals, enhances endothelial NO generation, and enhances the production of anti-inflammatory cytokines IL-4, and IL-10, corrects stress hyperglycemia and improves myocardial function. This supports my earlier proposal that insulin (with or without glucose and potassium) therapy to maintain euglycemia suppresses the inflammatory response, improves myocardial function, and thus, is of benefit in acute myocardial infarction, sepsis andseptic shock.
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PMID:Insulin in sepsis and septic shock. 1462 Oct 41

Individuals vary considerably in their susceptibility to infection and in their ability to recover from apparently similar infectious processes. These differences can be partially explained by polymorphisms of the genes encoding proteins involved in mediating and controlling the innate immune response, the inflammatory cascade, coagulation, and fibrinolysis. It is evident from experimental studies that dysregulation of the coagulation system, which is characteristic of the pathophysiology of septic shock (a procoagulant and antifibrinolytic state), contributes to systemic inflammation and death in sepsis. Several genetic variations in proteins that increase coagulation or impair anticoagulation and fibrinolysis have been described. Thus, polymorphisms have been reported in prothrombin, fibrinogen, factor V, tissue factor, endothelial protein C receptor, and plasminogen activator inhibitor-1 genes. Some of them are associated with an increased risk of pulmonary emboli, acute myocardial infarction, stroke, and severe sepsis. Hence, the deletion polymorphism (4G) within the promoter region of the plasminogen activator inhibitor-1 gene leads to impaired fibrinolysis and influences the severity and outcome of meningococcal disease and the susceptibility to severe sepsis and multiple organ failure after trauma. The factor V Leiden mutation is associated with thrombotic events and has been reported to exacerbate purpura fulminans in meningococcal infection. Surprisingly, this genetic variant seems to provide a survival advantage in severe sepsis, underlying the extreme complexity of the interaction between inflammation and coagulation. The study of genetic polymorphisms might provide important insights into the pathogenesis of severe sepsis and could make it possible to identify individuals who are at risk of developing or dying of severe infections. As genetic associations are discovered, medical practice can become more preemptive, using the predictive ability of genetics to anticipate disease and recommend therapy.
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PMID:Importance of hemostatic gene polymorphisms for susceptibility to and outcome of severe sepsis. 1511 37

Adrenomedullin (AM) is a peptide that possesses potentially beneficial properties. Since the initial discovery of the peptide by Kitamura et al. in 1993, the literature has been awash with reports describing its novel mechanisms of action and huge potential as a therapeutic target. Strong evidence now exists that AM is able to act as an autocrine, paracrine, or endocrine mediator in a number of biologically significant functions, including the endothelial regulation of blood pressure, protection against organ damage in sepsis or hypoxia, and the control of blood volume through the regulation of thirst. Its early promise as a potential mediator/modulator of disease was not, however, entirely as a result of the discovery of physiological functions but due more to the observation of increasing levels measured in plasma in direct correlation with disease progression. In health, AM circulates at low picomolar concentrations in plasma in 2 forms, a mature 52-amino acid peptide and an immature 53-amino acid peptide. Plasma levels of AM have now been shown to be increased in a number of pathological states, including congestive heart failure, sepsis, essential hypertension, acute myocardial infarction, and renal impairment. These earliest associations have been further supplemented with evidence of a role for AM in other pathologies including, most intriguingly, cancer. In this review, we offer a timely review of our current knowledge on AM and give a detailed account of the putative role of AM in those clinical areas in which the best therapeutic opportunities might exist.
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PMID:The clinical relevance of adrenomedullin: a promising profile? 1546 89

Inflammation is an important indicator of tissue injury. In the acute form, there is usually accumulation of fluids and plasma components in the affected tissues. Platelet activation and the appearance in blood of abnormally increased numbers of polymorphonucleocytes, lymphocytes, plasma cells and macrophages usually occur. Infectious disorders such as sepsis, meningitis, respiratory infection, urinary tract infection, viral infection, and bacterial infection usually induce an inflammatory response. Chronic inflammation is often associated with diabetes mellitus, acute myocardial infarction, coronary artery disease, kidney diseases, and certain auto-immune disorders, such as rheumatoid arthritis, organ failures and other disorders with an inflammatory component or etiology. The disorder may occur before inflammation is apparent. Markers of inflammation such as C-reactive protein (CRP) and urinary trypsin inhibitors have changed our appraisal of acute events such as myocardial infarction; the infarct may be a response to acute infection and (or) inflammation. We describe here the pathophysiology of an anti-inflammatory agent termed urinary trypsin inhibitor (uTi). It is an important anti-inflammatory substance that is present in urine, blood and all organs. We also describe the anti-inflammatory agent bikunin, a selective inhibitor of serine proteases. The latter are important in modulating inflammatory events and even shutting them down.
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PMID:Pathophysiology and diagnostic value of urinary trypsin inhibitors. 1565 36


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