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)

So-called "Postoperative Erythroderma" was experienced in a 68 year-old man who received CABG for unstable angina. After a seemingly uneventful recovery, he revealed high grade fever on 13th post operative day (POD), rashes over the whole body on 15th POD and pancytopenia on 20th POD. He died of sepsis, multiple organ failure and DIC on 21st POD. Blood transfusion (concentrated red cell: 3 units) was done on operation. In this case, the rate of premature and atypical lymphocytes increased, and the ratio of OKT4 (helper)/OKT8 (suppressor) decreased. These findings of the examination suggested that there was a possibility of cell-mediated immunological depression. We considered this to be acute GVHD after blood transfusion.
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PMID:[A case of "postoperative erythroderma" following coronary artery bypass grafting operation]. 183 33

As age and smoking are common risk factors, patients with lung cancer frequently have coexistent ischaemic heart disease. Ignoring the coronary disease results in an unacceptable operative mortality, whilst sequential coronary grafting and lung resection may prejudice the results of the resection. A series of 10 patients underwent combined coronary revascularization (average 2.9 grafts per patient) and lung resection for carcinoma (seven lobectomies, one bilobectomy, one sleeve lobectomy, and one pneumonectomy). The majority of patients had unstable angina, triple vessel or left main coronary artery stenosis and poorly staged tumours. There was no operative mortality and the average hospital stay was 20 days. Half the patients had significant peri-operative morbidity; seven are alive and well at between 12 and 38 months follow-up; but three have died of recurrent carcinoma (one with associated sepsis) at 3, 8, and 13 months. Combined coronary revascularization and lung resection can be safely performed in selected patients. The early morbidity is mainly related to the cardiac procedure and impaired respiratory function preoperatively, but the long-term results are dependent upon the control of the lung carcinoma.
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PMID:Concomitant coronary revascularization and resection of lung cancer. 848 Nov 33

The expression of tissue factor (TF) by monocytes/macrophages leads to thrombin generation and contributes to their physiological and pathophysiological roles in wound repair, disseminated intravascular coagulation linked to sepsis, postoperative thrombosis, unstable angina, atherosclerosis, chronic inflammation and cancer. Regulation of TF expression in monocytes is controlled by the transcription factors NF-kappaB and AP-1. In whole blood, the activation of the transcription factors is mediated through the phospholipase A2 pathway. Platelets play a crucial role in the expression of TF activity in monocytes, and granulocytes are mandatory in provoking the platelet effect in a P-selectin-dependent reaction. Although all induced or constitutive TF is expressed on the surface of monocytes, its catalytic activity is only about 10% compared to the activity of lysed cells. This phenomenon has been attributed to the increased availability of anionic phospholipid (phosphatidylserine) after cell lysis. At the surface of viable cells, the transmembrane phospholipid distribution and its regulation may be important for the expression of the catalytic activity of the complex of TF and activated factor VII. Phosphatidylserine pathophysiologically exposed at the outer surface of monocytes may, similar to that for platelet membranes, provide a strong stimulus for thrombin generation.
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PMID:Tissue factor expression by monocytes: regulation and pathophysiological roles. 981 23

This study evaluated the role of serum cardiac troponin I as a biochemical marker for the diagnosis of acute coronary syndromes in the presence of noncardiac diseases. Diagnostic characteristics were examined in 102 consecutive patients who were found to have serum cardiac troponin I levels higher than the upper reference limit of 0.6 ng/mL. Of 102 patients with cardiac troponin I levels of >0.6 ng/mL, 35 did not have the final diagnoses of acute coronary syndromes (myocardial infarction or unstable angina) but had various other final diagnoses, including nonischemic dilated cardiomyopathy, muscular disorders, central nervous system disorders, HIV disease, chronic renal failure, sepsis, lung diseases, and endocrine disorders. The mean value of serum cardiac troponin I in the patients with diseases other than acute coronary syndromes was significantly lesser than in those with acute coronary syndromes (2.0+/-1.9 [SD] v. 24.7+/-28.2 ng/mL; P<.0001). There were significantly fewer histories of chest pain and prior myocardial infarction in patients with diseases other than acute coronary syndromes than in those with acute coronary syndromes (history of chest pain, 3 v. 48 patients [P<.001]; history of prior myocardial infarction, 0 v. 30 patients [P<.001]). In conclusion, elevated serum levels of cardiac troponin I, especially in the lower ranges, should be interpreted with caution, particularly in patients suffering from acute illnesses who lack other diagnostic features suggestive of acute coronary ischemic events.
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PMID:Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes. 1033 75

High circulating levels of the procoagulant molecule tissue factor (TF) are associated with thrombosis in a variety of diseases including unstable angina, cancer, and sepsis. Currently, there are no clinical assays to measure the level of TF activity in whole blood. We present an assay called Tissue Factor Clotting Time ("TiFaCT") that detects fibrin formation in human blood. The mean baseline clotting time in a healthy population was 472 +/- 94 s (mean +/- SD, n = 150). Bacterial lipopolysaccharide (LPS or endotoxin) shortened the clotting time in a time-dependent manner. Inhibitory anti-TF antibodies prolonged the clotting time of LPS-stimulated blood, indicating that the shortened clotting time was due to induction of TF expression. Patients with unstable angina had shortened mean baseline clotting time (284 +/- 86, n = 13) compared with healthy volunteers (474 +/- 98, n = 30), suggesting that these patients had elevated levels of circulating TF. The TiFaCT assay should prove clinically useful in quantifying the levels of circulating TF in patients at risk of thrombosis.
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PMID:Measurement of tissue factor activity in whole blood. 1074 52

Tissue factor (TF) plays a crucial role in the pathogenesis of thrombotic, vascular and inflammatory disorders. Thus, the inhibition of this membrane protein provides a unique therapeutic approach for prophylaxis and/or treatment of various diseases. Tissue factor pathway inhibitor (TFPI), the only endogenous inhibitor of the TF/Factor VIIa (FVIIa) complex, has recently been characterised biochemically and pharmacologically. Studies in patients demonstrated that both TF and TFPI may be indicators for the course and the outcome of cardiovascular and other diseases. Based on experimental and clinical data, TFPI might become an important drug for several clinical indications. TFPI is expected to inhibit the development of post-injury intimal hyperplasia and thrombotic occlusion in atherosclerotic vessels as well as to be effective in acute coronary syndromes, such as unstable angina and myocardial infarction. Of special interest is the inhibition of TF-mediated processes in sepsis and disseminated intravascular coagulation (DIC), which are associated with the activation of various inflammatory pathways as well as of the coagulation system. A Phase II trial of the efficacy of TFPI in patients with severe sepsis showed a mortality reduction in TFPI- compared to placebo-treated patients and an improvement of organ dysfunctions. TFPI can be administered exogenously in high doses to suppress TF-mediated effects, alternatively high amounts of TFPI can be released from intravascular stores by other drugs, such as heparin and low molecular weight heparins (LMWH). Using this method high concentrations of the inhibitor are provided at sites of tissue damage and ongoing thrombosis. At present, clinical studies with TFPI are rather limited so that the clinical potential of the drug cannot be assessed properly. However, TFPI and its variants are expected to undergo further development and to find indications in various clinical states.
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PMID:Tissue factor pathway inhibitor: an update of potential implications in the treatment of cardiovascular disorders. 1177 96

We designed this study to define determinants of gastrointestinal complications after cardiac surgery. From January 1992 through December 2000, 11,058 patients underwent cardiac surgery on cardiopulmonary bypass at our institution. Data were prospectively collected and univariate and multivariate analyses conducted. A total of 147 gastrointestinal complications occurred in 129 patients (129/11,058; 1.2%) including gastroesophagitis (18, 12.2%), upper gastrointestinal hemorrhage (42, 28.6%), perforated peptic ulcer (7, 4.7%), cholecystitis (10, 6.8%), pancreatitis (13, 8.8%), intestinal ischemia (17, 11.5%), colitis (18, 12.2%), diverticulitis (5, 3.4%), intestinal occlusion (2, 1.1%), lower gastrointestinal hemorrhage (1, 0.7%), and mixed gastrointestinal complications (14, 9.5%). Patients with gastrointestinal complications were significantly older and had significantly higher comorbidity (unstable angina, chronic renal failure, and peripheral vascular disease), morbidity (prolonged mechanical ventilation, intraaortic balloon pumping, bleeding, acute renal failure, stroke, and infection), and mortality rates (22.5% vs 4%, P < 0.0001). They also had longer cardiopulmonary bypass times and higher valvular surgery rates. Multivariate analysis identified 6 independent predictors for gastrointestinal complications: prolonged mechanical ventilation (odds ratio [OR], 5.5), postoperative renal failure (OR, 4.2), sepsis (OR, 3.6), valve surgery (OR, 3.2), preoperative chronic renal failure (OR, 2.7), and sternal infection (OR, 2.4). Factors such as mechanical ventilation, renal failure, and sepsis are the stronger predictors for GI complications, causing splanchnic hypoperfusion, hypomotility, and hypoxia. Furthermore, excessive anticoagulation after valve replacement may lead to GI hemorrhage. Valve surgery, often requiring anticoagulation, increases bleeding. Monitoring mechanical ventilation and hemodynamic parameters, adopting early extubation and mobilization measures, preventing infections, and strictly monitoring renal function and anticoagulation may prevent catastrophic abdominal complications.
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PMID:Determinants of gastrointestinal complications in cardiac surgery. 1506 41

Tissue factor (TF) is a transmembrane glycoprotein that binds its zymogen cofactor, Factor VIIa (FVIIa) on the cell surface. Together (TF/FVIIa) they activate Factor X (FX) and Factor IX (FIX) and start the extrinsic pathway of blood coagulation. As such, the TF/FVIIa complex plays an important role in normal physiology as well as in thrombotic diseases such as unstable angina (UA), disseminated intravascular coagulation (DIC), and deep vein thrombosis (DVT). In addition to its function as an initiator of coagulation, TF/FVIIa plays an important role in inflammation. Expression of TF on the cell surface and its appearance as a soluble molecule are characteristic features of acute and chronic inflammation in conditions such as sepsis and atherosclerosis. Here we demonstrate that BCX-3607, a small molecule potent inhibitor of TF/FVIIa, reduces thrombus weight in an animal model of DVT. BCX-3607 also decreases the level of interleukin-6 (IL-6) in a LPS-stimulated mouse model of endotoxemia. Additionally, in vitro studies indicate that BCX-3607 blocks the generation of TF/FVIIa-induced IL-8 mRNA in human keratinocytes and reduces the TF/FVIIa-mediated generation of IL-6 and IL-8 in human umbilical vein endothelial cells (HUVEC). Therefore, BCX-3607 might block the TF/FVIIa-mediated coagulation and inflammation associated with pathological conditions.
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PMID:The antithrombotic and anti-inflammatory effects of BCX-3607, a small molecule tissue factor/factor VIIa inhibitor. 1637 35

Gastric perforation in association with incarceration of a hiatus hernia rarely features on a list of differential diagnoses of acute chest pain. A patient presented to the emergency department with acute chest pain characteristic of myocardial ischaemia. Several risk factors for ischaemic heart disease (IHD) were present. Investigations revealed normal cardiac enzymes and normal electrocardiography both initially and at 90 mins. A chest radiograph demonstrated the presence of a hiatus hernia. The patient was diagnosed with, and treated for, unstable angina. A troponin T test at 12 h post-admission was normal. The patient's clinical condition continued to deteriorate. The source of her pain was found to be gastric perforations in association with an incarcerated hiatus hernia. Her postoperative course was complicated by pulmonary and intra-abdominal sepsis necessitating admission to the intensive care unit where she remained for 23 days. This case highlights the challenge that non-cardiac chest pain presents to the acute care physician. Patients who present with risk factors for and symptoms consistent with a diagnosis of IHD may have non-cardiogenic pathology which can be life-threatening.
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PMID:Gastric perforation secondary to incarcerated hiatus hernia: an important differential in the diagnosis of central crushing chest pain. 1765 2

Staged or combined carotid endarterectomy (CEA) offers the potential benefit of decreased neurological morbidity during and after cardiac surgery; however, the strategy for treating unstable high-risk patients, who need urgent coronary artery surgery, remains unresolved. We report in-hospital and 30-day outcomes of 23 consecutive patients admitted with unstable angina, who underwent carotid angioplasty and stenting (CAS) immediately prior to urgent coronary artery surgery, from October 2007 to October 2008. Aspirin and unfractioned heparin were administrated during carotid stenting and clopidogrel was only started after cardiac surgery. All patients remained event-free during and immediately after the carotid stenting procedure. One patient died due to sepsis 22 days after cardiac surgery. There was neither stroke nor myocardial infarction at follow-up. No patient needed a cardiac or carotid re-intervention. This new approach (combined carotid stenting and coronary artery surgery) provides a less radical intervention, can be performed with a low periprocedural complication rate and may become a valuable alternative in the treatment of high-risk patients with combined carotid and cardiac disease.
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PMID:Combined carotid stenting and urgent coronary artery surgery in unstable angina patients with severe carotid stenosis. 1962 41


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