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 Parechovirus genus of the Picornaviridae family contains two species, Human parechovirus (HPeV) and Ljungan virus (LV). The HPeVs (including the former echoviruses 22 and 23, now HPeV type 1 (HPeV1) and HPeV2, respectively) cause a wide spectrum of disease, including aseptic meningitis, gastroenteritis, encephalitis, acute respiratory illness, and neonatal sepsis-like disease. The LVs were isolated from bank voles in Sweden during a search for an infectious agent linked to fatal myocarditis cases in humans. Because of the decline in use of cell culture and neutralization to investigate enterovirus-like disease, very few laboratories currently have the capability to test for parechoviruses. We have developed a real-time reverse transcription-PCR (RT-PCR) assay for detection of all known members of the genus Parechovirus. The assay targets the conserved regions in the 5' nontranslated region (5'NTR) of the parechovirus genome and can detect both HPeVs and LVs, unlike other published parechovirus 5' NTR assays, which only detect known HPeVs or only LVs. HPeV and LV can be differentiated by sequencing the 5'NTR real-time RT-PCR amplicon, when needed. The assay is approximately 100 times more sensitive than cell culture and may be used to test original clinical specimens. The availability of a broad-specificity PCR method should facilitate the detection of new human parechoviruses, as well as new parechoviruses in other mammalian species, and provide an opportunity to investigate the role of these viruses in human and animal disease.
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PMID:Detection of all known parechoviruses by real-time PCR. 1852 69

Since the ancient Greeks, we have learned that the pathophysiology of the human diseases relies on blood-borne humoral factors. This was the case with the sepsis myocardial depression, whose associated morbidity and mortality remained untouched during the last decades. Despite the growing knowledge of the possible involved mechanisms, our understanding of this serious condition is still in its infancy. Controversies have surrounded the real origin of septic-induced myocardial dysfunction, and it has been ascribed to inflammatory mediators, NO generation, interstitial myocarditis, coronary ischemia, calcium trafficking, endothelin receptor antagonist, and apoptosis. Although not fully understood, myocardial injury/depression remains a challenge for critical care practitioners.
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PMID:Myocardial depression in sepsis. 1870 15

Neonatal entero-viral sepsis is a rare but fulminant infection with multisystem involvement, often presenting with hepatitis, meningo-encephalitis, disseminated intravascular coagulation (DIC), and myocarditis. Neonatal myocarditis often proves fatal. We report here a case of neonatal enteroviral myocarditis with multisystem organ failure and ischemic cardiomyopathy that was managed medically.
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PMID:Enteroviral sepsis and ischemic cardiomyopathy in a neonate: case report and review of literature. 1881 54

The genetic expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF or ANP) and brain natriuretic peptide (BNP) have been studied mainly in the context of cardiac diseases associated with neuroendocrine and hemodynamic changes arising from cardiac dysfunction such as in chronic congestive heart failure. In this type of pathology, both ANF and BNP plasma levels change in an approximate coordinated fashion so that the use of these hormones as biomarkers of cardiac disease is, in principle, indistinctive. However, we reported that during an acute cardiac allograft rejection episode, BNP plasma levels can significantly increase in the absence of a similar increase in ANF plasma levels. We tested the hypothesis that these changes were related to cytokines and found that some pro-inflammatory cytokines, including TNFalpha and IL-1beta, selectively promote BNP synthesis and secretion in cultures of neonatal rat ventricular cardiocytes. This effect was found related to increased BNP promoter activity and sensitive to p38 mitogen-activated protein kinase inhibition.In order to determine in vivo if the selective up-regulation of BNP would be observed in inflammatory processes other than acute cardiac allograft rejection, we carried out investigation using the experimental autoimmune myocarditis rat model, which histologically resembles human giant cell myocarditis. It was found that this model is also accompanied by a specific increase in BNP-circulating levels although the cytokines involved seem to differ from those characterized earlier through in vitro studies.Recent studies in humans have found that in sepsis, plasma BNP levels increase in the absence of hemodynamic changes.In conclusion, BNP appears to be regulated uniquely in the setting of an inflammatory process. This sets it apart from ANF in terms of potential roles in the pathogenesis of disease and in its use as a biomarker of cardiac disease.
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PMID:Cardiac natriuretic peptides gene expression and secretion in inflammation. 1915 4

Drug-induced hypersensitivity syndrome (DIHS), also called drug rash with eosinophilia and systemic symptoms (DRESS), is a severe reaction usually characterized by fever, rash, and multiorgan failure, occurring 1-8 weeks after drug introduction. It is an immune-mediated reaction involving macrophage and T-lymphocyte activation and cytokine release, although no consensus has been reached as to its etiology. The skin, hematopoietic system, and liver are frequently involved. DIHS can mimic severe sepsis, viral infection, adult-onset Still disease (AOSD), or lymphoproliferation.We describe 24 consecutive patients with DIHS who were hospitalized between September 2004 and March 2008. Criteria for inclusion in this observational study were suspected drug reaction, eosinophilia >or=500/microL and/or atypical lymphocytes, involvement of at least 2 organs (skin being 1 of them), with suggestive chronology and exclusion of other diagnoses. Our cohort of 12 women and 12 men had a median age of 49 years (range, 22-82 yr), and 11 had skin phototype V or VI. Patients with mild or no rash were immunocompromised (7/24)- defined as treatment with prednisone (>or=10 mg/d) and another immunosuppressant drug, or human immunodeficiency virus infection. All patients were febrile (>38 degrees C), 14 had localized or generalized edema, 7 had pharyngitis, 8 had lymphadenopathy, 22 had hepatitis, 4 had nephritis, 2 had noninfectious and nonlithiasic angiocholitis or cholecystitis. Ten patients were hypotensive, 5 of whom had associated laboratory signs and/or imaging findings suggestive of acute myocardial dysfunction. Half of the patients had hemogram abnormalities, including eosinophilia. Nine DIHS patients fulfilled the Fautrel criteria for AOSD diagnosis, including glycosylated ferritin <20% in 4/11, with or without laboratory characteristics of hemophagocytosis. Twenty DIHS episodes occurred during the less sunny months of October to March.We determined 25-hydroxyvitamin D3 (25[OH]D3) levels in 18 patients and found that 9 patients had vitamin D deficiency (<25 nmol/L or <10 microg/L) and 5 had vitamin D insufficiency (25-50 nmol/L). Moreover, 25(OH)D3 levels were inversely correlated with ferritin values. After culprit-drug withdrawal, outcomes were favorable for all patients, including those with cardiac abnormalities under slow tapering of glucocorticoids.We recommend looking for the frequent but underdiagnosed hypersensitivity myocarditis with noninvasive diagnostic tools, such as N-terminal probrain natriuretic peptide, and promptly withdrawing the culprit drug and starting glucocorticoids. Vitamin D deficiency might be a DIHS risk or severity factor, especially for patients with high skin phototype and during the winter. Because DIHS clinical and laboratory patterns share similarities with AOSD and hemophagocytosis, DIHS should be included in their differential diagnoses.
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PMID:Drug-induced hypersensitivity syndrome: clinical and biologic disease patterns in 24 patients. 1944 Jan 16

Histophilus somni (Haemophilus somnus) is an important pathogen of cattle that is responsible for respiratory disease, septicemia, and systemic diseases such as thrombotic meningoencephalitis, myocarditis, and abortion. A variety of virulence factors have been identified in H. somni, including compositional and antigenic variation of the lipooligosaccharide (LOS). Phosphorylcholine (ChoP) has been identified as one of the components of H. somni LOS that undergoes antigenic variation. In this study, five genes (lic1ABCD(Hs) and glpQ) with homology to genes responsible for ChoP expression in Haemophilus influenzae LOS were identified in the H. somni genome. An H. somni open reading frame (ORF) with homology to H. influenzae lic1A (lic1A(Hi)) contained a variable number of tandem repeats (VNTR). However, whereas the tetranucleotide repeat 5'-CAAT-3' is present in lic1A(Hi), the VNTR in H. somni lic1A (lic1A(Hs)) consisted of 5'-AACC-3'. Due to the propensity of VNTR to vary during replication and cause the ORF to shift in and out of frame with the upstream start codon, the VNTR were deleted from lic1A(Hs) to maintain the gene constitutively on. This construct was cloned into Escherichia coli, and functional enzyme assays confirmed that lic1A(Hs) encoded a choline kinase, and that the VNTR were not required for expression of a functional gene product. Variation in the number of VNTR in lic1A(Hs) correlated with antigenic variation of ChoP expression in H. somni strain 124P. However, antigenic variation of ChoP expression in strain 738 predominately occurred through variable extension/truncation of the LOS outer core. These results indicated that the lic1(Hs) genes controlled expression of ChoP on the LOS, but that in H. somni there are two potential mechanisms that account for antigenic variation of ChoP.
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PMID:Molecular characterization of phosphorylcholine expression on the lipooligosaccharide of Histophilus somni. 1968 67

Since the introduction of cardiac plasma troponin measurements, a significant number of patients were seen with chest pain, elevated troponin levels but no significant coronary artery disease. Pulmonary embolism, aortic valve disease, myocarditis, sepsis, trauma, arrythmias, stress cardiomyopathy and dilated cardiomyopathy stand among possible causes for this syndrome. In some cases, myocardial strain could be the mechanism underlying this phenomenon, since it is known that the stimulation of stretch-responsive integrins may lead to the release of cardiac troponin I. In the present text, a case is made in favour of classifying this syndrome, of chest pain with increased values for plasma cardiac troponin, with or without ECG changes, in the absence of definite myocardial infarction or coronary artery disease, as pseudo myocardial infarction (PMI). This constitutes a new definition for a concept with decades, formerly centered on clinical and electrocardiographic changes mimicking infarct. The case is based on the search of scientific truth, on avoidance of unnecessary cardiac examinations, on avoidance of unnecessary drug therapy and on avoidance of unnecessary legal liability. PMI should be seen as a working diagnosis, since a more definitive diagnosis can be reached at all time. It should also be seen as a heterogeneous group of patients - several different diseases and conditions can lead to this phenomenon. But it must certainly not be seen as a benign condition, since published studies point in a totally different direction.
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PMID:Pseudo myocardial infarction - a condition in need to be redefined? 1985 81

The mortality and morbidity of salmonella infections is seriously underestimated. Salmonella myocarditis is an unusual complication of salmonella sepsis in adults. Cases that do occur may be associated with high morbidity and mortality. We present a rare case of salmonella myocarditis with multi-organ failure in a previously healthy young adult man who was brought to the emergency room with fever, diarrhea, shortness of breath, and altered sensorium, discovered to have acute pulmonary edema and respiratory compromise for which he was assisted with mechanical ventilation for 8 days. Blood culture grew Salmonella typhi. Biochemically he exhibited myocardial, hepatic, and muscular enzymatic surge with renal failure, features of rhabdomyolysis, and disseminated intravascular coagulation. The patient showed a progressive improvement on treatment with ceftriaxone for 2 weeks in addition to decongestive therapy. He was discharged in good condition afterward.
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PMID:Salmonella myocarditis in a young adult patient presenting with acute pulmonary edema, rhabdomyolysis, and multi-organ failure. 1994 25

For years, cardiac troponins (cTn) have been regarded as the preferred biomarkers for the diagnosis of myocardial infarction and for the risk stratification of patients with acute coronary syndromes, as well as for the selection of patients who need an early invasive strategy, and for the guidance of adjunctive pharmacological therapy. In addition, measurement of cTn has been found useful for detection of myocardial necrosis in conditions unrelated to myocardial ischemia including acute pulmonary embolism, myocarditis, heart failure, sepsis, and end-stage renal disease. In these conditions, an unfavorable prognosis is unequivocally associated with detectable concentrations of cTn.A major limitation of most currently available cTn assays is the lack of adequate precision, i.e., to measure cTn concentrations at the 99th percentile value with a coefficient of variation < 10%. As a consequence, many manufacturers have developed more sensitive cTn assays that now comply with precision criteria required by the Joint European Society of Cardiology/ American College of Cardiology/American Heart Association/World Heart Federation Task Force for the Redefinition of Acute Myocardial Infarction.Using assays with higher analytic sensitivity more patients will be seen in clinical practice with the high-sensitivity cardiac troponin T (TnThs) above the 99th percentile discriminator. The causes of these elevations may be due to acute, subacute and chronic cardiac disease such as heart failure or cardiomyopathies.
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PMID:Troponins and high-sensitivity troponins as markers of necrosis in CAD and heart failure. 2002 39

Human enteroviruses are associated with various clinical syndromes from minor febrile illness to severe, potentially fatal conditions like aseptic meningitis, paralysis, myocarditis, and neonatal enteroviral sepsis. Between June 2000 and August 2008 echovirus (E) type 2, 4, 6, 7, 9, 11, 13, 25, 30, coxsackievirus (CV) -A16, -A19, -B5, and enterovirus 71 (EV71) were reported in Hungary. In this study, 29 previously enterovirus positive samples from 28 patients diagnosed with hand, foot and mouth disease, meningitis and encephalitis, were molecularly typed. The genetic relationships of identified serotypes CV-A16, EV71, and E30 were assessed by direct sequencing of genomic region encoding the capsid protein VP1. The sequences were compared to each other and sequences from other geographical regions possessed in Genbank. The phylogenetic analysis of CV-A16 revealed that the viruses were mostly of Far-Eastern or Asia-Pacific origin. Typing of EV71 showed that one virus from 2000 belonged to genotype C1 and five viruses observed in 2004 and 2005 were identified as genotype C4. The 11 echovirus 30 strains showed homology with those of neighbor European countries. The molecular examination of E30 revealed that three separate lineages circulated in 2000, 2001, and 2004-2006 in Hungary.
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PMID:Detection of non-polio enteroviruses in Hungary 2000-2008 and molecular epidemiology of enterovirus 71, coxsackievirus A16, and echovirus 30. 2004 91


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