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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To save their patients from dialysis and transplantation, neurologists need simply remain alert to the possibility of renal failure, particularly in the context of systemic disease, diabetes, sepsis and drugs. Of the numerous territories shared by our respective specialities, we outline a pragmatic approach to the diagnosis and treatment of the vasculitides, underpinned by knowing which questions to ask, equally importantly when to ask them, and in the art of obtaining a tissue diagnosis. We consider the current evolving trial evidence that directs the usage of a growing arsenal of therapies in the induction and maintenance stages of vasculitis treatment, and extend this consideration to Lupus and Sjogren's.
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PMID:Notes on the kidney and its diseases for the neurologist. 1743 83

Theodore ("TR" or "Teddy") Roosevelt (1858-1919), who served as the twenty-sixth President of the United States from 1901 to 1909, was an "Icon of the American Century." Characterized by immense energy, numerous skills, zest for life, and enduring accomplishments, he made an impressive ascent to political importance. However, he also experienced serious, chronic, oral and systemic health problems. In spite of these significant health obstacles, he chose "the strenuous life," and cultivated a lifetime of joy, laughter and humor. TR was known as "the first president that smiled," and he was typically photographed and illustrated grinning from ear to ear. His flashing white teeth, wide smile, and engaging openness became welcome symbols of national and international acceptance. When Roosevelt died, suddenly and prematurely at the age of 60, dentists and physicians of that time began to investigate the probable medical causes of his untimely demise. The "focal infection hysteria" of the early 1900s convinced some of these health professionals that "a bad tooth", that previously had been endodontically treated, was the probable cause of death. Much of the early 20th century evidence-supporting the notion that oral sepsis was a "cause" of local or systemic disease-has now been proven, on closer inspection, to be anecdotal or of questionable scientific merit. Nevertheless, during those early days, it was common practice to extract all endodontically or periodontally involved teeth to eliminate any possible foci of infection that many clinicians believed could cause disease.
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PMID:Theodore Roosevelt's "presidential smile" and questionable dental health. 1784 49

Striking individual differences in severity of group A streptococcal (GAS) sepsis have been noted, even among patients infected with the same bacterial strain. We had provided evidence that HLA class II allelic variation contributes significantly to differences in systemic disease severity by modulating host responses to streptococcal superantigens. Inasmuch as the bacteria produce additional virulence factors that participate in the pathogenesis of this complex disease, we sought to identify additional gene networks modulating GAS sepsis. Accordingly, we applied a systems genetics approach using a panel of advanced recombinant inbred mice. By analyzing disease phenotypes in the context of mice genotypes we identified a highly significant quantitative trait locus (QTL) on Chromosome 2 between 22 and 34 Mb that strongly predicts disease severity, accounting for 25%-30% of variance. This QTL harbors several polymorphic genes known to regulate immune responses to bacterial infections. We evaluated candidate genes within this QTL using multiple parameters that included linkage, gene ontology, variation in gene expression, cocitation networks, and biological relevance, and identified interleukin1 alpha and prostaglandin E synthases pathways as key networks involved in modulating GAS sepsis severity. The association of GAS sepsis with multiple pathways underscores the complexity of traits modulating GAS sepsis and provides a powerful approach for analyzing interactive traits affecting outcomes of other infectious diseases.
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PMID:An unbiased systems genetics approach to mapping genetic loci modulating susceptibility to severe streptococcal sepsis. 1842 76

The ScpC protease of Streptococcus pyogenes degrades interleukin-8 (IL-8), a chemokine that mediates neutrophil transmigration and activation. The ability to degrade IL-8 differs dramatically among clinical isolates of S. pyogenes. Bacteria expressing ScpC overcome immune clearance by preventing the recruitment of neutrophils in soft tissue infection of mice. To study the role of ScpC in streptococcal sepsis, we generated an ScpC mutant that did not degrade IL-8 and thus failed to prevent the recruitment of immune cells as well as to cause disease after soft tissue infection. In a murine model of sepsis, challenge with the ScpC mutant resulted in more severe systemic disease with higher bacteremia levels and mortality than did challenge with the wild-type strain. As expected, the blood level of KC, the murine IL-8 homologue, increased in mice infected with the ScpC mutant. However, the elevated KC levels did not influence neutrophil numbers in blood, as it did in soft tissue, indicating that additional factors contributed to neutrophil transmigration in blood. In addition, the absence of ScpC increased tumor necrosis factor, IL-6, and C5a levels in blood, which contributed to disease severity. Thus, the ScpC mutant triggers high neutrophil infiltration but not lethal outcome after soft tissue infection, whereas intravenous infection leads to highly aggressive systemic disease.
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PMID:The ScpC protease of Streptococcus pyogenes affects the outcome of sepsis in a murine model. 1857

Infectious endocarditis is a systemic disease associated with high morbidity and mortality. Clinical recognition and effective management is challenging, but insights can be gleaned from relevant pathologic features. Risk factors include subaortic stenosis, possibly certain other congenital anomalies, and bacteremia. Auscultation can provide clues regarding valvular involvment, particularly when a diastolic left basilar murmur of aortic valve regurgitation is present. Aortic valve vegetations and insufficiency may also alter femoral arterial pulse characteristics. Echocardiography may facilitate diagnosis, particularly with aortic valve lesions, but may not be able to distinguish between small mitral valve vegetations and early chronic degenerative valve disease. Vegetative lesions develop along edges of valve closure on the ventricular aspect of the aortic valve and the atrial surface of atrioventricular valves. They may extend across valve leaflet, from valves to adjacent left atrial endocardium, interventricular or interatrial septum, or chordae tendineae. Vegetations can be friable and frequently embolize to spleen, kidney, and left ventricle - often before clinical recognition of the disease. Valvular insufficiency develops as a consequence of valvular vegetations, necrosis, perforation, or rupture of the chordae tendineae. Histopathologic appearance varies with respect to duration of disease and antimicrobial therapy. These factors influence the amount of necrotic material, blood clot, fibrin, and inflammatory cells which make up the vegetations. Bacteria are not always identified in valvular lesions, especially following antibacterial therapy, but may be detected in other organs. Common sequellae include congestive heart failure, sepsis, arrhythmias, and systemic organ infarction.
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PMID:Pathologic and clinical features of infectious endocarditis. 1908 8

Similar to apoptosis of nucleated cells, suicidal erythrocyte death or eryptosis is characterized by cell shrinkage, membrane blebbing and membrane phospholipid scrambling with phosphatidylserine exposure at the cell surface. Signaling of eryptosis involves formation of prostaglandin E(2) with subsequent activation of cation channels and Ca(2+)-entry and/or release of platelet activating factor (PAF) with subsequent activation of sphingomyelinase and formation of ceramide. Ca(2+) and ceramide stimulate cell membrane scrambling. Ca(2+) further activates Ca(2+)-sensitive K(+)-channels leading to cellular KCl loss and cell shrinkage and stimulates the protease calpain resulting in degradation of the cytoskeleton. Injuries triggering eryptosis may similarly compromise survival of nucleated cells. The case is made that analysis of enhanced eryptosis may direct to the pathophysiology of systemic disease. Examples presented include drug side effects, sepsis, haemolytic uremic syndrome, Wilson's disease, phosphate depletion and a rare condition caused by a mutation in GLUT1 turning the carrier into a cation channel.
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PMID:Eryptosis, a window to systemic disease. 1908 18

The term 'cardiorenal syndrome' (CRS) has increasingly been used in recent years without a constant meaning and a well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the CRS today includes 5 subtypes whose etymology reflects the primary and secondary pathology, the time frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can generally be defined as a pathophysiological disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical derangements, to make the rationale for management strategies and to design future clinical trials with accurate selection and stratification of the studied population.
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PMID:The cardiorenal syndrome. 1916 27

The term cardiorenal syndrome (CRS) has increasingly been used in recent years without a constant meaning and a well accepted definition. To include the vast array of interrelated derangements, and to stress the bi-directional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome includes today five sub-types whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal co-dysfunction secondary to systemic disease. The cardiorenal syndrome can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischaemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness.
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PMID:[Cardiorenal syndrome, current understanding]. 1955 20

The manifestations of perianal Crohn's disease vary from primary lesions such as skin tags and fissures, to diffuse septic destruction of tissue and sphincter muscle. These manifestations are often persistent and refractory to surgical treatment; however, a more disappointing scenario is when the treatment itself results in a chronic wound. The ideal approach for management involves basic surgical principles, careful patient selection, and realistic expectations. Choice of appropriate procedure, effective elimination of sepsis, thorough evaluation to rule out concomitant systemic disease, and appropriate use of fecal diversion are each an important principle. If proctectomy is necessary, several strategies such as intersphincteric dissection, avoidance of fecal contamination, and appropriate wound closure, are effective in diminishing the postoperative morbidity of an unhealed perineal wound. When an unhealed perineal wound develops in a patient with Crohn's disease, the initial management is conservative. When surgical treatment is necessary, success depends on careful patient selection, optimizing the patient's condition, elimination of sepsis, and choice of an effective technique for healing.
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PMID:Management of nonhealing perineal wounds. 2001 29

To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome (CRS) includes today five subtypes whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys, whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type 1 CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type 2 CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type 3 CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type 4 CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/ or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical disorders and to design future clinical trials.
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PMID:Cardiorenal syndromes: definition and classification. 2042 91


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