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

Acute and chronic liver disease contributes significantly to morbidity and mortality following hematopoietic cell transplantation (HCT). The best prognostic indicator for the development of severe liver dysfunction is an early rise in liver function test results after HCT. The leading causes soon after HCT are acute graft-versus-host disease (GVHD), sinusoidal obstruction syndrome, drug and total parenteral nutrition hepatotoxicity, sepsis, and viral infection. Hepatic herpesvirus and fungal infections after HCT, though uncommon, can be life-threatening and warrant immediate diagnosis and treatment. Hepatitis B, hepatitis C virus, iron overload, and chronic GVHD are among the most common causes for chronic liver disease after HCT. Because treatments are directed at the underlying etiology of liver disease, prompt diagnosis by means of laboratory tests, hepatic imaging, and often liver biopsy is required after HCT.
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PMID:Hepatic complications of hematopoietic cell transplantation. 1733 79

Following thorascopic thymectomy performed because of myasthenia gravis, a 25-year-old man was affected by fulminant hepatic failure (FHF) of unknown etiology. He was then transferred to our department, where his clinical situation worsened with the onset of renal failure, shock, coagulopathy and coma. Given the young age of the patient, the immediate availability of a donor, and the absence of a definite diagnosis of sepsis at the time, it was decided to proceed with liver transplantation. The results of a polymerase chain reaction (PCR) test (a technique that was unavailable at the referring hospital), which arrived only a few hours later, indicated the presence of herpes simplex virus (HSV) DNA in several of the patient's samples; this led to the formulation of a diagnosis of FHF due to HSV. It is worth noting that HSV-IgM and HSV-IgG assays had always been negative in this patient. Despite acyclovir therapy with initially encouraging clinical results, the patient died several days later because the viral infection had spread to the graft, lungs, heart, spleen, stomach and kidneys. Since evaluating antibody response is not always useful in diagnosing HSV infection, and particularly if PCR methodology is unavailable, it is worth initiating early empiric antiviral therapy when the etiology of FHF is indeterminate This is because the timeliness of treatment while awaiting virological confirmation may be critical to survival. If a liver transplantation becomes mandatory, careful consideration should be given to the extent of the viral infection and its response to therapy because of the possibility of viral spread to the graft.
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PMID:Liver transplantation due to Herpes Simplex virus-related sepsis causing massive hepatic necrosis after thoracoscopic thymectomy. 1752 22

Most children will have been evaluated for a febrile illness by 36 months of age. Although the majority will have a self-limited viral illness, studies done before the use of Haemophilus influenzae type b and Streptococcus pneumoniae vaccines showed that approximately 10 percent of children younger than 36 months without evident sources of fever had occult bacteremia and serious bacterial infection. More recent studies have found lower rates of bacterial infection (1.6 to 1.8 percent). Any infant younger than 29 days and any child that appears toxic should undergo a complete sepsis work-up. However, nontoxic-appearing children one to 36 months of age, who have a fever with no apparent source and who have received the appropriate vaccinations, could undergo screening laboratory analysis and be sent home with close follow-up. Empiric intramuscular antibiotics are suggested for some children; however, cerebrospinal fluid studies should be obtained first. Because immunizations have recently decreased infection rates for S. pneumoniae and H. influenzae type b, the recommendations for evaluation and treatment of febrile children are evolving and could involve fewer tests and less-presumptive treatment in the future. A cautious approach should still be taken based on the potential for adverse consequences of unrecognized and untreated serious bacterial infection.
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PMID:Evaluating fever of unidentifiable source in young children. 1761 20

Type I interferons (IFNs) are critical for antiviral responses. Here we generated a knockin mouse in which green fluorescence protein (GFP) was expressed under the control of the Ifna6 promoter. Virus-induced expression of GFP recapitulated various IFN-alpha subtypes. Systemic infection of the mice with Newcastle disease virus (NDV) increased GFP(+) plasmacytoid dendritic cells (pDCs) via the Toll-like receptor system, and GFP(+) conventional dendritic cells (cDCs) and macrophages via the RIG-I-like helicase system. By contrast, lung infection with NDV led to IFN-alpha production in alveolar macrophages (AMs) and cDCs, but not in pDCs. Specific depletion of AMs caused a marked defect in the initial viral elimination in the lung. pDCs produced IFN-alpha in the absence of AM-mediated viral recognition, suggesting that pDCs function when the first defense line is broken. Thus, AMs act as a type I IFN producer that is important for the initial responses to viral infection in the lung.
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PMID:Alveolar macrophages are the primary interferon-alpha producer in pulmonary infection with RNA viruses. 1772 16

The use of biomarkers provides a novel approach to diagnosing infection, its severity and treatment response. Biomarkers, especially procalcitonin and, to a lesser extent, C-reactive protein and interleukin 8, can improve the diagnostic and prognostic assessment of bloodstream infections. Both strengths and weaknesses of biomarkers must be recognized for rational and safe use in clinical settings. Cut-off ranges must be chosen within the specific clinical context. Ultrasensitive assays for procalcitonin, capable of measuring low levels in healthy individuals, may help to identify even 'subclinical' inflammatory states before the development of clinically evident sepsis. For immunocompromised patients, the use of biomarkers could lead to an earlier and more targeted antimicrobial therapy for patients at risk of sepsis, whereas those patients with viral illness or a non-infectious aetiology of inflammation who maintain low levels of procalcitonin over time can be withheld from antibiotic exposure. The time has arrived to move beyond the observational reporting of 'promising' biomarkers. Specific cut-off ranges must be proposed and intervention studies conducted to tackle the existing vicious cycle of diagnostic uncertainty, antibiotic overuse and emerging multi-resistance.
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PMID:Circulating biomarkers as surrogates for bloodstream infections. 1788 58

We present a case of a 60-year-old male patient with primary bone marrow anaplastic large cell lymphoma. He was admitted to the hospital with the symptoms of anemia and fever. There was no evidence of lymphadenopathy or splenomegaly. Immunoelectrophoresis showed the presence of a triple M gradient (double IgM and an IgG), with the IgG and one of the IgM paraproteins functioning as a cryoglobulin. The patient had no hepatitis C virus infection. Bone marrow biopsy showed massive CD30-positive, ALK-negative large lymphoid cell infiltration of T-cell origin with anaplastic morphology. PCR analysis of lymphoid cells separated from the bone marrow demonstrated the presence of a B/T hybrid genotype disorder with no evidence of the t(2;5), nor t(1;2) translocations. The patient entered a period of remission following CHOP chemotherapy. The patient subsequently died of sepsis as a consequence of serious humoral immunodeficiency.
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PMID:Primary bone marrow T-cell anaplastic large cell lymphoma with triple M gradient. 1792 57

This paper reviews a meeting at which basic pathophysiology of infections, mechanisms of action of hyperimmune products and pharmacokinetic and pharmacodynamic parameters, as well as currently available hyperimmunes and their potential new targets and uses, were discussed. A hyperimmune product was defined as either a monoclonal antibody or a polyclonal preparation enriched with antibody directed against one or more particular targets. A number of issues were emphasised, including: resistant bacterial pathogens, such as Staphylococcus aureus and Streptococcus pyogenes; the role of hyperimmune intravenous globulins in the prevention of sepsis in low birthweight infants; hepatitis B virus infection associated with liver transplantation; combination therapy; the potential role of hyperimmunes in the prevention and treatment of hepatitis C virus; and the use of immunoglobulins for the prophylaxis of Epstein-Barr virus-related lymphoproliferative disease. Routes of administration were also discussed. It was concluded that the development of hyperimmunes faces numerous obstacles. It was agreed that the use of hyperimmunes in clinical trials must be standardised; clinical trials must be large enough to have sufficient power to demonstrate efficacy with clear-cut end-points, and means need to be developed, in conjunction with regulatory agencies, for the feasible evaluation of combination products. However, progress in all these aspects will provide a wide range of hyperimmunes for future use.
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PMID:Hyperimmune products in the prevention and therapy of infectious disease: a report of a hyperimmune products expert advisory panel. 1803 67

Due attention has been given to infectious agents and immune responses to infection in sudden infant death syndrome (SIDS). It has been acknowledged that the pathological, epidemiological and genotypic findings in SIDS infants suggest an infectious aetiology possibly being potentiated by immunoregulatory polymorphisms, however, the cause of SIDS is a mystery and remains open to debate. Consistent pathological findings are seen which display similarities to the pathogenesis of toxaemic shock and/or sepsis. The major risk factors for SIDS parallel those for increased colonization and serious bacterial infections and the natural variation in the incidence of SIDS cases is typical of an infectious disease. The roles played by viral infection, immunoregulatory genes and suspected bacterial species are discussed herein.
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PMID:An infectious aetiology of sudden infant death syndrome. 1826 95

Hypercytokinemia is gaining recognition as the mechanism of fatality from influenza. No work to date has addressed the role of high mobility group box 1 protein (HMGB1) in influenza, the parallel being that in other severe proinflammatory cytokine syndromes (e.g., sepsis and malaria) levels of circulating HMGB1 are elevated and may correlate with death. Using a commercially available ELISA for HMGB1, we found that HMGB1 was not increased in the plasma of influenza virus-infected mice (A/Japan/305/57) on day 7 post infection, about the time of peak mortality, and peak levels of HMGB1 in the plasma did not occur until relatively late in infection, on day 9 post infection. In keeping with the late peak of HMGB1 being unassociated with mortality, administration of ethyl pyruvate, which inhibits active secretion but not passive release of HMGB1, to influenza virus-infected mice, did not affect their survival. Further work is required to determine whether influenza virus infection induces passive release of HMGB1, and whether HMGB1 neutralization with a specific Ab would improve survival.
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PMID:Systemic release of high mobility group box 1 protein during severe murine influenza. 1860

The haemophagocytic syndrome (HPS) is a rare but frequently fatal disorder of immune regulation caused by hypercytokinemia. Using cytometric bead array technique, the serum T-helper cell type 1 (Th1) and 2 (Th2) cytokines including interferon-gamma (IFN-gamma), tumour necrosis factor (TNF), interleukin (IL)-10, IL-6, IL-4 and IL-2 were determined in 24 children with de novo HPS and 87 children as control. The median levels of serum IFN-gamma, IL-10 and IL-6 in the acute phase of HPS were 901.7, 879.0 and 63.8 pg/ml, respectively, significantly higher than those after remission, and in the healthy volunteers and patients with viral infection. IL-4 was slightly elevated while IL-2 and TNF were within normal range in acute phase. Patients with bacterial sepsis showed an extremely high level of IL-6 and moderate level of IL-10, whereas IFN-gamma was only slightly elevated. Five patients were diagnosed with HPS according to the Th1/Th2 cytokine pattern 3-13 d earlier than they fulfilled the relevant diagnostic criteria. IL-10 level >2000 pg/ml was an unfavorable prognostic factor for HPS treatment response (P = 0.033) and outcome (P = 0.009). We conclude that the significant increase of IFN-gamma and IL-10 and a slightly increased level of IL-6 is an early, specific and prognostic cytokine pattern for childhood HPS.
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PMID:Early diagnostic and prognostic significance of a specific Th1/Th2 cytokine pattern in children with haemophagocytic syndrome. 1867 67


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