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

A 31-year-old man, who had undergone splenectomy 18 months previously because of hereditary spherocytosis, suddenly became ill, with fever, vomiting, epigastric pain and shock, and died 10 hours after the onset of his symptoms. Autopsy showed influenzal viremia, pneumococcemia and bilateral adrenal hemorrhage. The rapid course of the patient's illness emphasizes the serious risk of sepsis for individuals who have had a splenectomy. Anti-influenza immunization in such patients should be considered.
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PMID:Postsplenectomy sepsis due to influenzal viremia and pneumococcemia. 0 5

CMV infection is the major infectious complication following bone marrow transplantation. It is most often related to reactivation of latent infection in patients who were CMV seropositive before BMT. The incidence and severity have recently been modified by the use of preventive and curative treatments. Prevention of CMV infection with the transfusion of seronegative blood products is useful only when donor and recipient are seronegative. High-dose acyclovir has been shown effective in one randomized study. A multicenter study is currently being performed in Europe to confirm this result. Intravenous gammaglobulins seemed to lower the number of patients who incur interstitial pneumonitis but not the incidence of viremia. They also decreased the incidence of gram-negative sepsis and severe GVH and improved survival. The treatment is based on the use of gancyclovir. Several studies show that gancyclovir is more effective in asymptomatic patients with viral isolation from blood or bronchoalveolar lavage. The addition to gancyclovir of high-dose gammaglobulin improves survival in symptomatic patients with interstitial pneumonitis. This progress in the prevention and treatment of CMV infection has improved the overall results of allogeneic bone marrow transplantation.
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PMID:Prevention and treatment of CMV infection after allogeneic bone marrow transplant. 132 89

Cachexia in tumour-bearing patients involves loss of skeletal muscle proteins. In order to elucidate the mechanisms underlying this phenomenon, we tested the hypothesis of the presence of a circulating proteolytic factor (possibly interleukin-1, acting through an increased PGE2 release) in the plasma of cancer patients, because such a mechanism has been demonstrated in patients with sepsis or trauma and in animals with bacteraemia or viraemia. The effect of plasma from 13 malnourished cancer patients and 14 controls on PGE2 release and protein degradation (assessed as Tyr release) in rat diaphragm in vitro was evaluated; human recombinant interleukin-1 alpha (IL-1) was used for comparison. IL-1 increased PGE2 release (+44% at 5 U/ml), but did not greatly affect proteolysis. On the contrary, human plasma (125 microliters/ml) from both control and tumour-bearing individuals did not affect PGE2 release significantly, but greatly reduced Tyr release. The decrease in Tyr release by plasma was dose-dependent. In conclusion, our data indicate that, at variance with what was demonstrated in patients with trauma or sepsis, loss of skeletal muscle proteins in cancer patients is not mediated by a circulating factor. In addition, evidence is provided of dissociation between PGE2 and Tyr release and of lack of proteolytic activity for IL-1.
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PMID:Effect of plasma from cancer patients on rat skeletal muscle protein degradation and PGE2 release in vitro. 233 Mar 45

Severe hepatotoxicity from phenobarbital occurred in an infant boy who had a complicated illness with chronic bilateral subdural hematomas and sepsis. Skin rash began after 2 weeks of treatment, and signs of hepatocellular failure developed 3 weeks after phenobarbital had been started. Signs of severe liver disease included elevated aminotransferases, conjugated hyperbilirubinemia, significant coagulopathy, hepatosplenomegaly and ascites. Other features of this adverse drug reaction were unremitting fever, leukocytosis with eosinophilia and atypical lymphocytosis, and proteinuria. Sepsis, viral hepatitis, and metabolic liver disease were excluded. The child was on no other medication and had been previously well. In-vitro rechallenge of the patient's lymphocytes with cytochrome P-450 generated metabolites of phenobarbital showed extensive cytotoxicity compared to control. These data support the hypothesis that a defect in drug detoxification was responsible for the child's susceptibility to this drug hepatotoxicity.
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PMID:Phenobarbital hepatotoxicity in an 8-month-old infant. 233 96

2',3'-dideoxycytidine (ddC) inhibits replication of the immunodeficiency inducing strain of feline leukemia virus (FeLV-FAIDS) in vitro at concentrations ranging from 1-10 micrograms/ml. Additive antiviral effect is achieved when ddC is combined with either human recombinant alpha interferon (IFN alpha) or tumor necrosis factor (TNF) plus IFN alpha. Initial in vivo pharmacokinetic studies in cats, utilizing bolus intravenous administration of ddC (20 mg/kg), resulted in peak plasma concentrations of 15 micrograms/ml 1 min after administration and a half-life of approximately 1 h. These values could not be augmented with high levels of the deaminase blocker tetrahydrouridine administered prior to or concurrently with ddC. In vivo trials utilizing multiple, daily intravenous injections of ddC could not prevent the development of persistent viremia in cats infected with FeLV-FAIDS. To enhance ddC pharmacokinetics and antiviral activity, controlled release capsular implants were developed by blending ddC with a copolymer consisting of DL-lactide glycolide and hydroxypropyl cellulose, which was melt-spun into fibers and encapsulated in a sheath of polyethylene glycol for subcutaneous implantation. Pharmacokinetic studies, conducted in cats receiving an average dose of 600 mg of ddC, indicated an average peak plasma concentration of 17 micrograms/ml achieved at 6 h post implantation with 3.5 micrograms/ml noted at 48 h; and an extension of plasma half-life from 1.5 (bolus subcutaneous injection) to 20 h. sustained plasma concentrations of 1.5 to 10 micrograms/ml, equivalent to ddC levels previously shown to have anti-FeLV activity in vitro, were maintained throughout a 72 h period. Implantation devices could be replenished every 48 h and elevated plasma levels were sustained for four weeks without signs of clinical toxicity, sepsis or significant alterations in the hemogram. Initial clinical trials employing controlled release capsular ddC implants in vivo indicate significant retardation of FeLV-FAIDS replication throughout a four week treatment period.
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PMID:Treatment of FeLV-induced immunodeficiency syndrome (FeLV-FAIDS) with controlled release capsular implantation of 2',3'-dideoxycytidine. 254 37

In a prospective study during the summer and fall of 1982, enterovirus was isolated from 48 hospitalized children; in 29 (60%) enterovirus was isolated from CSF or blood, and in 19 (40%) only a presumptive diagnosis was established. Blood was positive in 21 (44%) and was the only positive specimen in two children. A presumptive diagnosis was provided within 4 days of admission in 38 (80%) and within 48 hours in 19 (40%) of the children from whom enterovirus was isolated. Viremia was most often detected in febrile infants younger than 3 months of age with a clinical picture simulating bacterial sepsis. The presence of viremia was inversely related to the presence of CSF pleocytosis and to virus isolation from CSF. The diagnosis of diseases caused by enterovirus is more accurate when blood culture is added to CSF stool and throat cultures.
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PMID:Viremia in hospitalized children with enterovirus infections. 298 58

The hypothesis has been advanced that the human systemic septic response is a function of the host and not of the type of infecting organism. Metabolic and physiologic data from five immunosuppressed transplant recipients with isolated cytomegaloviral sepsis and viremia were prospectively evaluated. Serial cultures obtained from lung, sputum, urine, wound, blood, and invasive lines were positive for virus and negative for bacterial or fungal pathogens. The results were compared with two data banks derived from either victims of multiple trauma without sepsis or surgical patients with early bacterial or fungal sepsis. Statistically significant differences between the patients and the nonseptic reference group were noted for cardiac index, total peripheral resistance, arteriovenous oxygen content difference, oxygen consumption, and levels of triglycerides, proline, phenylalanine, tyrosine, alpha-aminobutyrate, and alanine. No such differences were present for these data compared with the septic reference group. Physiologic data obtained just before death in three patients indicated a failure of oxygen transport. It appears that the systemic septic response to viral agents is indistinguishable by physiologic and metabolic criteria from that resulting from bacterial or fungal agents.
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PMID:Physiology and metabolism in isolated viral septicemia. Further evidence of an organism-independent, host-dependent response. 302 82

The systemic inflammatory response syndrome (SIRS) is the body's response to a multitude of chemical mediators. Conditions inciting the release of these mediators include bacterial sepsis, viremia, pancreatitis, trauma, neoplasia, heat stroke, and many others. The key to the successful management of SIRS lies in anticipation and not reaction. Resuscitation of the patient to supranormal levels, coupled with aggressive monitoring and support of target organs are essential.
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PMID:Systemic inflammatory response syndrome: septic shock. 787 61

Fibrosing cholestatic hepatitis (FCH) has been described as a specific manifestation of hepatitis B virus (HBV) infection in liver allograft recipients characterized by a rapid progression to liver failure. Only sporadic cases have been reported in other immunocompromised groups infected with HBV and in a few transplant recipients with hepatitis C virus (HCV) infection. We present the occurrence of FCH in 4 HCV-infected renal transplant recipients within a series of 73 renal transplant recipients with HCV infection followed up closely serologically and with consecutive liver biopsies. All 4 patients received the triple-immunosuppressive regimen (azathioprine, cyclosporine A, methylprednisolone). The interval from transplantation to the appearance of liver dysfunction was 1 to 4 months and to histological diagnosis, 3 to 11 months. The biochemical profile was analogous to a progressive cholestatic syndrome in 3 patients, whereas the fourth patient had only slightly increased alanine aminotransferase and gamma-glutamyl transferase (gammaGT) levels. Liver histological examination showed the characteristic pattern of FCH in 2 patients, whereas the other 2 patients had changes compatible with an early stage. All patients were anti-HCV negative at the time of transplantation, whereas 2 patients, 1 with incomplete and 1with complete histological FCH features, seroconverted after 3 and 31 months, respectively. The patients were HCV RNA positive at the time of the first liver biopsy and showed high serum HCV RNA levels (14 to 58 x 10(6) Eq/mL, branched DNA). HCV genotype was 1b in 3 patients and 3a in 1 patient. After histological diagnosis, immunosuppression was drastically reduced. Two patients died of sepsis and liver failure 16 and 18 months posttransplantation, whereas the seroconverted patients showed marked improvement of their liver disease, which was histologically verified in 1 patient. In conclusion, FCH can occur in HCV-infected renal transplant recipients. It seems to develop as a complication of a recent HCV infection during the period of maximal immunosuppression and is associated with high HCV viremia levels. There are indications that drastic reduction of immunosuppression may have a beneficial effect on the outcome of the disease.
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PMID:Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection. 1038 2

Sepsis is a condition at high risk for the patients to develop organ(s) or system dysfunction/failure and represent a very limiting process for survival. Researchers and clinicians proposed standardization of terminology for sepsis and related problems to improve communication and to evaluate the efficacy of preventive measures and therapeutic interventions. Interrelationship among systemic inflammatory response syndrome (SIRS), infection and sepsis are surrounded by non infectious satellite events such as trauma, burns, pancreatitis, haemorrhagic shock, immune-mediated organ injury and infectious cause such as fungemia, parasitemia, viremia. The prevalence of infections among intensive care patients has been reported to vary from 15 to 40%. Usually indicators of sepsis are persistent hyperlactatemia and supranormal level of DO2. These conditions may progress as a sort of dynamic process known as endotoxaemia condition which is mediated by derangement of biohumoral factors inducing immunological dissonance and ultimately concomitant or sequential organs dysfunction/failure. Multiple sources of sepsis is a phenomenon clearly associated with poor prognosis and all the sepsis trials managed in the last decades have failed on reducing mortality rate in enrolled patients. Development of scoring system routinely used at bedside represent an important method to establish cost-effectiveness in this exiting area of study and clinical management. Controversial results on sepsis need a sort of consensus at different level from researchers to clinician experiencing new strategies for prevention and more appropriately therapeutic approach for the management of this syndrome.
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PMID:Sepsis and organ dysfunction/failure. An overview. 1047 40


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