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)

Post-trauma immunosuppression is characterized by T-cell subpopulation changes and the presence of a low molecular weight suppressive active peptide (SAP), which suppresses T-cell blastogenesis and neutrophil chemotaxis. This study evaluated post-trauma T-cell antigens and suppressive active peptide/T-cell interactions to determine if the suppressive active peptide concentrations predictive of sepsis can cause changes in antigen expression predictive of sepsis. Human lymphocyte markers and differentiation antigens were analyzed post-trauma using flow cytometry for markers predictive of sepsis. Changes induced by purified suppressive active peptide incubated with normal human lymphocytes were similarly analyzed by flow cytometry. SAP concentrations for incubation were chosen which correlated with concentrations in patients developing clinical sepsis. Significant T-cell changes in patients who developed sepsis include: decreased total T-cells, decreased helper cells, decreased natural killer cells, increased Ia expressing mononuclear cells, increased activated T-cells, (L22) and increased IL-2 expressing cells (TAC). Suppressive active peptide can activate T-cells and cause significant increased expression of IL-2 receptors and natural killer cells. Other T-cell changes following trauma predictive of sepsis seem to occur independent of in vitro incubation with suppressive active peptides. IL-2 expressing cells are known to be more readily suppressed by the suppressive peptide. Suppressive peptide activation and subsequent inhibition of T-cells suggests a potential way to explain suppressive peptide-induced immunosuppression following trauma.
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PMID:Trauma peptide induction of lymphocyte changes predictive of sepsis. 326 88

Technical procedures normally used for open packing in our Institute (ICU) are described. Results of this procedure, utilized in thirteen patients suffering from infected pancreatic necrosis and multiple organ failure are reported. The grade of pancreatitis severity has been studied in detail. At admission patients presented a mean Ranson score of 6 and the morphological alteration sec. Balthazar was D in six patients and E in seven. At least two organs were insufficient at the beginning of our observation and the mean number of insufficient organs was 4. The mean APACHE II score was 20. Necrosis was documented in all patients. They were all admitted to ICU and the mean time of treatment was 50 days. Daily debridement was performed and continuous lavage was later added to daily open review. Three patients died, one from local bleeding and two from respiratory insufficiency. No patient died of sepsis and no mortality was observed in the last six cases. According to the severity of Ranson score, APACHE II, the number of insufficient organs and TAC morphological alteration predicted mortality rate should have been 70-80%; on the contrary, it was 25%. In conclusion open packing seems to be the correct treatment for infected pancreatic necrosis, particularly when it is complicated by multiple organ dysfunction.
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PMID:[Open treatment in acute severe pancreatitis]. 876 85

A 13-month-old Japanese female with Haemophilus influenzae type b meningitis presented with unusually severe septic shock and cerebral infarction in half a day of fever. The initial therapy of plasma-derived activated protein C (Anact C) led to an impressive effect on the aggressive condition. However, purpura fulminans and the consistent decline of plasma protein C activity (<20%) required prolonged activated protein C therapy and gene analysis. The patient carried a novel heterozygous mutation of PROC (exon 4; 335 GAC>TAC, Asp46Tyr). This is the first report of infectious purpura fulminans in a protein C-deficient heterozygote. The clinical onset and treatment course adequately corroborated the aggravated immune/hemostatic reactions and the cytoprotective effects of activated protein C replacement in human heterozygous protein C deficiency. The monitoring of plasma protein C activity and sufficient administration of activated protein C product could improve the outcome of severe sepsis in children.
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PMID:Fulminant sepsis/meningitis due to Haemophilus influenzae in a protein C-deficient heterozygote treated with activated protein C therapy. 1875 23