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)

Total hemolytic complement (CH50), conversion of C3 by inulin and cobra venom factor (CoVF), and immunochemical levels of Clq, C4, C2, C3, C5, factor B, properdin, C3b inactivator (KAF), and immunoglobulins (Igs) G, A, and M were measured in the sera of ten patients with abdominal trauma and ten medical patients with septicemia without trauma. Reduction in C3 conversion by CoVF and decrease in the levels of properdin and KAF were demonstrated in the trauma sera. CH50 and the level of C5 were also decreased. Conversion of C3 by inulin and levels of factor B, Clq, C4, C2, and C3 were found to be normal in the patients' sera. Complement levels and activities were found to be normal in the sera of the septic non-trauma patients. A decrease in serum IgM was observed in both patient groups; levels of IgG and IgA were normal. These results indicated that abnormalities of immunoglobulin and of the alternative and classical complement pathways were associated with nonburn trauma. Moreover, the data suggested that consumption of the classical complement pathway associated with septicemia in the thermally injured patient resulted from synergism between the trauma and infection rather than from septicemia per se.
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PMID:Host defense against opportunist microorganisms following trauma. II. Changes in complement and immunoglobulins in patients with abdominal trauma and in septic patients without trauma. 66 70

Total hemolytic complement (CH(50)), conversion of C3 by inulin, and immunochemical levels of Clq, C4, C2, C3, C5, factor B, C3b inactivator (KAF), and properdin were measured in the sera of 15 patients with severe thermal injury during nine weeks postburn. Five of the 15 patients had multiple episodes of septicemia as documented by positive blood cultures and clinical findings. Decrease in CH(50), Clq, C4, C2, C3, and C5 occurred prior to and during septic episodes in these patients. Although conversion of C3 by inulin was often reduced during septic episodes, levels of factor B and KAF were generally normal or elevated. In only one patient did consumption of complement occurring during septicemia decrease the opsonic capacity of the patient's sera for the patient's infecting microorganism, an isolate of E. coli; sera from the same patient opsonized her infecting strain of S. aureus normally. The microorganisms isolated from the other septic patients, which were opsonized normally by the patients' sera despite complement consumption, were also with one exception strains of Staphylococci. In the nonseptic burned patients, decrease in properdin and C3 conversion by inulin, and increase in C3, factor B and KAF were demonstrated as we have previously reported. The results indicate that the classical complement pathway was activated during septicemia in burned patients and that activation of this pathway occurred preferentially due to inhibition of the alternative pathway. In addition, the data show that complement consumption may reduce the opsonic capacity of a patient's sera for certain microorganisms and not for others.
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PMID:Host defense against opportunist microorganisms following trauma. I. Studies to determine the association between changes in humoral components of host defense and septicemia in burned patients. 66 83

Serum opsonic activity for E. coli 075, conversion of C3 by inulin, total hemolytic complement (CH(50)), levels of native C3, factor B, C3b inactivator (KAF), properdin (P), and immunoglobulins (Ig) were determined in 14 patients with burns involving 13% to 91% body surface during 6 to 8 weeks postburn. In the 12 uninfected patients, levels of IgG and IgA were reduced during the first 10 days postburn, and decreased concentrations of P and IgM were demonstrated from three to 6 weeks postburn. C3 conversion was reduced from 10 days to 6 weeks postburn. Levels of C3, factor B, and KAF were normal or elevated for the entire study period. No difference in the occurrence of humoral abnormalities was noted in patients with burns caused by flame, immersion scald, or acid contact. Reduction in C3 conversion and P concentration were the only abnormalities which correlated with increasing burn size. Bacteremia and/or fungemia was documented in the other two patients. In one of these patients, reduction in CH(50) occurred during septicemia due to S. aureus, and in the other, reduction in all measurements of complement was associated with candidemia and Pseudomonas septicemia and occurred prior to the development of shock. Serum opsonic activity was only reduced significantly during sepsis, suggesting that this abnormality occurred as a result rather than a cause of infection. These results indicate that consumption of components of the classical and/or alternative pathways of complement activation may be an important mechanism by which infection is perpetuated in the burn patient. They also emphasize the importance of the clinical management of the burn patient in preventing the development of septic complications.
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PMID:Changes in humoral components of host defense following burn trauma. 87 73