{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T08:15:03Z","timestamp":1775204103801,"version":"3.50.1"},"reference-count":16,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[1990,1,1]],"date-time":"1990-01-01T00:00:00Z","timestamp":631152000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1990,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Previous investigators suggested that increased plasma levels of the terminal complement complex (sC5b-9) are an early marker for the development of adult respiratory distress syndrome (ARDS) in septic patiente. We asked whether an increase in sC5b-9 was also associated with the development of ARDS from other etiologies and whether sC5b-9 measurements consistently reflected complement activation in vivo. We evaluated 75 patiente with sepsis, trauma, hypertrans-fusion, multiple fractures, aspiration, or pancreatitis who were at risk for ARDS but did not develop the syndrome and 23 patiente with similar histories who did develop ARDS. Of the latter patiente, seven were identified and studied both when they were at risk and when they had ARDS. Serial blood samples were obtained and analyzed for the complement activation products Bb, Ba, C4d, C3d, iC3b, and sC5b-9. All but one of the patiente studied had levels of one or more complement fragmente that were greater than 2 SD above the mean obtained from 18 normal subjects. In contrast to the report referred to previously, none of the fragmente measured, including sC5b-9, was a specific Indicator of ARDS, and no combination of complement fragmente predicted which patiente at risk would develop ARDS. Patiente demonstrated evidence of activation of the classical pathway only, alternative pathway only, or both pathways, but none of these was associated with greater risk or severity of disease. In addition, in several patiente only late components were activated, suggesting that enzymes other than those derived from complement activation may be responsible. In conclusion, complement can be activated by a variety of mechanisms in critically ill patiente. The measurement of neither individual split products nor sC5b-9 predicts which patiente will develop ARDS and which will not.<\/jats:p>","DOI":"10.1164\/ajrccm\/141.1.98","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T17:10:48Z","timestamp":1365095448000},"page":"98-103","source":"Crossref","is-referenced-by-count":28,"title":["The Terminal Complement Complex (sC5b-9) Is Not Specifically Associated with the Development of the Adult Respiratory Distress Syndrome"],"prefix":"10.1093","volume":"141","author":[{"given":"Polly E.","family":"Parsons","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patricia C.","family":"Giclas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[1990,1,1]]},"reference":[{"key":"p_7","unstructured":"ratory disease syndrome. 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