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Influence of mannan-binding lectin and MAp44 on outcome in comatose survivors of out-of-hospital cardiac arrest

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • John Bro-Jeppesen
  • Jesper Kjaergaard
  • Steffen Thiel
  • Jens Christian Jensenius
  • Mette Bjerre
  • Michael Wanscher
  • Jeppe V. Christensen
  • Hassager, Christian

Aim: The lectin complement pathway, initiated by mannan-binding-lectin (MBL) plays a role in tissue destruction following ischemia/reperfusion, and MBL deficiency has been associated with favorable outcome in stroke patients. MAp44 is produced in the heart and may theoretically function as an endogenous inhibitor of MBL-mediated activities. The aim of this study was to investigate the possible association between MBL deficiency, MAp44 levels and outcome in comatose survivors of out-of-hospital cardiac arrest (OHCA). Methods: In a single center post hoc analysis of the prospective multicenter randomized Target Temperature Management (TTM) trial, we measured MBL and MAp44 levels at baseline, 24, 48 and 72 h after OHCA in 169 consecutive patients randomly assigned to TTM at 33 °C or 36 °C for 24 h. Primary outcome was 30 days mortality and secondary outcome was favorable neurological outcome assessed by Cerebral Performance Category (CPC1-2) and modified Rankin Scale (mRS0-3) 180 days after OHCA. Results: Patients with MBL deficiency (defined as plasma levels ≤100 ng ml-1 at baseline) (n = 22) carried a 30-day mortality of 41% compared to 32% in MBL sufficient patient (n = 147), p = 0.55. Baseline MAp44 levels were not associated with mortality, p = 0.25. There was no significant difference in neurological outcome between the two MBL groups assessed by CPC (p = 0.69) and mRS (p = 0.91). In multivariable models, baseline MBL (OR = 1.0, p = 0.70), (OR = 1.5, p = 0.30) and MAp44 levels (OR = 1.0, p = 0.99), (OR = 1.6, p = 0.21) were not associated with favorable neurological outcome assessed by CPC and mRS, respectively. Conclusions: In comatose survivors after cardiac arrest, neither MBL deficiency nor levels of MBL and MAp44 were associated with mortality or neurological outcome.

OriginalsprogEngelsk
TidsskriftResuscitation
Vol/bind101
Sider (fra-til)27-34
Antal sider8
ISSN0300-9572
DOI
StatusUdgivet - 2016

ID: 179132996