OBJECTIVES: To assess the involvement of ficolin-3, the main initiator of the 
lectin complement pathway (LCP), in subarachnoid hemorrhage (SAH) pathology and 
outcome.
METHODS: In this preliminary exploratory study, plasma concentration of 
ficolin-3 and of ficolin-3-mediated functional LCP activity was measured, along 
with that of other LCP initiators (mannose-binding lectin, ficolin-2, and 
ficolin-1), C3 activation products, and soluble C5b-9 terminal complex, in a 
prospective cohort of 39 patients with SAH and 20 healthy controls. The 
following parameters were recorded: SAH severity, assessed using the World 
Federation of Neurosurgical Societies grading scale; vasospasm, defined as 
neuro-worsening with angiographic confirmation of vessel narrowing; cerebral 
ischemia, defined as hypodense lesion on CT scan performed before discharge; and 
6-month outcome, assessed using the Glasgow Outcome Scale.
RESULTS: In patients, no changes were detected for ficolin-3 compared with 
controls. Notably, however, ficolin-3-mediated functional LCP activity was 
reduced. Low levels of plasma ficolin-3 and ficolin-3-mediated functional LCP 
activity were related to SAH severity, vasospasm, and cerebral ischemia. 
Moreover, ficolin-3 functional LCP activity was decreased in patients with 
unfavorable outcome.
CONCLUSION: Our data provide evidence that LCP is activated after SAH and that 
the actual plasma concentrations of ficolin-3 reflect the severity of brain 
injury as evaluated by clinical and structural parameters. These results support 
the idea that ficolin-3-mediated functional LCP activity may be targeted to 
control injury progression in SAH.