Expression of pulmonary lactoferrin in sudden-onset and slow-onset asthma with fatal outcome

The objective of this forensic autopsy study was to determine the immunohistochemical expression pattern of lactoferrin (LF) in pulmonary tissue sections deriving from fatal slow-onset asthma (time interval between onset of asthma attack and death >2.5 h) and fatal sudden-onset asthma (cases in which death occurred within 1 h of the onset of an asphyxic asthma attack) relative to controls (sudden death due to diseases other than respiratory disorders). LF was applied to paraffin sections using a standard peroxidase-labelled streptavidin-biotin technique. LF immunoreactivity was graded semi-quantitatively in relation to different histoanatomic distribution sites of LF on a five category ordinal scale (maximum score of 15). We found a statistically significant difference between an enhanced expression of LF in both asthma groups relative to the controls (P<0.004 and P<0.001, respectively). When comparing both asthma groups, there was a statistically significant difference in LF immunoreactivity between the slow-onset and sudden-onset asthma group (P<0.001). Since LF immunoreactivity was far less intense in the sudden-onset asthma group (mean expression +/-SD: 7.3+/-1.3) than in the slow-onset asthma group (12.5+/-1), and an absent or weak LF expression pattern was observed in the control group (1.4+/-1.3), we assume that our results permit the following cautious estimations: (1) pulmonary LF expression is enhanced in asthma attacks with fatal outcome relative to controls and (2) a different expression pattern of LF can be observed in fatal sudden-onset asthma compared to slow-onset asthma in so far as the pulmonary expression of LF seems to be positively correlated with the preceding period of time between the asphyxic asthma attack and death. Further clinicopathologic studies including in-patient asthma fatalities with a well-known medical history are required to scrutinize if the pulmonary expression of LF is in fact positively associated with the time span of the asthma attack, thus possibly providing further therapeutic opportunities to intervene in severe asphyxic asthma.