I read the Washington Post article and learned about this disease that I had no idea existed. I am a scientist, and the descritiptions I found in that article triggered my memory. I worked on an artificial blood development project at Walter Reed Army Institute of Research and did a lot of experiments on blood loss and related hemorrhagic shock. The symptoms I observed there and the symptoms of SCLS share eary similarity. We published a couple of papers and succesfully completed the research phase of the blood subsitute we worked on, and described the importance of the intravascular activation of the complement system in the onset of the disease. I did one additional experiment to clarify why does the take hour(s) for the irreversible phase of the hemorrhagy shock to occure. Why is it that the massive and often fatal capillary leakage happens only after that irreversible phase occurs. The tentative (and unpublished) answer I found was that there is an important pro-enzyme in the blood that is activated together with the complement system and blood clothing during the very early phase of shock, but its half life is only about 5 minutes. The entire pool of this enzyme is depleted in couple of hours, or even as quickly as one hour. After that there is nothing to stop the full development of (hemorrhagic) shock, activation of granulocytes and multiple organ failure leading to and including capillary leakage.
The data I have are prety strong.
We were able to stop this process by inhibiting the complement system or blocking the C5a anaphylatoxin receptor.
I hypothesize that replacing the enzyme would be helpful as well. My question to the group is whether you know a research group that would be interested in working with me to decide whether this theory of mine has any merit?
If the SCLS patient's blood has low level or has a mutated form of that enzyme, it could be a perfect explanation of the symtpoms and could open the flodgate for finding therapy.
Lajos Baranyi, PhD;