The above paper, submitted for publication in March, 1972, raised the issues 'does endotoxin escape from the gut?' If is, is it rapidly eliminated by the normal liver?
The first query was answered almost immediately (to be more exact, just two months later) when two articles, appeared published back to back in the Lancet (in May, 1972), one by Triger et al from England, the other by Bjorneboe from Copenhagen.
Both papers indicated that the hyperglobulinemia observed in patients with liver cirrhosis is caused by an elevated antibody titer against the E Coli bacillus, an organism abundantly present in the gut.
This lead us to publish the following letter in the Lancet that tied, for the first time the escape of endotoxin from the gut to
the DIC observed in patients with liver cirrhosis. (E Wardle in: "Endotoxaemia in liver disease", Lancet 1 (1974): 930. conformed in print that we were the first to call attention to the connection of these two apparently unrelated clinical findings).
The first query was answered almost immediately (to be more exact, just two months later) when two articles, appeared published back to back in the Lancet (in May, 1972), one by Triger et al from England, the other by Bjorneboe from Copenhagen.
Both papers indicated that the hyperglobulinemia observed in patients with liver cirrhosis is caused by an elevated antibody titer against the E Coli bacillus, an organism abundantly present in the gut.
This lead us to publish the following letter in the Lancet that tied, for the first time the escape of endotoxin from the gut to
the DIC observed in patients with liver cirrhosis. (E Wardle in: "Endotoxaemia in liver disease", Lancet 1 (1974): 930. conformed in print that we were the first to call attention to the connection of these two apparently unrelated clinical findings).