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Biotech / Medical : XOMA. Bull or Bear?
XOMA 31.80-0.1%Nov 21 3:59 PM EST

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To: Cacaito who wrote (7357)10/31/1998 4:23:00 PM
From: Robert S.  Read Replies (2) of 17367
 
Cacaito, the press release from Xoma on 10/30/98 contained the following excerpt:

>>Endotoxin (lipopolysaccharide or LPS) is a structural component of gram-negative bacteria that can induce an overwhelming systemic inflammatory response.
In patients exposed to bacterial endotoxins this reaction can cause complications that in severe cases can result in shock, organ failure and death. LBP, a key
initiator of the inflammatory response, is secreted by the liver in direct response to exposure to bacterial endotoxin.<<

The Holzheimer study addressed the conflicting evidence pertaining to the role of endotoxin in sepsis and you minimized this research as being a review and not original (Holzhiemer has been publishing since the 80's). The original article below appeared in the peer-reviewed journal The Lancet and the abstract also illustrates that the role of endotoxins in sepsis is indeed perplexing:

Lancet 1993 May 1;341(8853):1133-5

Reappraisal of the role of endotoxin in the sepsis syndrome.

Hurley JC

Division of Infectious Diseases, Children's Hospital and Medical Center, Seattle, Washington 98105.

There is strong evidence to implicate endotoxin released from gram negative bacteria in the pathogenesis of the sepsis syndrome and related conditions, but
equally compelling data bring the role of endotoxin into doubt. Reappraisal of endotoxin and its release from gram negative bacteria suggests that it is not
directly responsible for the complications of sepsis syndrome. Rather, release of endotoxin is a marker for the transition of gram negative organisms to
cell-wall-deficient forms (L-forms) that may persist undetected despite antibiotic therapy directed against the parental form.
This transition has two
consequences in compromised patients: L-forms cause organ failure, and they serve as a sanctuary from which cell-wall-intact revertants may arise.

Comments:

Comment in: Lancet 1993 Jun 26;341(8861):1662

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