الفهرس 
The Criteria of Critically Ill PatientOnly 14 pages are availabe for public view
 |  | from | 140 |  |  |
| | | from | 140 | | |
Abstract
Data showing that bacterial translocation occurs are
substantial, but it seems that the frequency with which
translocation occurs in humans is much lower than that
observed in animal models.
Even more striking is the lack of strong data correlating
bacterial translocation with clinically significant problems in
humans. Still, extravagant postulations about the importance of
bacterial translocation are continually being put forth in the
literature. It seems that the hypothesis remains very attractive to
researchers despite many studies that yielded weak correlative
data.
Bacterial translocation could indeed be a critical
component to the development of SIRS, but human studies
addressing the question are plagued by methodologic problems.
Serial cultures of the mesenteric lymph nodes are not possible
in human studies, so indirect methods will continue to be
necessary tools. More frequent permeability studies and the use
of more reliable and specific markers of bacterial translocation
are urgently needed. Serial measurements of several proinflammatory and anti-inflammatory cytokines should be
studied simultaneously, but studies such as these are very labor
intensive.
More studies should be undertaken in which tissue
cytokine concentrations are measured, because these
concentrations may be more relevant to disease states than are
serum concentrations. Bacterial translocation may be a normal
physiologic event without deleterious consequences.
The baseline rate of translocation in most human studies
is 5% to 10%. Berg stated that there is a normal rate in animals
of approximately 10% to 20%. This may be a normal
physiologic process by which animals sample different luminal
antigens in order to produce immunocompetent cells.
Bacterial translocation may occur as an innocent
bystander. The vascular endothelium is injured after trauma and
shock. Immune cells such as macrophages and infiltrating
neutrophils become activated. Activated cells could engulf the
bacteria normally found in mesenteric lymph nodes, carrying
them to distant sites where they may cause disease.
Recently, Vazquez-Torres et al. (Vazquez-torres et al.,
1999) showed that Salmonella typhimurium can be carried from the intestinal lumen across the intestinal barrier and
disseminated by invading CD18+ mucosal macrophages that
routinely sample the lumen.
Human studies have not yet assessed factors such as
preexisting disease, age, sex, and host genetic factors that affect
cytokine responses.
When two patients have a similar insult, one may
experience SIRS with a downward course, whereas the other
may stabilize and recover. Host and genetic factors likely play
an important role in these individual differences.
Recently, genetic differences in cytokine responses have
been documented in different human conditions. Severe
rheumatoid arthritis, for example, has been associated with a
126-base pair allele related to a microsatellite polymorphism
within the interferon γ gene. Increased hepatic fibrosis occurs in
patients with hepatitis C who have certain high transforming
growth factor β-producing genotypes (Powell et al., 2000).
Finally, there is an association between interleukin 1 β
polymorphism, Helicobacter pylori, and gastric cancer (El-
Omar et al., 2000). Therefore, although bacterial translocation
may increase after a variety of injuries, the complications of translocation and patient outcome may be more dependent on
host factors than on the translocation itself.
Theoretically, bacterial translocation may be modulated
both quantitatively and qualitatively. Anumber of factors may
be significance in modulating gut barrier function and
consequently bacterial translocation in clinical practice. These
act at pre-epithelial, epithelial and post- epithelial levels. It is
recognized that these factors may act at more than one site, and
indeed at more than one level.
Probiotics, prebiotics, glutamine, curcumin and butyrate,
are of the general preventive measures of bacterial translocation.