The results of my genetic polymorphism study are
now complete and submitted for publication and meeting presentation.
Until it is accepted I will not provide specific details of the
findings but I can summarize them here:
The genes that produce cytokines in humans are polymorphic; there
are differences between individuals that control how much is produced
for a given stimulus. For instance, different people may produce
different amounts of IL-6 in response to identical types of bacterial
infections. High or low levels of pro- and anti-inflammatory cytokines
can confer high or low susceptibility to infectious and autoimmune
diseases. A current comprehensive database of polymorphisms and
their association with human disease (or lack thereof) can be found
We looked at genetic polymorphisms in men with CPPS and compared
them to a control population of 252 people without CPPS and to published
expected frequencies. In each case, the interesting numbers came
from the gene type associated with the "low expression"
for the given cytokine.
As a whole, CPPS patients had a significantly higher proportion
expressing the "low IL-10" gene. IL-10 is protective against
autoimmune disease, therefore having low IL-10 expression would
predispose to autoimmune disease. Interestingly, none of the patients
with positive cultures had the low IL-6 gene but the numbers in
this subgroup was too small for statistical significance.
Groups were analyzed according to many pretreatment and posttreatment
factors. The most interesting finding was that all patients who
failed therapy with Prosta-Q had the low TNF-alpha gene and a significantly
lower proportion had the low IL-10 gene. One would expect an inflammatory/autoimmune
condition to be associated with high TNF-alpha and low IL-10 expression
so the Prosta-Q appears to not be effective in those patients with
the opposite condition (low TNF and high IL-10). There were no differences
seen for any of the cytokines based on treatment response to antibiotics,
other anti-inflammatories, alpha-blockers or neuromuscular agents.
Thanks to all the patients who agreed to participate in these
studies, which is the only way we will advance understanding of
CPPS and hopefully learn how to treat it more effectively.
Daniel Shoskes MD
Cleveland Clinic Florida