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0:00
Hello.
My name is Andrew Menzies-Gow.
I'm a consultant
respiratory physician
at the Royal Brompton Hospital.
I'm going to talk to you about
Anti-IgE therapy for asthma.
0:11
During my talk, I'll
cover the evidence
for omalizumab
therapy in asthma,
the current situation
within the United Kingdom,
and evidence from
real life studies.
An important question that
I'm often asked about
omalizumab therapy is,
how long patients should
start it and stay on it,
if it is of benefit?
0:32
We know that the majority of
asthmatics attacks are also atopics.
They have positive skin tests
for common aeroallergens.
In large surveys of asthma
from across the world,
up to 90% of asthma occurs
in association with allergy.
We also know that allergen
specific IgE can both
initiate and maintain the
inflammatory response
which is characteristic of
asthma and associated with
Th2 inflammation and then
infiltration of eosinophils
into the airway mucosa.
Therefore, IgE becomes
a very logical target
for asthma therapy.
Whenever we think about
blocking part of
the immune system,
we need to be certain
that it's going to have
relatively few side
effects and not cause
a catastrophic failure
of the immune system.
We know that the
physiological root of IgE
appears to be fighting
parasitic infections,
primarily anti-nematode
infections.
Therefore, certainly
in the western world,
blocking IgE is likely to
prevent allergic inflammation
with no significant impact on
the immune system's ability
to fight infections.
1:34
Anti-IgE is a
monoclonal antibody
that's injected subcutaneously.
It finds its way to the serum
where it binds to free IgE
and produces multimers
that are removed
by the reticular
endothelial system.
It prevents IgE binding to
the surface of mast cells,
so it very quickly
depletes pre-serum IgE,
but it can take up to
eight weeks before
the levels of IgE on the
surface of mast cells
and basophils start to decrease,
which is why the treatment takes
at least 8 to 16 weeks before
we see any improvement
in asthma symptoms.
Importantly, anti-IgE
does not bind to IgE
that's already on the surface
of mast cells or basophils.
Therefore, it can't induce
an anaphylactic reaction
by directly cross-linking IgE on
the surface of mast
cells and basophils.
