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[Pathogenesis of inclusion body myositis: autoimmune or degenerative disease?].
[inclusion body myositis]
While
the
pathogenesis
of
inclusion
body
myositis
(
IBM
)
remains
undetermined
,
there
are
two
major
hypotheses
:
the
autoimmune
hypothesis
and
the
degeneration
hypothesis
.
Herein
,
we
review
these
hypotheses
as
well
as
potential
therapeutic
approaches
.
Evidence
in
favor
of
a
primary
autoimmune
etiology
includes
the
frequent
complication
of
other
autoimmune
diseases
in
patients
with
IBM
and
the
presence
of
autoantibodies
against
cytosolic
5
'
-
nucleotidase
1
A
.
Interleukin
(
IL
)
-
1
β
reportedly
leads
to
accumulation
of
amyloid
β
via
nitric
oxide
stress
in
vitro
.
The
degeneration
hypothesis
addresses
the
following
aspects
of
IBM
:
accumulation
of
amyloid
β
and
other
abnormal
proteins
that
are
observed
in
neurodegenerative
diseases
such
as
Alzheimer
's
disease
and
Parkinson
's
disease
;
relation
to
aging
;
and
poor
response
to
immunotherapy
.
Overexpression
of
IL
-
1
β
in
skeletal
muscles
of
patients
with
IBM
and
its
secretion
from
skeletal
muscle
cells
suggests
an
important
role
for
IL
-
1
β
in
the
pathogenesis
of
IBM
.
Thus
,
IL
-
1
β
is
a
potential
treatment
target
.
Diseases
Validation
Diseases presenting
"skeletal muscles"
symptom
focal myositis
inclusion body myositis
pyomyositis
systemic capillary leak syndrome
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