Celiac
Disease & neuropathy
Neuropathy

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Neuropathy in Celiac Disease
Antibodies to gangliosides and Purkinje cells have
been reported in patients with
celiac disease (CD) with neuropathy
and ataxia, respectively. The response of
neurological symptoms and antibody
titers to a gluten-free diet is
still controversial. The objective
of our study was to assess whether
neurological manifestations in CD
patients correlate with antibody
titers and a gluten-free diet. Thirty-five
CD patients (9 males, 26 females,
mean age 37.1 +/- 12.6 yrs) were
followed prospectively. At initial
evaluation, 23 were on a gluten-free
diet, 12 were not. At recruitment
and during follow-up, patients
underwent neurological and
electrophysiological evaluation. IgG,
IgM, and IgA anti-ganglioside
antibodies were assayed by ELISA;
anti-neuronal antibodies were
assessed by immunohistochemistry and
Western blot. Four patients, all
males, had electrophysiological
evidence of neuropathy; three had
been on a gluten-free diet for
several months, and one was newly
diagnosed. One had reduced tendon
reflexes; another complained of
distal paresthesias. With regard to
anti-ganglioside antibodies, three
patients had a moderate increase in
antibodies without symptoms or signs
of neuropathy. No patients had
ataxia or cerebellar dysfunction,
although in four patients reactivity
to neuronal antigens was found. In
17 patients, an electrophysiological
follow-up (mean duration of
follow-up, 9 months) showed no
changes.
Department of
Neurosciences, University of Padua,
Via Giustiniani Padua, Italy.
In conclusion, the
preliminary results of this
prospective study indicate that
neuropathy, usually subclinical, may
accompany CD. Antibody titers do not
seem to correlate with neurological
symptoms/signs or diet. Ongoing
follow-up will help confirm these
data and clarify the role, if any,
of antibodies in neurological
involvement in CD
.
CIDPUSA
Concludes that other treatments are needed
to help these patients rather then the usual
Gluten free diet.
The following study
shows that a sign fact number of migraine
patients have CD. These patients are helped
by a gluten free diet.
Department of
Internal Medicine, Catholic
University of the Sacred Heart,
Gemelli Hospital, Rome, Italy.
OBJECTIVES:
Subclinical celiac disease (CD) has
been associated with various
neurological disorders, the most
common being neuropathy and
cerebellar ataxia. The aims of the
present study were to assess the
following: 1) the prevalence of CD
in patients affected by migraine; 2)
whether there are regional cerebral
blood flow abnormalities in migraine
patients with CD compared to
migraine patients without CD; and 3)
the effects of a gluten free diet in
migraine patients with CD. METHODS:
A total of 90 patients affected by
idiopathic migraine were enrolled,
and 236 blood donors were used as
controls. Serum IgG
antitransglutaminase (TgA) and IgA
antiendomysial (EmA) were measured.
In positive cases, diagnosis was
confirmed endoscopically. A gluten
free diet was started in the
patients diagnosed with CD, who were
followed for 6 months. A single
photon emission CT brain study was
performed before and after a gluten
free diet. RESULTS: Four of 90
(4.4%; 95% CI = 1.2-11.0) migraine
patients were found to have CD
compared with 0.4% (95% CI =
0.01-2.3) blood donor controls (p <
0.05). During the 6 months of gluten
free diet, one of the four patients
had no migraine attacks, and the
remaining three patients experienced
an improvement in frequency,
duration, and intensity of migraine.
Single photon emission CT studies
showed a regional baseline reduction
in brain tracer uptake in all four
patients. Such reduction in uptake
completely resolved at follow-up.
CONCLUSIONS: Our results suggest
that a significant proportion of
patients with migraine may have CD,
and that a gluten free diet may lead
to a improvement in the migraine in
these patients.
BACKGROUND: About 2.5% of patients with
idiopathic peripheral neuropathy or
idiopathic dysautonomia have underlying
celiac disease (CD). Antibodies to
ganglioside have been reported in CD
patients with neuropathy. No data are so
far available on the presence in CD of
acetylcholine receptor (AChR)
antibodies. Muscle AChR antibodies are
found in patients with myasthenia
gravis, and ganglionic AChR antibodies
in patients with autoimmune autonomic
neuropathy.
BACKGROUND: Idiopathic autonomic
neuropathy is a severe, subacute
disorder with a presumed autoimmune
basis. It is indistinguishable from the
subacute autonomic neuropathy that may
accompany lung cancer or other tumors.
Autoantibodies specific for nicotinic
acetylcholine receptors in the autonomic
ganglia are potentially pathogenic and
may serve as serologic markers of
various forms of autoimmune autonomic
neuropathy. METHODS: We tested serum
from 157 patients with a variety of
types of dysautonomia.
Immunoprecipitation assays with
iodine-125-labeled epibatidine and
solubilized human neuroblastoma
acetylcholine receptors were used to
detect autoantibodies that bound to or
blocked ganglionic receptors. RESULTS:
Ganglionic-receptor-binding antibodies
were found in 19 of 46 patients with
idiopathic or paraneoplastic autonomic
neuropathy (41 percent), in 6 of 67
patients with postural tachycardia
syndrome, idiopathic gastrointestinal
dysmotility, or diabetic autonomic
neuropathy (9 percent), and in none of
44 patients with other autonomic
disorders. High levels of the binding
antibodies correlated with more severe
autonomic dysfunction (including the
presence of tonic pupils). Levels of
these antibodies decreased in patients
who had clinical improvement. All seven
patients with ganglionic-receptor-blocking
antibodies had ganglionic-receptor-binding
antibodies and had idiopathic or
paraneoplastic autonomic neuropathy.
CONCLUSIONS: Seropositivity for
antibodies that bind to or block
ganglionic acetylcholine receptors
identifies patients with various forms
of autoimmune autonomic neuropathy and
distinguishes these disorders from other
types of dysautonomia. The positive
correlation between high levels of
ganglionic-receptor antibodies and the
severity of autonomic dysfunction
suggests that the antibodies have a
pathogenic role in these types of
neuropathy.