Document 6478302

Vol.23 March 2009
BTXA Treatment for Vasomotor Rhinitis
Rhinitis is the inflammation of nasal mucosa. Its symptoms include itching, sneezing, congestion and
rhinorrhea of nasal system. It constitutes a major worldwide health problem. Vasomotor Rhinitis
(VMR) is known as non-allergic and non-infectious rhinitis. It is unrelated to allergy, infection,
structural abnormalities and systemic diseases. Patients with VMR always suffer from nasal
obstruction and numerous watery nasal discharge. Use of botulinum toxin to treat hypersecretory
disorders is increasing in popularity in recent years. In this issue, further information concerning
this topic will be introduced to the readers.
Introduction
Rhinitis is inflammation of nasal mucous membranes,
"dry" patients, in which nasal obstruction and airflow
characterized by nasal discharge, itching, and
resistance exist with minimal rhinorrhea. Triggers of
congestion. It
vasomotor rhinitis symptoms vary among patients.
infectious,
occupational
can be classified into
idiopathic
rhinitis.
It
allergic,
rhinitis,
nares,
and
Odors or irritants in air, changes in weather,
always
coexists
with
medications, foods and chronic health conditions are
respiratory disorders such as asthma and greatly
some possible factors.
impacts life quality of patients. It may contribute to
Cause
sinus problem, ear problem, sleep problem and
Exact pathogenesis of VMR is not fully known. It is
learning problem.
thought to be the result of autonomic imbalance with
Vasomotor Rhinitis (VMR), almost 50% of chronic
a relative dominance of the parasympathetic nervous
rhinitis, is non-allergic rhinitis. Possible reasons are
system in the nasal mucosa. Emotional disturbance,
thought to be allergy, infection, structural lesions,
hormones, physical agents, and trauma are some
possible factors.
systemic disease and drug abuse. Its symptoms
include nasal blockage to rhinorrhea; sneezing. The
nasal airway is under the control of the autonomic
nervous
system.
Sympathetic
nervous
system
decreases nasal airway resistance; parasympathic
system produces nasal discharge.
Patients with vasomotor rhinitis are divided into two
subgroups: "runners", who have "wet" rhinorrhea; and
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ICBA Newsletter Vol. 23
Some studies showed that VMR is caused by an
Botulinum Toxin Type A Treatment
autonomic nervous system dysfunction (relative
Botulinum Toxin Type A selectively inactivates
parasympathetic
of
peripheral cholinergic nerve terminals by blocking the
Parasympathetic
release of acetylcholine. Its most important effect is
hyperactivity in the nasal cavity causes clear nasal
at the neuromuscular junction where it causes
discharge from submucosal glands; on the other hand,
temporary and reversible weakness and atrophy of
sympathetic hypoactivity can give rise to nasal
striated muscle. Botulinum Toxin Type A also
blockage. Therapeutic efforts to decrease rhinorrhea
provokes
in human beings have attempted to either cut the
sympathetic and parasympathetic ganglion cells and
parasympathetic
vidian
postganglionic parasympathetic neurons. It exerts
neurectomy or chemically block the receptors with
action at the molecular level by selectively cleaving
the short-acting, topical ipratropium.
the
sympathic
hyperactivity)
as
hypoactivity.
nerve
supply
a
result
through
medical
decongestants,
treatment
nasal
of
VMR
ipratropium
bromide,
blocking
(synaptosomal-associated
on regulated exocytosis, the release of synaptic
and
vesicles in response to electrical depolarization.
Blocking the release of acetylcholine from the
potential side effects. Nasal steroids may be
cholinergic nerve terminal in the nasal mucosa or
appropriate treatment option, but the efficacy of
preganglionic
these drugs has been inconsistent. Surgical treatment
short-term
effect
and
cholinergic
nerve
endings
in
sphenopalatine ganglion are the two suggested
such as concha resections, vidian nerve section
has
SNAP-25
by
BTX-A damages SNAP-25, the most obvious effect is
including
antihistamines needs long time usage and has some
generally
protein
dysfunction
protein with a molecular weight of 25 kD). When the
Current treatment
The
autonomic
mechanisms of BTX-A action in the nasal cavity.
some
Rohrbach
complications.
and
colleagues
demonstrated
a
degeneration of nasal glands and ducts in addition to
Exercise may be a useful treatment addition because
diffuse glandular apoptosis in guinea pigs after nasal
it produces decreased airway resistance and assists
application of 20U BTX-A. They also observed the
natural nasal decongestion by I-adrenergic-mediated
absence of necrosis or inflammation after application
mechanisms. However, the effect of exercise on nasal
of BTX-A.
decongestion is rather short-lived.
The cost-effectiveness is an important issue in the
Traditional oral antihistamines have no established
management of chronic diseases such as vasomotor
beneficial effect in patients with vasomotor rhinitis
rhinitis. With the high price of the treatment of VMR
and may be associated with sedation. Newer,
with nasal steroids or oral antihistamines, intranasal
less-sedating antihistamines also have no proven
injection of BTX-A is a highly effective, safe, and
effectiveness for vasomotor rhinitis, and their
simple
administration delays proper treatment and incurs
long-lasting effect for patients with VMR. Botulinum
significant cost and burden to the health care system.
Toxin Type A provides good alternative for the
symptomatic
treatment
option
with
a
treatment of resistant VMR cases.
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ICBA Newsletter Vol. 23
The Effect of Botulinum Toxin Type A on Vasomotor Rhinitis and Frey’s Syndrome
and Morphological Study
Wang Jinling, Chen Fuquan, Zhang Xu, Liu Shunli1, Wang Yinchun2
(1Department of Otolaryngology, Xijing Hospital, Fourth Military Medical University, Xi’ an 710032; 2Lanzhou
Institute of Biological Prodcuts)
Abstract
Objective: To investigate the effect and mechanisms of botulinum toxin type A (BTXA) on vasomotor
rhinitis and Frey’s syndrome.
Method: A retrospective study of 82 patients with vasomotor rhinitis who received BTXA injection at 4
points in bilateral nasal cavities with 2.5U each point had been done. The state of rhinorrhea, nasal
obstruction, sneeze and nasal mucosa edema of each patient were recorded and scored before and after
the application of BTXA respectively. 1 patient of gustatory sweating who had done operation for
hemifacial spasm underwent Minor’s starch iodine test before and after treatment with intracutaneous
injections of botulinum toxin A. 48 guinea pigs were randomly divided respectively into 3 groups:
BTXA group and control group. Merocel sponge soaked with 10U (0.2ml) BTXA was put into left nasal
cavity for one hour in BTXA group. Saline replaced BTXA in control group. The inferior turbinate
mucosa of guinea pigs was harvested under general anesthesia at 1, 2 and 4 weeks after BTXA
treatment. The first group was observed with HE staining and electron microscope. The tissues of the
second group were fixed in 4% paraformaldehyde and paraffin embedded. The concentration of
acteylcholinesterase was determined with immunohistochemistry staining. Apoptosis was detected
with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling
(TUNEL) staining and the types of gland cells were determined with AB-PAS staining in the third
group.
Result: Rhinorrhea improved significantly in all 82 patients while sneeze, nasal obstruction and mucosa
edema reduced partly. The reducing of rhinorrhea lasted averagely 10 weeks. Patients had an episode of
nasal dryness or increased rhinorrhea at the day of injection. No other complications were found. 1
patient of Frey’s syndrome did not experience any gustatory sweating at follow-up. The only side effect
was a transitory affection of the lower orbicularis oris muscle. 1 and 2 weeks after local BTXA
application in nasal mucosa of guinea pigs, the degenerations of glandular epithelium and canal
epithelium were observed. Most of the glandular cells showed normal at 4 weeks after BTXA treatment.
1 and 2 weeks after local BTXA application, the expression of acteylcholinesterase in nasal glandular
and canal cells decreased significantly (P<0.01). It became normal at 4 weeks after BTXA treatment. 1
and 2 weeks after local BTXA application, apoptosis of glandular and canal cells in nasal mucosa of
guinea pigs increased significantly (P<0.01). The apoptosis index became normal at 4 weeks after BTXA
treatment. Apoptosis mainly occurred in serous gland.
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Conclusion: BTXA can induce the degeneration of glandular cells in nasal mucosa of guinea pig, and
induce apoptosis in nasal serous glands, decrease the concentration of acetylcholinesterase in nasal
glands. BTXA can obviously relieve rhinorrhea of patients with vasomotor rhinitis, and disappearance
of gustatory sweating with Frey’s syndrome that was effective, simple and minimally invasive method
of treatment.
References
1.
Tae YY, Yoon GJ, Young HK, Tae YJ. A comparison of the effects of botulinum toxin A and
steroid injection on nasal allergy. Otolaryngology-Head and Neck Surgery 2008;
139:367-71.
2.
Cengiz O, Yusuf V, Okan D, Kemal G. The effect of intranasal injection of botulinum toxin
A on the symptoms of vasomotor rhinitis. American Journal of Otolaryngology-Head and
Neck Medicine and Surgery 2006; 27:314-8.
For further information, please feel free to contact us by
the following means:
International C-BTXA Association (ICBA)
Room 1312, New East Ocean Centre, 9 Science
Museum Road, Tsim Sha Tsui East, Kowloon, HK
+852 2771 6622
+852 2782 5249
hughs@hughsource.com
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