ASSOCIATION BETWEEN THE
CATECHOL-O-METHYLTRANSFERASE Val158Met
POLYMORPHISM WITH SUSCEPTIBILITY
AND SEVERITY OF CARPAL TUNNEL SYNDROME
Erkol İnal E1,*, Eroğlu P2, Görükmez O3, Özemri Sağ Ş4, Yakut T4
*Corresponding Author: Dr. Esra Erkol İnal, Department of Physical Medicine and Rehabilitation, Süleyman
Demirel University, Faculty of Medicine, Afyon yolu, Çünür, Isparta, Turkey. Tel: +90-246-211-9280. GSM:
+90-507-563-6511. Fax: +90-246-211-2830. E-mail: esraerkol@hotmail.com
page: 43
|
|
DISCUSSION
Lower COMT gene activity that is linked to Met/
Met genotype, results in elevated levels of catecholamines,
which stimulate β2 adrenergic receptors in
the peripheral and central nervous system [13,14]. The
clinical status in CTS is generally thought be a result
of the entrapment of the median nerve, nevertheless,
current results revealed the association of the Met/Met
genotype with higher pain sensitivity and disability in
a number of chronic musculoskeletal disorders such as
fibromyalgia [15], temporomandibular pain [16] and
CTS [9]. However, our data suggested that there was
no relationship between pain severity and disability
and the COMT gene Val158Met SNP in the patients
with CTS, similar to some previous studies investigating
chronic musculoskeletal disorders [17] and
neuropathic [18] and widespread pain [19]. These discrepancies
may be due to the fact that a patient’s SNP
in a potential candidate gene does not act alone, but
in interaction with environmental and ethnic factors
to reveal personal manifestation in the disease course.
The COMT gene Val158Met SNP Met/Met genotype
was found to be related with higher anxiety,
depression and disability in fibromyalgia [20,21]. The
COMT gene SNPs related to pain sensitivity such as
Val158Met was found to be related with severity of fibromyalgia
in Spanish patients, whereas there was no
relation in Mexican patients [22]. The patients with
the Met/Met genotype had worse clinical features in
long-lasting low-back pain, sciatica and lumbar disc
herniation [23,24]. Nevertheless, the exact role of the
COMT gene Val158Met SNP remains controversial.
Supporting all these results: gender, ethnicity and
psychological state were accepted to interact with
the genes in pain responses to painful conditions [5].
Similar to a recent study, we did not find any relationships
between the COMT gene Val158Met SNP
and development of CTS [9]. The patient population
in the latter study also consisted of solely female
patients similar to the present study.
There are several limitations in the present study.
The population in this study includes only female patients
and the participants were all from a secondary
hospital. These conditions may limit the results to the
general population. Moreover, only one SNP of the
COMT gene was investigated in this study; therefore,
we could not exclude the other genetic influences.
In conclusion, we found no relationships between
the Val158Met SNP, CTS and clinical outcomes.
Genetic researches can help to offer special
care to the patients; however, the results of the reports
investigating the relationships between the COMT
gene Val158Met SNP and pain perception in painful
conditions are conflicting. New studies with a greater
number of candidate genes to CTS and pain, in a
larger population including both male and female patients
from several hospitals and geographic regions,
should be designed to establish precise relations.
Declaration of Interest. The authors report no
conflicts of interest. The authors alone are responsible
for the content and writing of this article.
|
|
|
|
 |
Number 27
VOL. 27 (2), 2024 |
Number 27
VOL. 27 (1), 2024 |
Number 26
Number 26 VOL. 26(2), 2023 All in one |
Number 26
VOL. 26(2), 2023 |
Number 26
VOL. 26, 2023 Supplement |
Number 26
VOL. 26(1), 2023 |
Number 25
VOL. 25(2), 2022 |
Number 25
VOL. 25 (1), 2022 |
Number 24
VOL. 24(2), 2021 |
Number 24
VOL. 24(1), 2021 |
Number 23
VOL. 23(2), 2020 |
Number 22
VOL. 22(2), 2019 |
Number 22
VOL. 22(1), 2019 |
Number 22
VOL. 22, 2019 Supplement |
Number 21
VOL. 21(2), 2018 |
Number 21
VOL. 21 (1), 2018 |
Number 21
VOL. 21, 2018 Supplement |
Number 20
VOL. 20 (2), 2017 |
Number 20
VOL. 20 (1), 2017 |
Number 19
VOL. 19 (2), 2016 |
Number 19
VOL. 19 (1), 2016 |
Number 18
VOL. 18 (2), 2015 |
Number 18
VOL. 18 (1), 2015 |
Number 17
VOL. 17 (2), 2014 |
Number 17
VOL. 17 (1), 2014 |
Number 16
VOL. 16 (2), 2013 |
Number 16
VOL. 16 (1), 2013 |
Number 15
VOL. 15 (2), 2012 |
Number 15
VOL. 15, 2012 Supplement |
Number 15
Vol. 15 (1), 2012 |
Number 14
14 - Vol. 14 (2), 2011 |
Number 14
The 9th Balkan Congress of Medical Genetics |
Number 14
14 - Vol. 14 (1), 2011 |
Number 13
Vol. 13 (2), 2010 |
Number 13
Vol.13 (1), 2010 |
Number 12
Vol.12 (2), 2009 |
Number 12
Vol.12 (1), 2009 |
Number 11
Vol.11 (2),2008 |
Number 11
Vol.11 (1),2008 |
Number 10
Vol.10 (2), 2007 |
Number 10
10 (1),2007 |
Number 9
1&2, 2006 |
Number 9
3&4, 2006 |
Number 8
1&2, 2005 |
Number 8
3&4, 2004 |
Number 7
1&2, 2004 |
Number 6
3&4, 2003 |
Number 6
1&2, 2003 |
Number 5
3&4, 2002 |
Number 5
1&2, 2002 |
Number 4
Vol.3 (4), 2000 |
Number 4
Vol.2 (4), 1999 |
Number 4
Vol.1 (4), 1998 |
Number 4
3&4, 2001 |
Number 4
1&2, 2001 |
Number 3
Vol.3 (3), 2000 |
Number 3
Vol.2 (3), 1999 |
Number 3
Vol.1 (3), 1998 |
Number 2
Vol.3(2), 2000 |
Number 2
Vol.1 (2), 1998 |
Number 2
Vol.2 (2), 1999 |
Number 1
Vol.3 (1), 2000 |
Number 1
Vol.2 (1), 1999 |
Number 1
Vol.1 (1), 1998 |
|
|
