Significance of catechol-O-methyltransferase gene polymorphism in fibromyalgia syndrome

被引:184
作者
Gürsoy, S [1 ]
Erdal, E
Herken, H
Madenci, E
Alasehirli, B
Erdal, N
机构
[1] Gaziantep Univ Med Hosp, Dept Phys Med & Rehabil, TR-2700 Kolejtepe Gaziantep, Turkey
[2] Mersin Univ, Fac Med, Dept Genet & Biol, Mersin, Turkey
[3] Gaziantep Univ, Fac Med, Dept Psychiat, Gaziantep, Turkey
[4] Gaziantep Univ, Fac Med, Dept Pharmacol, Gaziantep, Turkey
[5] Mersin Univ, Fac Med, Dept Biophys, Mersin, Turkey
关键词
adrenergic system; catechol-O-methyltransferase (COMT) fibromyalgia syndrome; COMT polymorphism;
D O I
10.1007/s00296-002-0260-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Fibromyalgia syndrome (FS) is associated with a neuroendocrinal disorder characterized by abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis, including hyperactive ad renocortico tropic hormone (ACTH) release and adrenal hyporesponsiveness. Catechol-O-methyltransferase (COMT) enzyme inactivates catecholamines and catecholamine-containing drugs. Polymorphism in the gene encodes for the COMT enzyme. For this study, the significance of COMT polymorphism was assessed in FS. There were three polymorphisms of the COMT gene: LL, LH, and HH. The analysis of COMT polymorphism was performed using polymerase chain reaction (PCR). Sixty-one patients with FS and 61 healthy volunteers were included in the study. Although no significant difference was found between LL and LH separately, the LL and LH genotypes together were more highly represented in patients than controls (P = 0.024). In addition, HH genotypes in patients were significantly lower than in the control groups (P = 0.04). There was no significant difference between COMT polymorphism and psychiatric status of the patients as assessed by several psychiatric tests (P > 0.05). In conclusion, COMT polymorphism is of potential pharmacological importance regarding individual differences in the metabolism of catechol drugs and may also be involved in the pathogenesis and treatment of FS through adrenergic mechanisms as well as genetic predisposition to FS.
引用
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页码:104 / 107
页数:4
相关论文
共 16 条
[1]  
BENNET MR, 1997, TXB RHEUMATOLOGY, P511
[2]  
BERKER E, 2000, J RHEUM MED REHAB, V11, P138
[3]  
BRADLEY AL, 2001, ARTHRITIS ALLIED CON, P1811
[4]  
Daniels JK, 1996, AM J PSYCHIAT, V153, P268
[5]  
Erdal ME, 2001, MOL BRAIN RES, V94, P193
[6]   Association of T102C polymorphism of the 5-HT2A receptor gene with pyschiatric status in fibromyalgia syndrome [J].
Gürsoy, S ;
Erdal, E ;
Herken, H ;
Madenci, E ;
Alasehirli, B .
RHEUMATOLOGY INTERNATIONAL, 2001, 21 (02) :58-61
[7]   Absence of association of the serotonin transporter gene polymorphism with the mentally healthy subset of fibromyalgia patients [J].
Gursoy, S .
CLINICAL RHEUMATOLOGY, 2002, 21 (03) :194-197
[8]   Noradrenergic suppression of synaptic transmission may influence cortical signal-to-noise ratio [J].
Hasselmo, ME ;
Linster, C ;
Patil, M ;
Ma, D ;
Cekic, M .
JOURNAL OF NEUROPHYSIOLOGY, 1997, 77 (06) :3326-3339
[9]  
Herken H, 2001, INT MEC J, V8, P41
[10]  
MartinezLavin M, 1997, J RHEUMATOL, V24, P714