No differences between fibromyalgia and controls were found by measuring IL-1β,IL-2,IL-10,sIL-2R,IFN-γ
,TNF-a
there were additional increases in IL-1Ra,IL-8,IL-6 over control values.
通過測量IL-1β,IL-2,IL-10,sIL-2R,IFN-γ,TNF-α,沒有發現纖維肌痛與對照之間的差異
IL-1Ra,IL-8,IL-6比對照值增加。
IL-8 promotes sympathetic pain and IL-6 induces hyperalgesia,fatigue and depression.
IL-8促進交感神經痛,IL-6誘導痛覺過敏,疲勞和抑鬱
Systematic review of the selected 25 articles revealed that FMS patients had higher serum levels of
interleukin (IL)-1 receptor antagonist, IL-6, and IL-8, and higher plasma levels of IL-8.
所選25篇文章的系統評價顯示,FMS患者血清白細胞介素(IL)-1受體拮抗劑(IL-1Ra),IL-6和IL-8水平升高,IL-8水平升高。
No intergroup difference was found for serum IL-6, IL-1β/IL-1, TNF, IL-2, IL-10, IFN-γ, IL-4.
血清IL-6,IL-1β/ IL-1,TNF,IL-2,IL-10,IFN-γ,IL-4沒有發現組間差異。
IL-8 levels were significantly higher among fibromyalgia patients compared with controls
纖維肌痛患者IL-8水平明顯高於對照組
由以上可知降低IL-8是治療纖維肌痛的重點
如何降低IL-8
能降低IL-8:鎂、牛磺酸、錳、硒、維生素C、維生素D、維生素E、兒茶素、花青素、薑黃素、茄紅素、異黃酮、鞣花酸、ω-3脂肪酸(DHA、EPA)
而且鋅、銅會增加IL-8
CRH(促腎上腺皮質激素釋放激素)值的升高以FM(纖維肌痛Fibromyalgia,FM)患者最明顯
會調節CRH的興奮性神經傳導物質主要有乙醯膽鹼和5-羥色胺(血清素),而抑制性神經傳導物質為兒茶酚胺和γ-氨基丁酸(γ-aminobutyric acid )。
促腎上腺皮質激素釋放激素(Corticotropin-releasing hormone,CRH)
Mg(2+) deficiency caused an increase in the transcription of the corticotropin releasing hormone
in the paraventricular hypothalamic nucleus (PVN)
Mg(2+)鎂離子缺乏導致室旁下丘腦核(PVN)中促腎上腺皮質激素釋放激素的轉錄增加
It is concluded that 5-HT via activation of 5-HT1A, 5-HT2A, 5-HT2C and possibly also 5-HT1B receptors
increases the synthesis of CRH in the PVN and POMC in the anterior pituitary lobe,
which results in increased ACTH secretion.
得出結論:5-HT(血清素)通過激活5-HT1A,5-HT2A,5-HT2C和可能還有5-HT1B受體增加了垂體前葉中PVN和POMC中CRH的合成
所以會調節CRH的興奮性神經傳導物質是會增加CRH的物質
由這篇文章
The γ-aminobutyric acid (GABA) degradation blocker γ-vinyl-GABA (VGB)
γ-氨基丁酸(GABA)降解阻滯劑γ-乙烯基GABA(VGB)
may decrease seizures also by reducing the levels of the convulsant molecule, CRH.
可以藉由降低CRH來減少癲癇發作
因此
阻止γ-氨基丁酸(GABA)降解就是讓更多GABA存在
所以
會調節CRH的抑制性神經傳導物質γ-氨基丁酸(GABA)
應能抑制CRH的釋放
維生素B6的脫羧作用(decarboxylation):
GABA( γ-amino-butyric acid γ-胺基丁酸),是由色胺酸、酪胺酸、【麩胺酸】經脫羧反應轉變而成。
研究也發現纖維肌痛症病人體內重要抑制疼痛的神經傳導物質血清素及正腎上腺素濃度較正常人來得低
可是
Cerebrospinal fluid (CSF)
腦脊液(CSF)
norepinephrine (NE)
去甲基腎上腺素(舊稱正腎上腺素)
increased CSF NE levels and appeared to increase CSF CRH levels
腦脊液NE水平升高,似乎增加腦脊液CRH水平
總結以上:
我感覺
也許纖維肌痛
講的
低鎂血症時,神經纖維和骨骼肌的應激性就增高,故在臨床上可出現
一系列神經-肌肉應激性增高的表現如小束肌纖維收縮、震顫
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