過敏與梅尼爾的關係?

Is Allergy Related to Meniere’s Disease?

原文：  https://www.researchgate.net/publication/223136937_Is_Allergy_Related_to_Meniere's_Disease

過敏與梅尼爾氏病的關係之前有跟大家分享國外許多研究對梅尼爾氏病的不同面向，有自體免疫, 過敏, 病毒, 壓力, 等等, 這篇論文則是review過敏這個因素，其中提到幾個重點跟大家分享

*在一個大型的研究中，從734個MD病人當中survey，發現過敏在MD病人中的盛行率約為41%

*有過敏性鼻炎的人，可能會有氣喘,鼻瘜肉,中耳炎,或慢性鼻竇炎。而有氣喘與過敏性鼻炎的人則會有較高的食物過敏盛行率。在2000年的一份研究中指出在MD病人中，小麥是最常見的食物過敏原68%。麥膠蛋白被認為是造成小麥過敏的人們對"IgE誘導產生的過敏"(第1型過敏)最主要的原因

*Derebery等人認為有三種過敏機制可能造成梅尼爾症狀，第1種是IgE誘導的過敏反應在內淋巴囊造成局部發炎, 第2種是免疫複合物在內耳淋巴囊附近的微血管堆積造成局部發炎，有研究顯示MD病人的循環免疫複合物的檢驗結果比控制組高了21~96%, 第3種是病毒侵入造成內淋巴囊的輕微發炎反應

*Derebery等人建議病人使用過敏免疫治療(allergen immunotherapy)並且/或是移除過敏源，在113個接受治療的病人中，所有人都回報症狀有所改善

摘錄一些重點如下


• In a large study, Derebery and Berliner investigated the prevalence of allergy in MD. In a survey of 734 patients with MD, concurrent allergic disease was found in 41 %.

在一個大型的研究中，從734個MD病人當中survey，發現過敏在MD病人中的盛行率約為41%

•  Likewise, in allergy-susceptible patients, an allergic response can evoke responses in distal sites.

在疑似過敏的患者身上，過敏反應可能會觸發末梢的反應

• This likely occurs via an integration of neurological, immunologic, and allergic responses involved in inflammation.

這可能會經由神經性,免疫性, 與有發炎之過敏反應的結合而發生

• People with ARmay have asthma, nasal polyposis, otitis media, or chronicrhinosinusitis [36]. People with asthma and AR have a higherprevalence of food allergies, the estimated prevalence ofwhich in America is 3.5 % to 6 % 

有過敏性鼻炎的人，可能會有氣喘,鼻瘜肉,中耳炎,或慢性鼻竇炎。而有氣喘與過敏性鼻炎的人則會有較高的食物過敏盛行率

• Derebery and Berliner [18] in 2000 reported wheat as the most common food allergen found in patients with MD(68.2 %).

2000年的一份研究中指出在MD病人中，小麥是最常見的過敏原68%

• Gliadin is considered the major cause of IgE-mediated hypersensitivity in people with wheat allergy.

麥膠蛋白被認為是造成小麥過敏的人們對"IgE誘導產生的過敏"(第1型過敏)最主要的原因

• Allergic reactions are considered to be one of the many causes of migraines. Numerous studies have reported an association between migraines and allergies. They found that the incidences of both allergy and migraine were significantly higher in the Meniere’s group and that the incidence of allergy in the MD migraine group was significantly higher than that in the group with MD alone.
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• Derebery and Berliner [21] outlined three proposed mechanisms by which allergy can produce MD symptoms.
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• The first mechanism, the endolymphatic sac, could be atarget organ of the allergic reaction. The antigen enters the endolymphatic sac andcauses an IgE-mediated degranulation of mast cells. Thisproduces a local inflammatory response that impairs theendolymphatic sac’s filtering function, and a buildup oftoxic metabolic products results, interfering with hair cell function. Histamine and other vasoactive mediators releasedin an allergic response elsewhere may also exert an effecton the well-vascularized fenestrated blood vessels of the endolymphatic sac, thereby affecting reabsorption. 
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• The second mechanism proposed is deposition of circu-lating immune complexes (CICs). These CICs are depositedand accumulate in the fenestrated blood vessels of the en-dolymphatic sac and stria vascularis. This results in inflam-mation and an increased permeability of the leaky capillariesthat surround the endolymphatic sac. The inflammationinterferes with the capability of the endolymphatic sac’shomeostasis function. Several studies demonstrated an in-crease in circulating immune complexes: 21 % to 96 % ofpatients with MD compared with controls 
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• The third mechanism is the viral antigen–allergic inter-action. This mechanism suggests that a viral insult canantigenically stimulate Waldeyer’s ring, with T-cell homingto the endolymphatic sac, causing a low-grade inflammatoryresponse. This impairs absorption of the endolymphatic sacbut does not produce symptoms. Then, later in life, anunknown trigger in the system stimulates excessive fluidproduction. Then, later in life, anunknown trigger in the system stimulates excessive fluidproduction.  Derebery and Berliner [21] referenced howviruses are capable of exacerbating allergic symptoms by avariety of means, including causing histamine release,thought to be mediated by interferon. They can also damageepithelial surfaces, enhancing antigen entry and increasingresponsiveness of target organs to histamine. Derebery[22••]noted heat shock protein 70 (HSP70), an antibodyfrequently seen increased in both MD and autoimmuneinner ear disease, is often upregulated in viral infections. They concluded that patients with clinically “certain” MD do not have a significantly raised incidence of HSP70 antibodies.
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• Derebery [19] (2000): 113 patients accepted treatment;all 113 reported improvementof symptoms after treatmentof allergy
• In Derebery’s clinicalexperience, patients who have both MD and allergybenefit from immunotherapy and/or dietary avoidanceof reactive food allergens. The symptoms of MD aregenerally better controlled, with fewer vertigo attacksand more stable hearing
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• The association of allergy andMD is well-documented. At the present time, it is generallyaccepted that the cause of MD is likely to be multifactorial,consisting of an underlying genetic predisposition, com-bined with an extrinsic insult. Allergy may well be involvedin the final common inflammatory pathway in a selectsubpopulation of patients with MD 
• 有點懶，之後再繼續讀這篇論文

關於第一二三型過敏反應的解釋 可參照這裡
https://smallcollation.blogspot.tw/2013/10/hypersensitivity.html#gsc.tab=0
"1.第Ⅰ型過敏反應－IgE誘導發生的過敏反應
造成第I型過敏反應的機制為：當過敏原第一次進入人體在與特定B細胞上的抗體結合後，會引起特定IgE的大量製造，分泌出的IgE與過敏原結合後，會附著在肥大細胞(Mast cell)表面的Fcε受體。當相同的過敏原再度入侵人體，過敏原和肥大細胞表面上的IgE結合，會誘發肥大細胞釋出發炎物質，如組織胺、介白素、細胞激素，造成紅腫發癢等症狀"

"3.第Ⅲ型過敏反應－免疫複合體(immune complex)引發的過敏反應
...複合物如果沒有被清除，且在腎、血管壁、心臟瓣膜等處沉積，進而引發過度的免疫反應，如吞噬細胞企圖吞噬複合物，但複合物太大無法吞噬，於是釋放出酵素，導致發炎並造成該部位的傷害...複合物沉積的位置可以是全身性或局部性...造成的原因有可能是病患自己產生自體抗體與自體抗原形成免疫複合體而引發，如全身紅斑性狼瘡(systemic lupus erythematosus) 、類風濕關節炎的患者；或者是持續性感染，其抗原的量雖然不多，但一直存在，使得免疫複合物持續產生，並堆積在各個器官，如麻瘋病、瘧疾、B型肝炎"