馬菁茹 黃晶晶 肖寬林

·綜述·

兒童阻塞性睡眠呼吸暫停低通氣綜合征與常見炎癥因子及相關(guān)疾病的關(guān)系

馬菁茹 黃晶晶 肖寬林

兒童阻塞性睡眠呼吸暫停低通氣綜合征(OSAHS)最主要的發(fā)病原因是扁桃體、腺樣體肥大(AH)，可影響兒童的生長發(fā)育。其發(fā)病機制與炎癥有關(guān)。OSAHS患兒可發(fā)生全身及局部炎癥反應(yīng)，但相關(guān)機制尚未明確。本文回顧了近年來有關(guān)OSAHS及AH與多種細胞因子的研究，對兒童OSAHS與變應(yīng)性鼻炎及分泌性中耳炎關(guān)系的研究結(jié)果進行了初步分析。(中國眼耳鼻喉科雜志，2017，17：366-369)

阻塞性睡眠呼吸暫停低通氣綜合征；腺樣體肥大；炎癥；腫瘤壞死因子α；白細胞介素6；白三烯；兒童

腺樣體又稱咽扁桃體，是兒童免疫系統(tǒng)的重要組成部分，位于鼻咽頂后壁中線處。正常情況下6～7歲發(fā)育最大，10歲之后開始萎縮。當(dāng)鼻咽部及其毗鄰部位或腺樣體自身炎癥反復(fù)刺激時，腺樣體發(fā)生病理性增生，并引起相應(yīng)癥狀，稱為腺樣體肥大(adenoid hypertrophy, AH)。AH是兒童阻塞性睡眠呼吸暫停低通氣綜合征(obstructive sleep apnea hypopnea syndrome, OSAHS)最常見的病因，其主要臨床表現(xiàn)為鼻塞、睡眠打鼾、張口呼吸等，長期發(fā)展引起面骨發(fā)育障礙，出現(xiàn)“腺樣體面容”。兒童OSAHS及AH的病理生理學(xué)機制尚不清楚，但目前研究顯示可能與全身及局部炎癥反應(yīng)有關(guān)。本文主要綜述炎癥因子及炎癥相關(guān)疾病與兒童OSAHS關(guān)系的最新進展。

1 兒童OSAHS與炎癥

OSAHS可使患兒出現(xiàn)心血管疾病、神經(jīng)系統(tǒng)疾病、認知障礙等的風(fēng)險增高，這可能與炎癥反應(yīng)有關(guān)。

1.1 全身炎癥 多項研究表明OSAHS與全身炎癥反應(yīng)有關(guān)。Gozal等[1]發(fā)現(xiàn)非肥胖OSAHS患兒血漿白細胞介素6(interleukin-6，IL-6)水平升高，行扁桃體和腺樣體切除術(shù)(tonsillectomy and adenoidectomy，T&A)后逐漸恢復(fù)至對照水平。Huang等[2]發(fā)現(xiàn)OSAHS患兒血漿高敏C反應(yīng)蛋白(high-sensitivity C-reactive protein，hs-CRP)、IL-17、IL-23均顯著增加。外周血細胞因子常用來反映全身炎癥水平，OSAHS患兒血清細胞因子改變且治療后恢復(fù)，說明OSAHS可引起患兒全身炎癥改變，且這種改變可逆。

1.2 局部炎癥 近年來，國內(nèi)外學(xué)者對OSAHS患兒扁桃體、腺樣體組織進行檢測發(fā)現(xiàn)多種細胞因子水平增高。Kim等[3]研究發(fā)現(xiàn)OSAHS患兒扁桃體組織中腫瘤壞死因子α(tumor necrosis factor-α，TNF-α)、IL-6、IL-1α等促炎因子高表達。梁敏等[4]發(fā)現(xiàn)AH患兒腺樣體組織中半胱氨酸白三烯受體1(cysteinyl leukotriene receptors-1，CysLTR-1)和CysLTR-2基因mRNA存在高表達。Kheirandish-Gozal等[5]亦發(fā)現(xiàn)鼻內(nèi)激素可使OSAHS患兒體外扁桃體細胞的增殖能力減弱，混合細胞體系中TNF-α、IL-8、IL-6等促炎因子顯著減少?？梢奜SAHS患兒扁桃體、腺樣體組織發(fā)生局部炎癥反應(yīng)。

2 兒童OSAHS與細胞因子

OSAHS患兒外周血及局部組織存在多種細胞因子改變。近年來國內(nèi)外學(xué)者對OSAHS患兒血清及組織中TNF-α、IL-6和白三烯(leukotriene，LT)等細胞因子進行了深入研究，對更深層機制進行探討，然而所得結(jié)論存在一定差異。

2.1 TNF-α TNF-α是一種多功能促炎因子，在細胞免疫過程中發(fā)揮重要作用。既往研究[3, 5]表明，OSAHS患兒血清中TNF-α高表達，且抗炎治療后TNF-α水平下降。此后Gozal等[6]亦發(fā)現(xiàn)TNF-α水平在中重度OSAHS患兒血清中明顯升高，且與睡眠呼吸暫停低通氣指數(shù)(apnea hypopnea index，AHI)和體重指數(shù)(body mass index，BMI)相關(guān)，T&A治療后血漿TNF-α水平下降。這種改變可能與OSAHS患兒長期處于間歇性低氧(intermittent hypoxia, IH)狀態(tài)，血清缺氧誘導(dǎo)因子1α(hypoxia-inducible factor -1α，HIF-1α)增加有關(guān)。Huang等[7]認為HIF-1α可誘導(dǎo)TNF-α產(chǎn)生。楊曉剛等[8]發(fā)現(xiàn)TNF-α拮抗劑通過有效中和TNF-α并阻斷其生物學(xué)活性，抑制致炎性細胞因子釋放，減弱HIF-1α蛋白表達。這也證實HIF-1α確實與TNF-α存在一定關(guān)聯(lián)，IH是OSAHS患兒血清TNF-α發(fā)生改變的重要原因。也有學(xué)者認為，TNF-α與OSAHS相關(guān)性不強。Chu等[9]研究表明，肥胖OSAHS患兒在T&A治療前后血漿TNF-α水平無明顯變化，且TNF-α血漿水平與AHI無相關(guān)性。Alexopoulos等[10]發(fā)現(xiàn)血漿TNF-α水平與OSAHS的嚴重程度不相關(guān)。這些差異可能與肥胖有關(guān)，但TNF-α基因多態(tài)性對OSAHS患兒血漿TNF-α水平可變性的影響亦不容忽視。1992年，Wilson等[11]率先報道等位基因G-A位于TNF-α啟動子區(qū)域第308位(-308A/G)，隨后有研究[12]發(fā)現(xiàn)-308G可增加TNF-α啟動子活性，從而在轉(zhuǎn)錄水平改變TNF-α的合成和表達。Khalyfa等[13]發(fā)現(xiàn)OSAHS患兒清晨血漿TNF-α水平增加，且在TNF-α-308G單核苷酸多態(tài)性(single nucleotide polymorphism，SNP)患者中增加尤為顯著。隨后，Wu等[14]對10項病例對照研究(包括成人和兒童)進行Meta分析，顯示TNF-α-308G/A多態(tài)性增加了患者對OSAHS風(fēng)險的敏感度。TNF-α基因多態(tài)性可能增加兒童OSAHS及AH的易感性，從而使血清TNF-α水平產(chǎn)生差異。

2.2 IL-6 IL-6是機體生理病理過程中重要的多功能和多向性細胞因子，在炎癥、免疫防御及組織損傷中具有重要作用，參與趨化因子誘導(dǎo)白細胞遷移，調(diào)節(jié)白細胞激活、分化和增殖，指導(dǎo)固有免疫和適應(yīng)性免疫轉(zhuǎn)換[15]。Rudmik等[16]研究表明，腺樣體組織中存在樹突細胞、巨噬細胞、漿細胞、肥大細胞、淋巴細胞等。炎癥時，肥大細胞被激活釋放組胺、類胰蛋白酶等多種分泌性介質(zhì)，使外周血單個核細胞釋放IL-6。既往研究[1, 3, 5]已證實OSAHS患兒發(fā)生全身及局部炎癥反應(yīng)，使IL-6升高。此后，沈康等[17]發(fā)現(xiàn)腺樣體組織內(nèi)IL-6濃度與AH程度呈正相關(guān)，表明IL-6與腺樣體局部免疫有關(guān)。Kheirandish-Gozal等[18]證實不僅抗炎治療降低OSAHS患兒IL-6水平，T&A手術(shù)亦使患兒血漿IL-6水平降低。Wang等[19]研究發(fā)現(xiàn)腺樣體組織中血管內(nèi)皮生長因子(vascular endothelial growth factor, VEGF)水平顯著增高，且與AH程度及鼻咽分泌物中的IL-6相關(guān)。體外培養(yǎng)發(fā)現(xiàn)IL-6可促進VEGF表達，因VEGF參與血管生成的病理生理過程，由此推測IL-6促使VEGF表達，促進血管生成，從而誘導(dǎo)腺樣體進一步增生。但目前OSAHS合并AH患兒與外周血及局部IL-6的關(guān)系尚不明確，有待進一步論證。

2.3 LT LT是細胞膜磷脂分子層中的花生四烯酸在5-脂氧酶作用下合成的一系列炎性介質(zhì)，包括LTB4、LTC4、LTID4、LTE4，后三者含有半胱氨酰基，故又稱為半胱氨酰白三烯(cysteinyl leukotriene，CysLT)。國際藥理聯(lián)合理事會將LTs受體分為2大類，即BLT受體和CysLTR，后者分為CysLTR-1和CysLTR-2。CysLT是重要的免疫及炎癥因子。Tsaoussoglou等[20]使用qRT-PCR技術(shù)、流式細胞技術(shù)和免疫熒光技術(shù)，發(fā)現(xiàn)OSAHS患兒扁桃體組織中CysLT-1和CysLT-2高表達。馬冬梅等[21]研究發(fā)現(xiàn)OSAHS患兒血清CysLTs水平與OSAHS的嚴重程度密切相關(guān)。梁敏等[4]也得出了相似的結(jié)論。近年來，有關(guān)各類型LTs的研究逐漸深入。Lefebvre等[22]發(fā)現(xiàn)OSAHS患兒外周血多形核白細胞(polymorphonuclear leukocytes，PMNs)較對照組產(chǎn)生更多LTB4，且LTB4水平與平均血氧飽和度及最低血氧飽和度相關(guān)。Shu等[23]研究證實LTD4可促使OSAHS患兒腺樣體T細胞增殖，參與OSAHS病理生理過程?；谶@些研究，臨床上使用孟魯司特等白三烯受體拮抗劑治療AH。研究表明孟魯司特治療可使76%的OSAHS患兒腺樣體減小，改善睡眠不適、打鼾、張口呼吸等癥狀[24]，尤其是對輕度患兒，孟魯司特聯(lián)合鼻內(nèi)激素可改善80%輕度AH患兒的病情[25]。

除TNF-α、IL-6、LTs外，CRP、IL-17等都是常見的兒童OSAHS炎癥生物標(biāo)記，但其具體作用機制亦未明確。目前對正五聚蛋白-3(pentraxin-3，PTX-3)、Nesfatin-1、Fibrinogen等新型炎癥標(biāo)記因子與OSAHS的研究也在逐步開展，但主要集中在成人病例，其與兒童OSAHS及AH的關(guān)系尚缺乏有效數(shù)據(jù)支持。

3 兒童OSAHS與相關(guān)疾病

隨著OSAHS和炎癥關(guān)系研究的深入，近年來，越來越多的學(xué)者開始關(guān)注OSAHS與變應(yīng)性鼻炎(allergic rhinitis，AR)及分泌性中耳炎(otitis media with effusion，OME)等兒童常見疾病的關(guān)系。本文主要從炎癥角度綜述兒童OSAHS與AR和OME之間的聯(lián)系。

3.1 兒童OSAHS與AR 臨床研究[26]表明，OSAHS患兒中，有43%合并AR，明顯高于同年齡兒童10%～15%的AR患病率，且AH可加重AR病情，使其病程延長[27]。從解剖上分析：AR患兒鼻腔阻力增加產(chǎn)生鼻內(nèi)湍流，患兒為緩解鼻腔阻塞而張口呼吸，下頜骨發(fā)育的改變使咽部直徑減小，氣流通過狹窄的咽部引起震動導(dǎo)致打鼾。鼻腔阻塞使咽部產(chǎn)生負壓，引起咽部收縮，睡眠時低氧最終導(dǎo)致OSAHS[28]。李明華[29]認為鼻黏膜的過敏性炎癥產(chǎn)生分泌物，反復(fù)刺激鼻腔后部的腺樣體，可引起或加重AH，進而導(dǎo)致OSAHS。AR和OSAHS患者外周血均發(fā)現(xiàn)組胺、CysLTs、IL-1β、IL-4等炎癥因子的改變，鼻內(nèi)激素治療AR可改善OSAHS病情[30]。Th17/Treg細胞平衡有助于評估OSAHS及AR的病情，二病共患時AR所致Th17/Treg細胞失衡與OSAHS所致失衡相互影響，加重病情[31]。這說明OSAHS與AR存在相似炎癥反應(yīng)，二者相互影響。然而，Di Francesco等[32]研究發(fā)現(xiàn)AR并未使患兒AHI增加?？梢?，AR與OSAHS的相關(guān)作用及其機制仍有待進一步研究。

3.2 兒童OSAHS與OME 近年來，OME與AH的相關(guān)性一直是學(xué)者們研究的熱點。Nwosu等[33]研究發(fā)現(xiàn)AH患兒OME發(fā)病率為55.9%，遠高于排除AH癥狀的兒童，且AH病情越重，與OME相關(guān)性越強。腺樣體壓迫咽鼓管咽口曾被認為是誘發(fā)OME的主要原因，但研究[34]發(fā)現(xiàn)OME患兒與非OME患兒相比腺樣體大小無明顯差異。OME患兒內(nèi)耳黏膜檢測出多種致病菌生物膜，與扁桃體、腺樣體組織檢出的致病菌一致，說明扁桃體、腺樣體在OME發(fā)病中起到慢性感染“蓄菌池”作用[35]。A&H可清除上氣道黏膜“蓄菌池”，促進OME恢復(fù)[36]。OME患兒血清TNF-α、IL-1β、IL-6及IL-8均顯著升高，OSAHS患兒亦有類似發(fā)現(xiàn)[37]。Bhargava等[38]發(fā)現(xiàn)鼻內(nèi)激素治療可明顯改善AH伴OME患兒的聽力及相關(guān)癥狀。AH加重OME病情，但兒童OSAHS及AH是否與OME發(fā)病相關(guān)仍未有定論。Braun等[39]在實驗中未發(fā)現(xiàn)兒童OSAHS與OME有關(guān)聯(lián)。Zelazowska-Rutkowska等[40]發(fā)現(xiàn)AH伴OME患兒的腺樣體細胞分泌IL-5和TNF-α較單純AH患兒高，而IL-6、IL-8、IL-10無變化，說明AH伴OME較AH產(chǎn)生了不同的免疫反應(yīng)。OME與OSAHS及AH的關(guān)系仍需驗證，但不可否認抗炎治療及T&A可緩解OME病情。

大多數(shù)兒童OSAHS是由扁桃體、腺樣體肥大引起，患兒血清及扁桃體、腺樣體組織內(nèi)均可發(fā)現(xiàn)TNF-α、IL-6、LTs等細胞因子發(fā)生改變，表明兒童OSAHS與全身及局部免疫密切相關(guān)。AR及OME與OSAHS的關(guān)聯(lián)尚不明確，其具體關(guān)系及機制仍需進一步研究。

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Relationshipbetweenpediatricobstructivesleepapneahypopneasyndromeandcommoninflammatoryfactorsandrelateddiseases

MAJing-ru,HUANGJing-jing,XIAOKuan-lin.

DepartmentofOtolaryngology,EyeEarNoseandThroatHospitalofFudanUniversity,Shanghai200031,China

XIAO Kuan-lin, Email: xiaokuanlin@hotmail.com

Tonsil and adenoid hypertrophy are the most important causes of pediatric obstructive sleep apnea hypopnea symptom (OSAHS), which could affect the growth of children. The pathogenesis of OSAHS is not clear. Some studies showed that it was associated with inflammation. OSAHS children might get systemic and local inflammation. This paper reviewed the research of OSAHS and adenoid hypertrophy with some common cytokines, and made a preliminary analysis on the relationship between OSAHS and allergic rhinitis and otitis media with effusion. (Chin J Ophthalmol and Otorhinolaryngol,2017,17:366-369)

Obstructive sleep apnea hypopnea syndrome; Adenoid hypertrophy; Inflammation; Tumor necrosis factor α; Interleukin 6; Leukotriene; Children

2016-11-16)

(本文編輯 楊美琴)

復(fù)旦大學(xué)附屬眼耳鼻喉科醫(yī)院耳鼻喉科 上海 200031

肖寬林(Email: xiaokuanlin@hotmail.com)

10.14166/j.issn.1671-2420.2017.05.017