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Article(id=1208055580506296841, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208055572495179979, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2022.06.0625, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1624809600000, receivedDateStr=2021-06-28, revisedDate=null, revisedDateStr=null, acceptedDate=1636560000000, acceptedDateStr=2021-11-11, onlineDate=1765952494979, onlineDateStr=2025-12-17, pubDate=1656345600000, pubDateStr=2022-06-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1765952494979, onlineIssueDateStr=2025-12-17, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1765952494979, creator=13701087609, updateTime=1765952494979, updator=13701087609, issue=Issue{id=1208055572495179979, tenantId=1146029695717560320, journalId=1189873630562394117, year='2022', volume='47', issue='6', pageStart='533', pageEnd='638', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1765952493070, creator=13701087609, updateTime=1765952764848, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208056712481841868, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208055572495179979, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208056712481841869, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208055572495179979, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=625, endPage=630, ext={EN=ArticleExt(id=1208055581672313367, articleId=1208055580506296841, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress in diagnosis and treatment of portal hypertensive enteropathy, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Portal hypertensive enteropathy (PHE) is the appearance of intestinal mucosal capillary stasis and expansion,ultrastructural changes in mucosal epithelial cells, and ectopic varicose veins in patients with portal hypertension (PH), and its scope is limited to intestinal lesions characterized by vascular changes. PHE, including portal hypertensive small bowel disease and portal hypertensive colonopathy (PHC), is one of the important causes of PH complicated by gastrointestinal bleeding. The pathogenesis of PHE is not fully understood, the lack of specificity of histopathological findings, atypical clinical symptoms, and the uniqueness of anatomical location makes its diagnosis difficult. Abdominal CT, multi-slice spiral CT perfusion imaging, 99mTc-RBC and single photon emission CT (SPECT)/CT can provide certain diagnostic information and help guide follow-up treatment. This article summarizes the research progress of PHE from the aspects of pathogenesis, histopathological findings, clinical manifestations,examination and diagnosis and treatment methods, in order to deepen clinicians' understanding of this disease.

, correspAuthors=Hui-Ru Zhang, authorNote=null, correspAuthorsNote=
*E-mail:
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门静脉高压性肠病(PHE)是在门静脉高压(PH)患者中出现的肠黏膜毛细血管淤血、扩张，黏膜上皮细胞超微结构改变，以及异位静脉曲张等，其范围仅限于以血管改变为特征的肠道病变。PHE包括门静脉高压性小肠病及门静脉高压性结肠病(PHC)，是PH并发消化道出血的重要原因之一。PHE的发病机制尚不完全清楚，其组织病理学表现缺乏特异性，临床症状不典型，且病变解剖位置独特，导致其诊断具有一定难度。腹部CT、多层螺旋CT灌注成像、99mTc标记红细胞及单光子发射CT(SPECT)/CT等检查手段能提供一定的诊断信息并有助于指导后续治疗。本文从发病机制、组织病理学表现、临床表现、检查与诊断及治疗方法等方面总结PHE的研究进展，以加深临床医师对该疾病的认识。

, correspAuthors=张慧茹, authorNote=null, correspAuthorsNote=
张慧茹，E-mail：
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白婷婷，硕士研究生，主要从事慢性肝病方面的研究

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白婷婷，硕士研究生，主要从事慢性肝病方面的研究

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白婷婷，硕士研究生，主要从事慢性肝病方面的研究

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门静脉高压性肠病研究进展
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白婷婷 , 文良志 , 陈东风 , 张慧茹 *
解放军医学杂志 | 综述 2022,47(6): 625-630
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解放军医学杂志 | 综述 2022, 47(6): 625-630
门静脉高压性肠病研究进展
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白婷婷, 文良志, 陈东风, 张慧茹*
作者信息
  • 陆军特色医学中心大坪医院消化内科，重庆 400042

    • 白婷婷，硕士研究生，主要从事慢性肝病方面的研究

通讯作者:

张慧茹，E-mail：
Research progress in diagnosis and treatment of portal hypertensive enteropathy
Ting-Ting Bai, Liang-Zhi Wen, Dong-Feng Chen, Hui-Ru Zhang*
Affiliations
  • Department of Gastroenterology, Daping Hosptial of Army Special Medical Center, Chongqing 400042, China
出版时间: 2022-06-28 doi: 10.11855/j.issn.0577-7402.2022.06.0625
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摘要
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门静脉高压性肠病(PHE)是在门静脉高压(PH)患者中出现的肠黏膜毛细血管淤血、扩张，黏膜上皮细胞超微结构改变，以及异位静脉曲张等，其范围仅限于以血管改变为特征的肠道病变。PHE包括门静脉高压性小肠病及门静脉高压性结肠病(PHC)，是PH并发消化道出血的重要原因之一。PHE的发病机制尚不完全清楚，其组织病理学表现缺乏特异性，临床症状不典型，且病变解剖位置独特，导致其诊断具有一定难度。腹部CT、多层螺旋CT灌注成像、99mTc标记红细胞及单光子发射CT(SPECT)/CT等检查手段能提供一定的诊断信息并有助于指导后续治疗。本文从发病机制、组织病理学表现、临床表现、检查与诊断及治疗方法等方面总结PHE的研究进展，以加深临床医师对该疾病的认识。

门静脉高压  /  门静脉高压性肠病  /  门静脉高压性结肠病  /  出血  /  内镜检查

Portal hypertensive enteropathy (PHE) is the appearance of intestinal mucosal capillary stasis and expansion,ultrastructural changes in mucosal epithelial cells, and ectopic varicose veins in patients with portal hypertension (PH), and its scope is limited to intestinal lesions characterized by vascular changes. PHE, including portal hypertensive small bowel disease and portal hypertensive colonopathy (PHC), is one of the important causes of PH complicated by gastrointestinal bleeding. The pathogenesis of PHE is not fully understood, the lack of specificity of histopathological findings, atypical clinical symptoms, and the uniqueness of anatomical location makes its diagnosis difficult. Abdominal CT, multi-slice spiral CT perfusion imaging, 99mTc-RBC and single photon emission CT (SPECT)/CT can provide certain diagnostic information and help guide follow-up treatment. This article summarizes the research progress of PHE from the aspects of pathogenesis, histopathological findings, clinical manifestations,examination and diagnosis and treatment methods, in order to deepen clinicians' understanding of this disease.

portal hypertension  /  portal hypertensive enteropathy  /  portal hypertensive colonopathy  /  bleeding  /  endoscopy
白婷婷, 文良志, 陈东风, 张慧茹. 门静脉高压性肠病研究进展. 解放军医学杂志, 2022 , 47 (6) : 625 -630 . DOI: 10.11855/j.issn.0577-7402.2022.06.0625
Ting-Ting Bai, Liang-Zhi Wen, Dong-Feng Chen, Hui-Ru Zhang. Research progress in diagnosis and treatment of portal hypertensive enteropathy[J]. Medical Journal of Chinese People’s Liberation Army, 2022 , 47 (6) : 625 -630 . DOI: 10.11855/j.issn.0577-7402.2022.06.0625
正文
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门静脉高压(portal hypertension，PH)是指肝静脉压力梯度(HVPG) >5 mmHg，当HVPG>12 mmHg时，PH具有临床意义。肝硬化是PH最常见的病因之一。1985年，McCormack等[1]首次将PH引起的胃黏膜改变描述为充血性胃病。1989年，Thiruvengadam等[2]发现PH不仅能导致充血性胃病，还可引起十二指肠及空肠黏膜出现多发红斑性改变，这些部位的病变与胃内病变相似，被认为是门静脉高压性充血性胃病的延伸，也是导致门静脉高压非静脉曲张性消化道出血的原因之一。因此，他们建议使用“充血性胃肠病”代替“充血性胃病”，使表达更加全面、准确。1991年，Kozarek等[3]对PH患者进行结肠镜检查，发现患者出现类似胃部樱桃色红斑、蜘蛛样毛细血管扩张及血管发育不良等多发肠黏膜血管性病变，并将上述病变命名为“门静脉高压性结肠病(portal hypertensive colonopathy，PHC)”。门静脉高压性肠病(portal hypertensive enteropathy，PHE)是指在PH基础上出现的肠黏膜毛细血管淤血、扩张，黏膜上皮细胞超微结构改变，以及PH所致的异位静脉曲张，其范围仅限于以血管改变为特征的肠道病变，包括门脉高压性小肠病及PHC[4]。在肝硬化PH患者中，PHE的发生率为15%~82%，不同个体间存在较大异质性[5]。PHE目前尚无统一的内镜分型、诊断标准及治疗方案，本文主要对其发病机制、临床表现、诊断及治疗现状进行综述。
1 发病机制
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1.1 肠道血流动力学改变
PH导致肠道血液回流受阻。Zwiebel等[6]对20例肝硬化合并PH患者行多普勒超声检查发现，患者肠系膜上动脉及内脏动脉血流量较健康组明显增加。此外，有研究表明，PH合并食管静脉曲张患者行内镜治疗后出现小肠黏膜损伤，且与肠系膜上静脉血流速度降低及肠系膜循环充血相关[7]。由于门静脉高动力循环，肠道血流量增加，肠黏膜及黏膜下毛细血管和小静脉扩张、通透性增加，血浆成分外渗，导致肠黏膜下广泛水肿、充血、糜烂，而动-静脉短路开放使黏膜的有效血流量减少，肠黏膜微循环发生障碍。Prieto等[8]对大鼠行部分门静脉结扎术建立PH模型，并于术后6周检测十二指肠、空肠、回肠及肠系膜淋巴结中的肥大细胞密度，结果显示，与对照组相比，PH组大鼠小肠及肠系膜淋巴结中的肥大细胞密度增高，提示肥大细胞参与了PHE的发生。PH患者的肠系膜静脉压力明显升高，导致肠绒毛上皮层及间质中的肥大细胞和淋巴管内皮细胞发生炎症反应，并通过肠系膜进入全身淋巴管，造成肠黏膜屏障受损及肠淋巴管渗漏，由肠源性病原体相关分子模式物质引起肠道损伤乃至全身系统性炎症[9]。
1.2 血管活性物质的变化
PH患者结肠黏膜下层血管内皮细胞中的肿瘤坏死因子-α(tumor necrosis factor-α，TNF-α)及一氧化氮合酶(nitric oxide synthase，iNOS)表达升高，导致上调的一氧化氮(nitric oxide，NO)通过介导黏膜血管扩张以及黏膜微循环障碍参与PHE的发病过程[10]。有研究显示，PH大鼠肠组织中的降钙素相关基因肽(calcitonin gene related peptide，CGRP)表达升高，其在肠黏膜病变中可能发挥一定作用[11]。此外，PHE患者体内的扩血管物质(如胰高血糖素)表达增加，外周动脉对缩血管物质的反应性降低，导致内脏血管舒缩功能紊乱，上述过程也参与了PHE的发生[12]。
1.3 肠黏膜屏障损伤
PH患者肠黏膜缺血、缺氧、代谢紊乱，肠上皮细胞多种功能受到影响，其中肠道分泌功能降低造成非致病性细菌在肠腔内过度生长及定植，导致肠道菌群稳态发生改变，并产生内毒素及蛋白水解酶，损伤肠黏膜屏障[13]。PH患者肠道菌群中产生短链脂肪酸(short chain fatty acids，SCFAs)的菌属(如厚壁菌属、拟杆菌属及梭菌属)明显减少[13]。有研究表明，SCFAs能增强芳香烃受体(aromatic hydrocarbon receptor，AhR)的反应性[14]，而AhR的激活可调节肠道干细胞(intestinal stem cells，ISCs)的Wnt、Notch及表皮生长因子(epidermal growth factor receptor，EGFR)/丝裂原活化蛋白激酶(mitogen-activated protein kinase，MAPK)等信号通路，从而调节ISCs的干性及分化，以保持ISCs干性、增殖及分化间的平衡[15]。因此，PH患者体内SCFAs的产生受到抑制，可能影响ISCs的功能，无法维持肠黏膜屏障的完整性。目前ISCs维持肠黏膜屏障完整性与PHE之间的关系尚不明确，值得进一步研究。
2 组织病理学改变
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PHE的组织病理学改变主要为肠黏膜固有层内的毛细血管扩张、血管壁增厚、血管壁周围组织有嗜伊红物质沉积，小肠绒毛萎缩、绒毛/隐窝比值降低，新生血管丰富，血管内出现纤维素性血栓及淋巴细胞浸润等[5,16]。文献报道，PHE患者存在肠黏膜内淋巴管扩张，被认为是肠道丢失蛋白的原因之一[16]。由于PHE的组织病理学改变是非特异性的，因此其诊断不应仅依靠组织病理学检查结果，还应结合PH患者的临床症状、内镜检查结果及影像学表现综合判断。
3 临床表现
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3.1 消化道出血
大多数PHE患者无特异性临床症状，部分患者可出现急性或慢性消化道出血，以慢性隐匿性出血居多，主要表现为大便隐血阳性及血便，大出血发生率仅为4%[4]。PHE患者也可表现为慢性失血及慢性贫血。肝硬化患者由门静脉高压性小肠病及PHC导致的急性消化道出血率分别为5.5%~11.0%及1%~2%[17]。
3.2 营养不良
PH患者肠道的运动、分泌及吸收能力下降，会影响三大营养物质、维生素及微量元素的吸收，患者可出现低蛋白血症、贫血、体重减轻及肌少症等临床表现；PH还可降低患者的生活质量，缩短生存期，增加感染、腹水、肝性脑病、围手术期并发症等的发生风险以及患者等待肝移植期间的死亡风险，是肝移植围手术期不良结局的独立危险因素[18]。一项纳入12例PH患者(PH组)、12例单纯肝硬化患者(肝硬化组)及32例健康志愿者(对照组)的研究表明，PH组患者小肠消化间期移行复合运动(migrating motor comlpexes，MMC)Ⅱ期及餐后十二指肠逆性压力波与对照组比较差异均有统计学意义，PH组患者MMCⅡ期的长簇波明显高于对照组，而肝硬化组与对照组上述指标比较差异无统计学意义，提示PH患者可能合并小肠运动功能紊乱，从而导致营养不良[19]。此外，PH组中33%的患者伴有小肠细菌过度增生(small intestinal bacterial overgrowth，SIBO)，而肝硬化组患者未出现SIBO，伴有SIBO的PH患者MMC周期长于未合并SIBO的PH患者[19]，表明在肝硬化PH患者中，MMC的持续时间延长，小肠聚集性收缩频率增快，可能是其发生SIBO的机制之一。当肝硬化PH患者出现肠道运动功能异常或SIBO时，更易导致肝硬化PH相关并发症，如吸收不良、自发性细菌性腹膜炎、菌血症、全身感染及肝性脑病等[20]。
3.3 肠易激综合征(irritable bowel syndrome，IBS)样症状
PHE患者常出现腹胀、纳差、腹痛、便秘及腹泻等IBS样症状，其中腹胀、便秘等可能与肝硬化PH患者的肠道消化、吸收、分泌、运动功能及神经调节功能紊乱有关，且与Child-Pugh分级有密切关系[21]。有研究显示，肝硬化失代偿期患者的左半结肠出现运输加速，与腹泻症状明显相关[22]。一项研究表明，1033例腹泻型IBS患者中有401例合并SIBO，发生率为38.8%；而对照组656名健康体检者中有141名合并SIBO，发生率为21.5%，表明当PH患者出现腹泻型IBS样表现时更易合并SIBO，SIBO可能导致腹胀、纳差、腹痛及腹泻等症状[23]。
3.4 食管静脉曲张
目前对于PHE的发病率是否与PH患者合并食管静脉曲张相关，尚存在不同的观点。杨汉勤等[24]的研究纳入62例肝硬化PH患者，其中轻度食管静脉曲张17例，中度24例，重度21例，出现结肠病变的分别有6例(35.3%)、15例(62.5%)、17例(81.0%)。严正平等[25]发现，轻、中、重度食管静脉曲张患者PHC的发生率分别为25.0%(2/8)、58.9%(10/17)、72.7%(8/11)。由此可见，PHE的发生率随PH患者食管静脉曲张程度的加重而增高，且与PH程度关系密切。但也有学者认为，PHE的发生与肝硬化PH的病因、肝功能不全程度及PH程度无关[3,24]。Nagral等[26]发现，PHE的发生率与肝硬化患者的Child-Pugh评分及接受治疗的次数无关，且门静脉宽度与其侧支循环的建立并不能很好地预测PHE的发生。此外，尚无研究表明不同类型PH所致PHE的临床表现有差异，因此PHE发生的影响因素还需要进一步研究。
4 临床检查与诊断
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4.1 内镜检查
4.1.1 门静脉高压性小肠病
诊断主要依赖于胶囊内镜及小肠镜。de Palma等[27]使用胶囊内镜研究肝硬化PH患者的小肠改变，将内镜下表现分为两类：(1)黏膜炎性病变，如水肿、红斑、颗粒样改变、黏膜脆性增加；(2)血管性病变，如樱桃红斑、毛细血管扩张、血管发育不良样病变及静脉曲张。Higaki等[28]将门静脉高压性小肠病的小肠镜下表现分为两类：(1)小肠绒毛异常，包括黏膜网状结构、水肿性黏膜、黏膜颗粒样充血、鲱鱼子外观样充血；(2)血管病变，如红色斑点、红色斑点伴黏膜颗粒样改变、血管扩张、静脉曲张伴蓝色征、小囊状静脉曲张伴血管表面透亮、囊状静脉曲张充血、静脉曲张破裂出血及渗血。
4.1.2 PHC
PHC典型的内镜下表现为外观正常的黏膜上有直径<10 mm轻微隆起的红色病变[4]。目前，尚无理想的分级系统对PHC患者黏膜异常的严重程度进行分级。PHC典型血管病变的组织学表现主要有两种[29]：初期病变特征为黏膜下层血管轻度扩张迂曲；晚期病变表现为黏膜下静脉明显扩张，黏膜小静脉及毛细血管明显扩张迂曲。内镜下典型的血管扩张或弥漫性红斑可分为3种类型：1型为扁平、蕨类植物样血管病变(或蜘蛛样病变)；2型为直径<10 mm的扁平或轻微隆起红色病变或樱桃红色病变；3型为轻微隆起的黏膜下瘤样病变，中心呈红色并有凹陷[30]。de Palma等[27]进一步提出了PHC的3级分类系统：1级为结肠黏膜红斑；2级为结肠黏膜红斑呈马赛克样改变；3级为结肠血管病变，包括樱桃红斑、毛细血管扩张或血管发育不良样病变。
4.1.3 门静脉高压性息肉样变肠病
该病是PHE的罕见表现，发生率仅为0.3%[31]。病理活检提示黏膜固有层大量血管扩张，部分毛细血管内有纤维素性血栓，这些改变与炎性息肉截然不同，与PH直接相关。Huang等[32]报道了1例肝硬化PH患者，肠镜下表现为结肠息肉，但病理活检提示黏膜及黏膜下层血管广泛扩张，淋巴细胞浸润较少。临床上以反复消化道出血为突出表现，对肠镜下可见息肉样改变的患者，可根据其病理活检的典型表现最终诊断为结肠门静脉高压性息肉样肠病。
4.2 影像学及核医学检查
PHE患者的影像学表现无特异性，腹部增强CT主要表现为肠壁黏膜层、浆膜层过灌注及肠壁水肿，呈“三带征”，结合患者肝硬化合并PH的影像学特征性改变，可以考虑诊断为PHE。有研究显示，多层螺旋CT灌注成像中肠系膜上静脉内径>1.2 cm可判断患者患有PH，进而测量并分析胃肠壁血流量、对比剂平均通过时间(mean transit time，MTT)、血管渗透性参数(permeability，PMB)等的变化，能够对门脉高压性胃肠病作出明确诊断[33]。在PH早期患者胃肠壁血流量增加，PH晚期时微血管管壁增厚，管腔狭窄，胃肠壁血流量降低[<100 ml/(100 g.min)]；PH患者的PMB较对照组降低[<25 ml/(100 g.min)]，MTT延长(>13 s)[33]。测量肠系膜上静脉内径、胃肠壁血流量、PMB、MTT等指标能够为PH患者(尤其是胃镜无法观察到空回肠的情况下及胃镜检查出血风险较大的患者)发生门静脉性胃肠病提供重要的诊断信息。
有研究表明，99mTc标记红细胞闪烁显像可显示十二指肠、空肠或回盲瓣区域等隐匿部位的活动性出血，但难以确定确切位置。因此，可进一步行99mTc标记红细胞单光子发射CT(single photon emission CT，SPECT)/CT检查，根据SPECT值着色的三维容积渲染CT图像，获得出血部位更精确的解剖学信息[34-35]。对有隐匿性消化道出血的PHE患者，利用99mTc标记红细胞闪烁显像以及SPECT/CT检查能够定位其活动性出血部位，指导后续动脉栓塞或内镜下止血等治疗方法的选择。随着人工智能在医学领域的广泛应用，影像组学及核医学技术或许对PHE的诊断有重要价值。
5 治疗方法
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5.1 基础治疗
PHE的成因主要是肝硬化性PH，基础治疗包括有效清除肝炎病毒，合理使用抗炎、抗肝纤维化药物(如甘草酸制剂、多烯磷脂酰胆碱、水飞蓟素类、腺苷甲硫氨酸、还原型谷胱甘肽等)，从而减轻肝组织损伤，促进肝细胞修复及再生，延缓肝纤维化、肝硬化的进展及PH的形成。益生菌、谷氨酰胺等药物有助于维持肠黏膜屏障功能并促进其修复，而纠正低蛋白血症、营养支持治疗等对预防PHE患者出现感染、腹水、肝性脑病等肝硬化相关并发症具有重要作用。
5.2 降低门静脉压力的治疗方案
5.2.1 药物治疗
(1)非选择性β受体阻滞剂(non-selective beta-blockers，NSBB)：可减少心排血量，收缩内脏血管，从而减少门静脉血流量。(2)血管加压素及其衍生物：可直接收缩内脏血管，降低肝窦内压，从而降低门静脉压力。(3)生长抑素及长效生长抑素类似物：可选择性收缩内脏血管，降低门静脉压力，从而减少曲张静脉血流。(4)肾素-血管紧张素-醛固酮系统(renin angiotensin aldosterone system，RAAS)抑制剂：可抑制RAAS系统激活，减轻水钠潴留，减低肝硬化患者的肝内血流阻力，降低门静脉压力，进而减轻PHE。(5)他汀类药物：长时间使用辛伐他汀可显著降低HVPG[36]；但Uschner等[37]研究发现，在非肝硬化PH大鼠模型中，他汀类药物可刺激肝外血管生成，从而导致PH加重，因此他汀类药物降低PH的疗效仍需进一步研究。
5.2.2 介入治疗
一项关于PHC患者持续出血的研究表明，接受颈静脉肝内门体分流术(transjugular intrahepatic portosystemic shunt，TIPS)的PHC患者术前结肠镜检查提示肠黏膜毛细血管广泛扩张、迂曲，给予TIPS治疗后出血得到控制，HVPG明显降低，术后第9天复查结肠镜提示肠黏膜扩张血管数量减少且血管扩张程度降低，术后第4周及第12周结肠镜检查提示结肠血管病变消失，随访18个月患者消化道出血未复发[38]。TIPS可明显降低门静脉压力，对严重PHE导致消化道出血、使用NSBB治疗效果不佳及外周血红蛋白<60 g/L的患者，建议采用TIPS治疗[39]。此外，有学者认为脾动脉栓塞能减少脾静脉血流量，改善门静脉血流动力学，可用于PHE患者的止血治疗及预防出血，尤其适用于巨脾伴脾功能亢进的患者[40]，但其长期疗效及安全性仍需更充分的证据证实。
5.3 内镜下治疗
1982年，Sauerbruch等[41]首次报道了内镜下硬化剂注射(endoscopic sclerosing agent injection，EIS)治疗门静脉十二指肠静脉曲张出血的成功病例，随访15个月后患者未再发生出血。多项研究表明，超声内镜(endoscopic ultrasonography，EUS)引导弹簧线圈注射联合或不联合组织胶注射治疗异位静脉曲张出血均具有较好的效果[42-43]。目前PHE的内镜下治疗方法包括硬化剂注射及组织胶注射等，但先前研究报道均基于小样本病例，尚未形成统一规范，需根据PHE出血的严重程度及血管病变的位置、数量、程度选择个体化的治疗方式。
5.4 手术治疗
研究表明，行近端脾肾分流术联合脾切除术后，PH所致的右半结肠黏膜下毛细血管扩张明显缓解，下消化道出血风险降低[44]。对于药物、内镜以及介入治疗均难以治愈的肠道出血，可考虑手术治疗，包括脾肾分流术、脾切除术、部分肠切除术等。有研究报道，携带丙型肝炎病毒的肝硬化患者在肝移植前的结肠镜检查显示直肠及左半结肠出现樱桃斑样改变，这些结肠血管性病变在肝移植术后2周消失，因此肝移植可作为晚期肝硬化合并PHE的治疗选择[45]。
6 总结与展望
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PHE发病率较高，且易被临床医师忽视。当PH患者出现腹胀、纳差、腹痛、腹泻，尤其是不能用食管胃静脉曲张破裂出血解释的贫血、黑便、血便时，更应警惕PHE。由于小肠镜、胶囊内镜及结肠镜在肝硬化PH患者中的临床应用并不多，较难获得直观明确的诊断，临床上可从常见的CT影像学征象(如小肠、结肠肠壁增厚，黏膜及肠壁过灌注等)中获得提示，适时安排相应内镜检查以确诊。PHE治疗的重点在于预防消化道出血、再出血，以及发生出血后的及时止血。在综合治疗的基础上，可个体化应用内镜治疗、TIPS、肝移植乃至肠切除等方案，以获得更好的治疗效果。PHE的发病机制、相关危险因素，以及建立基于临床表现、组织病理表现、内镜检查、影像学及核医学检查的诊断标准，拟定规范的治疗方案等问题，都值得进一步研究。
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  • 国家自然科学基金(81972305)
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2022年第47卷第6期
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doi: 10.11855/j.issn.0577-7402.2022.06.0625
  • 接收时间：2021-06-28
  • 首发时间：2025-12-17
  • 出版时间：2022-06-28
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  • 收稿日期：2021-06-28
  • 录用日期：2021-11-11
基金
National Natural Science Foundation of China(81972305)
国家自然科学基金(81972305)
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    陆军特色医学中心大坪医院消化内科，重庆 400042

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张慧茹，E-mail：
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2种不同金属材料的力学参数
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genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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