Inflammatory bowel disease and thromboembolism

Patients with inflammatory bowel disease (IBD) have an increased risk of vascular complications. Thromboembolic complications, both venous and arterial, are serious extraintestinal manifestations complicating the course of IBD and can lead to significant morbidity and mortality. Patients with IBD are more prone to thromboembolic complications and IBD per se is a risk factor for thromboembolic disease. Data suggest that thrombosis is a specific feature of IBD that can be involved in both the occurrence of thromboembolic events and the pathogenesis of the disease. The exact etiology for this special association between IBD and thromboembolism is as yet unknown, but it is thought that multiple acquired and inherited factors are interacting and producing the increased tendency for thrombosis in the local intestinal microvasculature, as well as in the systemic circulation. Clinicians’ awareness of the risks, and their ability to promptly diagnose and manage tromboembolic complications are of vital importance. In this review we discuss how thromboembolic disease is related to IBD, specifically focusing on: (1) the epidemiology and clinical features of thromboembolic complications in IBD; (2) the pathophysiology of thrombosis in IBD; and (3) strategies for the prevention and management of thromboembolic complications in IBD patients.

Intestinal microbiota, probiotics and prebiotics in inflammatory bowel disease

It has been presumed that aberrant immune response to intestinal microorganisms in genetically predisposed individuals may play a major role in the pathogenesis of the inflammatory bowel disease, and there is a good deal of evidence supporting this hypothesis. Commensal enteric bacteria probably play a central role in pathogenesis, providing continuous antigenic stimulation that causes chronic intestinal injury. A strong biologic rationale supports the use of probiotics and prebiotics for inflammatory bowel disease therapy. Many probiotic strains exhibit anti-inflammatory properties through their effects on different immune cells, pro-inflammatory cytokine secretion depression, and the induction of anti-inflammatory cytokines. There is very strong evidence supporting the use of multispecies probiotic VSL#3 for the prevention or recurrence of postoperative pouchitis in patients. For treatment of active ulcerative colitis, as well as for maintenance therapy, the clinical evidence of efficacy is strongest for VSL#3 and Escherichia coli Nissle 1917. Moreover, some prebiotics, such as germinated barley foodstuff, Psyllium or oligofructose-enriched inulin, might provide some benefit in patients with active ulcerative colitis or ulcerative colitis in remission. The results of clinical trials in the treatment of active Crohn’s disease or the maintenance of its remission with probiotics and prebiotics are disappointing and do not support their use in this disease. The only exception is weak evidence of advantageous use of Saccharomyces boulardii concomitantly with medical therapy in maintenance treatment.

Significant risk and associated factors of active tuberculosis infection in Korean patients with inflammatory bowel disease using anti-TNF agents

AIM:To evaluate the incidence and risk factors of Korean tuberculosis(TB) infection in patients with inflammatory bowel disease(IBD) undergoing anti-TNF treatment.METHODS:The data of IBD patients treated with anti-TNFs in 13 tertiary referral hospitals located in the southeastern region of Korea were collected retrospectively.They failed to show response or were intolerant to conventional treatments,including steroids or immunomodulators.Screening measures for latent TB infection(LTBI)and the incidence and risk factors ofactive TB infection after treatment with anti-TNFs were identified.RESULTS:Overall,376 IBD patients treated with antiTNF agents were recruited(male 255,mean age of anti-TNF therapy 32.5±13.0 years);277 had Crohn’s disease,99 had ulcerative colitis,294 used infliximab,and 82 used adalimumab.Before anti-TNF treatment,screening tests for LTBI including an interferon gamma release assay or a tuberculin skin test were performed in 82.2%of patients.Thirty patients(8%)had LTBI.Sixteen cases of active TB infection including one TB-related mortality occurred during 801 personyears(PY)follow-up(1997.4 cases per 100000 PY)after anti-TNF treatment.LTBI(OR=5.76,95%CI:1.57-21.20,P=0.008)and WBC count<5000 mm3(OR=4.5,95%CI:1.51-13.44,P=0.007)during follow-up were identified as independently associated risk factors.CONCLUSION:Anti-TNFs significantly increase the risk of TB infection in Korean patients with IBD.The considerable burden of TB and marked immunosuppression might be attributed to this risk.

Thiopurine metabolites variations during co-treatment with aminosalicylates for inflammatory bowel disease:Effect of N-acetyl transferase polymorphisms

AIM: To evaluate variation of the concentration of thiopurine metabolites after 5-aminosalicylate(5-ASA) interruption and the role of genetic polymorphisms of N-acetyl transferase(NAT) 1 and 2. METHODS: Concentrations of thioguanine nucleotides(TGN) and methymercaptopurine nucleotides(MMPN), metabolites of thiopurines, were measured by high performance liquid chromatography in 12 young patients(3 females and 9 males, median age 16 years) with inflammatory bowel disease(6 Crohn's disease and 6 ulcerative colitis) treated with thiopurines(7 mercaptopurine and 5 azathioprine) and 5-ASA. Blood samples were collected one month before and one month after the interruption of 5-ASA. DNA was extracted and genotyping of NAT1, NAT2, inosine triphosphate pyrophosphatase(ITPA) and thiopurine methyl transferase(TPMT) genes was performed using PCR assays. RESULTS: Median TGN concentration before 5-ASA interruption was 270 pmol/8 x 108 erythrocytes(range: 145-750); after the interruption of the aminosalicylate, a 35% reduction in TGN mean concentrations(absolutemean reduction 109 pmol/8 × 108 erythrocytes) was observed(median 221 pmol/8 × 108 erythrocytes, range: 96-427, P value linear mixed effects model 0.0011). Demographic and clinical covariates were not related to thiopurine metabolites concentrations. All patients were wild-type for the most relevant ITPA and TPMT variants. For NAT1 genotyping, 7 subjects presented an allele combination corresponding to fast enzymatic activity and 5 to slow activity. NAT1 genotypes corresponding to fast enzymatic activity were associated with reduced TGN concentration(P value linear mixed effects model 0.033), putatively because of increased 5-ASA inactivation and consequent reduced inhibition of thiopurine metabolism. The effect of NAT1 status on TGN seems to be persistent even after one month since the interruption of the aminosalicylate. No effect of NAT1 genotypes was shown on MMPN concentrations. NAT2 genotyping revealed that 6 patients presented a genotype corresponding to fast enzymatic activity and 6 to slow activity; NAT2 genotypes were not related to thiopurine metabolites concentration in this study. CONCLUSION: NAT1 genotype affects TGN levels in patients treated with thiopurines and aminosalicylates and could therefore influence the toxicity and efficacy of these drugs; however the number of patients evaluated is limited and this has to be considered a pilot study.

Role of the gut microbiota in inflammatory bowel disease pathogenesis: What have we learnt in the past 10 years?

Our understanding of the microbial involvement in inflammatory bowel disease (IBD) pathogenesis has increased exponentially over the past decade. The development of newer molecular tools for the global assessment of the gut microbiome and the identification of nucleotide-binding oligomerization domain-containing protein 2 in 2001 and other susceptibility genes for Crohn&#x02019;s disease in particular has led to better understanding of the aetiopathogenesis of IBD. The microbial studies have elaborated the normal composition of the gut microbiome and its perturbations in the setting of IBD. This altered microbiome or &#x0201c;dysbiosis&#x0201d; is a key player in the protracted course of inflammation in IBD. Numerous genome-wide association studies have identified further genes involved in gastrointestinal innate immunity (including polymorphisms in genes involved in autophagy: ATG16L1 and IGRM), which have helped elucidate the relationship of the local innate immunity with the adjacent luminal bacteria. These developments have also spurred the search for specific pathogens which may have a role in the metamorphosis of the gut microbiome from a symbiotic entity to a putative pathogenic one. Here we review advances in our understanding of microbial involvement in IBD pathogenesis over the past 10 years and offer insight into how this will shape our therapeutic management of the disease in the coming years.

Epidemiological studies of migration and environmental risk factors in the inflammatory bowel diseases

Inflammatory bowel diseases(IBD)are idiopathic chronic diseases of the gastrointestinal tract well known to be associated with both genetic and environmental risk factors.Permissive genotypes may manifest into clinical phenotypes under certain environmental influences and these may be best studied from migratory studies.Exploring differences between first and second generation migrants may further highlight the contribution of environmental factors towards the development of IBD.There are few opportunities that have been offered so far.We aim to review the available migration studies on IBD,evaluate the known environmental factors associated with IBD,and explore modern migration patterns to identify new opportunities and candidate migrant groups in IBD migration research.

Oral manifestation in inflammatory bowel disease:A review

Inflammatory bowel diseases (IBDs), including Crohn&#x02019;s disease (CD) and ulcerative colitis, not only affect the intestinal tract but also have an extraintestinal involvement within the oral cavity. These oral manifestations may assist in the diagnosis and the monitoring of disease activity, whilst ignoring them may lead to an inaccurate diagnosis and useless and expensive workups. Indurated tag-like lesions, cobblestoning, and mucogingivitis are the most common specific oral findings encountered in CD cases. Aphthous stomatitis and pyostomatitis vegetans are among non-specific oral manifestations of IBD. In differential diagnosis, side effects of drugs, infections, nutritional deficiencies, and other inflammatory conditions should also be considered. Treatment usually involves managing the underlying intestinal disease. In severe cases with local symptoms, topical and/or systemic steroids and immunosuppressive drugs might be used.

Temporal trends in inflammatory bowel disease publications over a 19-years period

AIM: To determine whether temporal changes occurred in the pediatric vs adult inflammatory bowel disease(IBD), both in terms of number and type of yearly published articles.METHODS:We aimed to evaluate all Pub Med-registered articles related to the field of IBD from January1,1993 and until December 31,2011.We searched for articles using the key words"inflammatory bowel disease"or"Crohn’s disease"or"ulcerative colitis"or"undetermined colitis",using the age filters of"child"or"adult".We repeated the search according to the total number per year of articles per type of article,for each year of the specified period.We studied randomized controlled trials,clinical trials,case reports,meta-analyses,letters to the editor,reviews,systematic reviews,practice guidelines,and editorials.RESULTS:We identified 44645 articles over the 19year-period.There were 8687 pediatric-tagged articles vs 19750 adult-tagged articles.Thus 16208 articles were unaccounted and not assigned a"pediatric"or"adult"tag by Pub Med.There was an approximately3-fold significant increase in all articles recorded both in pediatric and adult articles.This significant increase was true for nearly every category of article but the number of clinical trials,meta-analysis,and randomized controlled trials increased proportionally more than the number of"lower quality"articles such as editorials or letters to the editor.Very few guidelines were published every year.CONCLUSION:There is a yearly linear increase in publications related to IBD.Relatively,there are more and more clinical trials and higher quality articles.

Prevention of post-operative recurrence of Crohn's disease

Endoscopic and clinical recurrence of Crohn&#x02019;s disease (CD) is a common occurrence after surgical resection. Smokers, those with perforating disease, and those with myenteric plexitis are all at higher risk of recurrence. A number of medical therapies have been shown to reduce this risk in clinical trials. Metronidazole, thiopurines and anti-tumour necrosis factors (TNFs) are all effective in reducing the risk of endoscopic or clinical recurrence of CD. Since these are preventative agents, the benefits of prophylaxis need to be weighed-against the risk of adverse events from, and costs of, therapy. Patients who are high risk for post-operative recurrence should be considered for early medical prophylaxis with an anti-TNF. Patients who have few to no risk factors are likely best served by a three-month course of antibiotics followed by tailored therapy based on endoscopy at one year. Clinical recurrence rates are variable, and methods to stratify patients into high and low risk populations combined with prophylaxis tailored to endoscopic recurrence would be an effective strategy in treating these patients.

Neuroanatomy of lower gastrointestinal pain disorders

Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal,immune and endocrine signaling pathways within the intestines,the peripheral and the central nervous system.In this article we review how the sensory nerve information from the healthy and the hypersensitive bowel is encoded and conveyed to the brain.The gut milieu is continuously monitored by intrinsic enteric afferents,and an extrinsic nervous network comprising vagal,pelvic and splanchnic afferents.The extrinsic afferents convey gut stimuli to second order neurons within the superficial spinal cord layers.These neurons cross the white commissure and ascend in the anterolateral quadrant and in the ipsilateral dorsal column of the dorsal horn to higher brain centers,mostly subserving regulatory functions.Within the supraspinal regions and the brainstem,pathways descend to modulate the sensory input.Because of this multiple level control,only a small proportion of gut signals actually reaches the level of consciousness to induce sensation or pain.In inflammatory bowel disease(IBD)and irritable bowel syndrome(IBS)patients,however,long-term neuroplastic changes have occurred in the brain-gut axis which results in chronic abdominal pain.This sensitization may be driven on the one hand by peripheral mechanisms within the intestinal wall which encompasses an interplay between immunocytes,enterochromaffin cells,resident macrophages,neurons and smooth muscles.On the other hand,neuronal synaptic changes along with increased neurotransmitter release in the spinal cord and brain leads to a state of central wind-up.Also life factors such as but not limited to inflammation and stress contribute to hypersensitivity.All together,the degree to which each of these mechanisms contribute to hypersensitivity in IBD and IBS might be diseaseand even patient-dependent.Mapping of sensitization throughout animal and human studies may significantly improve our understanding of sensitization in IBD and IBS.On the long run,this knowledge can be put forward in potential therapeutic targets for abdominal pain in these conditions.

误诊为炎症性肠病、阑尾炎的肠白塞病临床分析

目的探讨肠白塞病的临床特点、诊断及鉴别诊断要点,总结分析误诊原因和防范措施。方法对2014年1月至2024年5月收治的病初曾误诊为炎症性肠病和阑尾炎的肠白塞病7例的临床资料进行回顾性分析。结果7例以腹痛、腹泻、消化道出血、发热和腹部压痛、反跳痛为主要临床表现。4例白细胞、中性粒细胞升高;6例红细胞沉降率增快;5例C反应蛋白升高;全部患者抗中性粒细胞胞浆抗体、抗核抗体、抗双链DNA抗体及抗ENA抗体阴性;IgG升高4例,补体C3、C4降低5例,核周型抗中性粒细胞胞浆抗体阳性2例,抗心磷脂抗体阳性1例、类风湿因子阳性1例、便潜血试验阳性4例。胃镜示反流性食管炎1例。结肠镜检查示结直肠多发溃疡形成,伴有不同程度黏膜充血、糜烂、肠腔狭窄变形、结肠多发性息肉等。7例肠黏膜活检病理示回盲部/结肠黏膜急性和(或)慢性炎。于基层医院误诊为炎症性肠病4例,阑尾炎3例。入住我院后根据临床表现、实验室检查、胃肠镜检查及相关诊疗指南确诊为肠白塞病,误诊时间23 d~12年。确诊后7例给予糖皮质激素和(或)联合免疫抑制剂治疗,合并胃溃疡、反流性食管炎患者同时予抑酸剂及黏膜保护剂治疗,并发肠道穿孔或大出血者予手术治疗,7例均病情控制好转出院。结论肠白塞病易误诊,临床医师应提高对该病的警惕性,遇及疑似患者应及时行肠镜和病理检查,并根据临床表现及其他医技检查结果综合分析,以及早明确诊断并治疗。

Cancer risk in IBD: How to diagnose and how to manage DALM and ALM

The risk of developing neoplasia leading to colorectal cancer is significantly increased in ulcerative colitis (UC) and most likely in Crohn's disease. Several endoscopic surveillance strategies have been implemented to identify these lesions. The main issue is that colitisassociated neoplasms often occurs in flat mucosa, often being detected on taking random biopsies rather than by identification of these lesions via endoscopic imaging. The standard diagnostic procedure in long lasting UC is to take four biopsies every 10 cm. Image enhancement methods, such as chromoendoscopy and virtual histology using endomicroscopy, have greatly im- proved neoplasia detection rates and may contribute toreduced random biopsies by taking targeted "smart" biopsies. Chromoendoscopy may effectively be performed by experienced endoscopists for routine screening of UC patients. By contrast, endomicroscopy is often only available in selected specialized endoscopic centers. Importantly, advanced endoscopic imaging has the poten- tial to increase the detection rate of neoplasia whereas the interplay between endoscopic experience and interpretation of histological biopsy evaluation allows the physician to make a proper diagnosis and to find the appropriate therapeutic approach. Colitis-associated intraepithelial neoplasms may occur in flat mucosa of endoscopically normal appearance or may arise as dysplasia-associated lesion or mass (DALM), which may be indistinguishable from sporadic adenomas in healthy or non-colitis mucosa [adenoma-like mass (ALM)]. The aim of this review was to summarize endoscopic and histological characteristics of DALM and ALM in the context of therapeutic procedures.

逍遥舒坤颗粒对大鼠盆腔炎性疾病后遗症的治疗作用及其机制

目的 探讨逍遥舒坤颗粒灌胃治疗对大鼠盆腔炎性疾病后遗症(SPID)的治疗作用及其机制。方法 将39只Wistar雌性大鼠随机分为对照组、模型组、药物干预组,每组各13只。对照组常规饲养,模型组和药物干预组以疲劳、饥饿辅助大肠杆菌上行感染法建立SPID模型。药物干预组于造模成功后给予逍遥舒坤颗粒浓缩药液灌胃,对照组和模型组给予等量生理盐水灌胃,连续14 d。治疗结束后,取各组大鼠子宫、输卵管组织,先观察外观形态,然后采用HE染色法观察组织形态和结构;Western blotting法检测子宫组织纤维化相关蛋白Ⅰ型胶原蛋白α1链(COL1A1)、基质金属蛋白酶9(MMP-9)蛋白表达情况。结果 与对照组比较,模型组和药物干预组均有不同程度的输卵管增粗、阻塞、积水,输卵管卵巢粘连、包块、囊肿,盆腔结缔组织增生、粘连。与模型组比较,药物干预组子宫和输卵管外观形态、病理形态均有所改善。与对照组比较,模型组子宫组织COL1A1表达升高、MMP-9表达下降;与模型组比较,药物干预组子宫组织COL1A1表达下降、MMP-9表达升高(P均<0.05)。结论 逍遥舒坤颗粒能够抑制SPID大鼠子宫成纤维细胞增殖,减轻纤维化程度,防止和减轻粘连形成,从而治疗SPID;其机制可能与上调子宫组织中MMP-9表达、抑制COL1A1合成有关。

半乳糖凝集素-9与炎症性肠病关系的研究进展

半乳糖凝集素-9(galectin-9,Gal-9)是能特异性识别、结合半乳糖苷的半乳糖凝集素家族成员之一.该蛋白广泛表达于机体组织,参与细胞生长、分化、黏附、聚集、凋亡等,与炎症性疾病、自身免疫性疾病、肿瘤、细菌病毒感染等多类疾病密切相关.近年研究发现,G a l-9与炎症性肠病的发生、发展关系密切,本文就Gal-9与炎症性肠病的关系进行综述.

miRNA在炎症性肠病发病过程中的作用

微小RNA(microRNA,miR)是一类非编码的内源性小分子RNA,能在转录后水平负性调节靶mRNA表达.炎症性肠病(inflammatory bowel disease,IBD)的发病机制与免疫异常、炎症损伤、遗传等因素密切相关.miRNA在肠道的差异性表达是调控肠黏膜屏障功能的重要环节,影响肠道上皮细胞的增殖、分化以及肠道黏膜的免疫功能,与IBD的发生发展密切相关.目前已发现多种miRNA在IBD患者在血清和肠黏膜组织异常表达,活动性溃疡性结肠炎较正常肠黏膜表达明显下调如miR-192、miR-375、miR-422b,而miR-16、miR-21、let-7等表达明显上调;活动性克罗恩病较正常肠黏膜表达明显下调如miR-19b、miR-629,miR-23b、miR-106和miR-191的表达明显上调.这为IBD的早期诊断、预防和治疗提供了分子靶标.

胶囊内镜下小肠黏膜特征分析53例

目的:回顾性分析胶囊内镜检查患者53例,认识胶囊内镜下小肠正常黏膜特征及小肠病变黏膜特征.方法:2010-08/2011-08,利用Miro Cam胶囊内镜系统对患者53例行胶囊内镜检查.统计患者的年龄、性别、症状、体征等临床资料,将受检者分为不明原因的消化系出血,疑为功能性胃肠病,腹痛、腹泻、腹胀,便秘,体检等共5组;通过查阅病案及电话回访,搜集资料,将胶囊内镜下所见作出最终的临床诊断;分析胶囊内镜下小肠正常及病变黏膜特征.结果:在53例患者中,1例因吞服胶囊后无图像信号,未能顺利完成胶囊内镜检查;1例因患者吞咽胶囊困难而无法进行;其余51例均顺利到达结肠,到达结肠率为96.22%.胃的平均运行时间为69.78 min,小肠的平均运行时间为513.25 min.48例有消化系疾病的阳性结果,3例未见异常,阳性率为90.57%.在所有疑诊小肠疾病的51例患者中,胶囊内镜小肠病变总的诊断率为92.15%(47/51);空肠及回肠阳性诊断率为52.94%,包括炎症12例(1例临床确诊为Crohn's病),息肉3例,不明肿块3例,淋巴滤泡增生1例,疑似小肠淋巴管扩张7例,钩虫病1例;同时检出反流性食管炎1例;慢性胃炎26例,糜烂性胃炎7例,胃部息肉3例;结肠炎症3例,结肠息肉5例,大肠黑变病2例.胶囊均自然排出体外,无梗阻等并发症的发生.结论:Miro Cam胶囊内镜是一种非侵入性的检查手段,检查安全,顺应性好;在胶囊内镜下,正常小肠黏膜及病变黏膜均呈现出一定的特征.

防御素与炎症性肠病

目前普遍认为炎症性肠病是在遗传背景的前提下,环境因素(如感染等)导致肠道免疫紊乱而发病.近年来,防御素(defensin)家族在先天性防御体系中的作用日益受到研究学者的重视.本文就防御素的种类、分布、基因表达调控、其抗微生物作用,以及其与炎症性肠病的关系和应用前景作一综述.

巨噬细胞移动抑制因子_173G/C基因多态性与炎性肠疾病的Meta分析

目的:探讨巨噬细胞移动抑制因子(macrophage migration inhibitoryfactor,MIF)_173G/C基因多态性与炎性肠疾病(inflammatory bowel disease,IBD)易感性的关系.方法:计算机检索CBM、CNKI、PubMed和EMbase数据库,收集关于MIF_173G/C基因多态性与溃疡性结肠炎(ulcerative colitis,UC)或克罗恩病(Crohn's disease,CD)的易感性病例-对照研究研究,以IBD组与对照组人群基因型分布的比值比(odds ratio,OR)及95%CI可信区间(confidence interval,95%CI)其为效应指标,采用固定或随机效应模型进行合并分析,并进行偏倚评估.应用STATA10.0软件进行统计学处.结果:纯合子比较模型,显性遗传模型,隐性遗传模型Meta分析表明MIF_173G/C基因多态性与UC易感性有统计学意义(C/CvsG/G:OR=1.54,95%CI:1.08-2.19;显性遗传模型:OR=1.15,95%CI:1.00-1.32;隐性遗传模型:OR=1.52,95%CI:1.07-2.17);各遗传模型Meta分析结果显示:MIF_173G/C基因多态性与CD的易感性无统计学意义.结论:基于目前研究结果显示,MIF_173G/C可能是UC的易感性基因,但与CD无明显相关性.受纳入研究质量和数量限制,上述结论尚待开展更多高质量的前瞻性研究进一步验证.

无创正压通气对慢性阻塞性肺疾病患者气道炎症因子的影响

目的探讨无创正压通气对慢性阻塞性肺疾病患者气道炎症因子的影响。方法选取慢性阻塞性肺疾病患者60例,采用随机数字法分为对照组和观察组各30例。对照组采用常规对症支持治疗,观察组在对照组基础上联合无创正压通气治疗。比较2组临床疗效,IL-8、TNF-α水平,中性粒细胞占白细胞百分比等指标。结果观察组治疗后pH、p(O_2)水平显著高于对照组(P<0.05),p(CO_2)水平显著低于对照组(P<0.05)。2组治疗前、后中性粒细胞占白细胞百分比无显著差异(P>0.05)。观察组治疗后IL-8、TNF-α显著低于对照组(P<0.05)。观察组治疗后并发症发生率为3.33%,显著低于对照组的10.00%(P<0.05)。结论慢性阻塞性肺疾病患者在常规治疗基础上联合无创正压通气治疗效果理想。

急性多灶性缺血性脉络膜病变临床分析

目的探讨急性多灶性缺血性脉络膜病变（AMIC）发病机制、诊断及其治疗。方法将8例AMIC患者的15只眼眼底彩照、吲哚氰绿血管造影（ICGA）和荧光素钠眼底血管造影（FFA）检查结果进行对比分析，并予抗炎、抗病毒或抗结核及改善微循环等药物治疗，抗炎选用非甾体类药物，未用糖皮质激素。结果ICGA：1只眼急性期病变呈斑片状充盈缺损；3只眼陈旧病灶色素遮蔽荧光。FFA：8例15眼中1眼急性病变病灶早期为弱荧光，之后着染荧光；3眼陈旧病灶为色素上皮脱色素的窗样缺损及色素沉着的遮蔽荧光。恢复期11眼兼有急性和陈旧性病变特征。急性期病例经3个月、恢复期病例经3～6周治疗后，视力、FFA及ICGA恢复。结论AMIC属脉络膜缺血性疾病，应查找病因积极治疗，大多预后良好。