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CHANGES OF STOMACH MICROFLORA AFTER TOTAL COLECTOMY. 全结肠切除术后胃菌群的变化。
R M Shermatov

The purpose of the study: to study the nature of the changes of the microbiota of the stomach after total colectomy.

Materials and methods: The research was conducted on 50 outbred white male rats by means of microbiological and electron microscopic methods with statistical data processing.

Conclusion: In adaptive-adaptive changes of the microbiota of the stomach after total colectomy clearly stages, where it is possible to allocate two periods - the period of early post-operative changes (7-30 days) and the adaptation period 160-go days). Changes of the microbiota was characterized by a significant decrease in anaerobic non-sporulating Bacillus, lactic acid bacteria and staphylococci and the increase of yeast and yeast-like fungi of the genus Candida, pathogens, enterococci, Escherichia coil, and Bacillus Proteus.

研究目的:研究全结肠切除术后胃微生物群变化的性质。材料与方法:采用微生物学、电镜等方法对50只远交系白种雄性大鼠进行研究,并对数据进行统计学处理。结论:在全结肠切除术后胃微生物群的适应-适应变化中分期明确,其中可分为术后早期变化期(7-30天)和适应期(160- 10天)两个阶段。微生物群的变化表现为无孢子厌氧芽孢杆菌、乳酸菌和葡萄球菌的显著减少,念珠菌属酵母和酵母样真菌、病原菌、肠球菌、螺旋杆菌和变形杆菌的增加。
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引用次数: 0
40 YEARS OF MICROBIOLOGY LABORATORY AT STATE RESEARCH INSTITUTE OF HIGHLY PURE BIOPREPARATIONS. 在国家高纯度生物修复研究所微生物实验室工作了40年。
T Ya Vakhitov
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引用次数: 0
THE INCIDENCE OF PRIMARY AND SECONDARY RESISTANCE TO THE ANTI-CYTOKINE THERAPY IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE. 炎症性肠病患者抗细胞因子治疗的原发性和继发性耐药发生率
L B Lazebnik, V E Sagynbaeva

Long-term experience of using irifliximab in patients with inflammatory bowel disease (IBD) have shown that 20-30% of patients couldn't achieve clinical improvement (primary failure) or have developed acquired drug resistance (secondary failure). The frequency of antibody formation to infliximab is to 28-61%, for adalimumab 4-12%, to certolizumab the guests to 12.3%, for etanercept to 2.5%. The ways to overcome the primary and secondary inefficiency of anti-cytokine the(apy (loss of response to therapy) at the present time are: increasing the dose, shortening the interval between infusions of genetically engineered biological drugs, additional immunosuppressive agents, as well as switching to another biologic drug. Search of primary and secondary inefficiency of anti-cytokine therapy in patients with IBD currently remains topical and requires new approaches to the solution of this problem.

长期使用伊利利昔单抗治疗炎症性肠病(IBD)患者的经验表明,20-30%的患者不能达到临床改善(原发性失败)或出现获得性耐药(继发性失败)。英夫利昔单抗产生抗体的频率为28-61%,阿达木单抗产生抗体的频率为4-12%,塞妥珠单抗产生抗体的频率为12.3%,依那西普产生抗体的频率为2.5%。目前克服抗细胞因子治疗原发性和继发性无效的方法是:增加剂量,缩短基因工程生物药物的输注间隔,增加免疫抑制剂,以及切换到另一种生物药物。寻找IBD患者抗细胞因子治疗的原发性和继发性无效目前仍然是热门话题,需要新的方法来解决这一问题。
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引用次数: 0
MEDICAL AND SOCIAL REASONS FOR LATE DIAGNOSIS OF ULCERATIVE COLITIS. 溃疡性结肠炎晚期诊断的医学和社会原因。
M A Fedosova, E I Kashkina, V N Shemyatenkov

Purpose of the study: medico-social factors, influencing upon the date of visiting the doctor for the patients with ulcerative colitis manifestation have been analyzed.

Materials and methods: under observation there were 38 patients with ulcerative colitis. The diagnosis was made on the availability of the typical symptoms and was confirmed by the endoscopy of the colon and histological biopsy of the mucosa samples.

Conclusion: light and moderately severe colitis is still remaining not identified for a long time due to the lack of population's awareness about that disease as well as insufficient attention of the doctors to such problems. The belated visit to a doctor is more common for mail patients up to 30.,years old with high education.

研究目的:分析医学社会因素对溃疡性结肠炎患者就诊日期的影响。材料与方法:对38例溃疡性结肠炎患者进行观察。诊断是根据典型症状的可用性,并通过结肠内窥镜检查和粘膜标本的组织学活检证实。结论:轻、中重度结肠炎长期未被发现,主要是由于人群对该疾病的认识不足,以及医生对该问题的重视程度不够。对于30岁以下的邮差患者来说,延迟就医更为常见。岁,受过高等教育。
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引用次数: 0
LOCAL RENIN-ANGIOTENSIN SYSTEM OF SMALL INTESTINE. 小肠局部肾素-血管紧张素系统。
T S Zamolodchikova, B B Shoibonov, S M Tolpygo

The renin-angiotensin system (RAS) is the universal multiple-factor regulator of many vital processes at the organismal, tissue and cellular levels. Classical (circulating) RAS provides maintenance of arterial pressure, a water and salt balance, lipid and glucose homeostasis. Local tissue RAS are functioning independently and participating in metabolic processes and protective reactions. Local RAS of a small intestine mucosa is presented practically by a complete rangeof the components (renin, angiotensinogen, angiotensin-converting enzymes, angiotensin receptors) localized, mainly, in an intestinal epithehum, lamina propria and muscularis mucosa. Local RAS participates in regulation of the most levels of activity ofa small intestine, influencing on an intestinal motility, secretory-transport processes, adaptation and protective reactions. The experimental data presented in this review are very promising for the detection of possible complications when using drugs that alter the activity of the RAS-related unexplored effects of the interaction of these drugs with their potential targets, localized not only in the blood vessels, but also directly to the niucosa of the gastrointestinal tract. This is especially important in connection with the extensive use of drugs that modulate the activity of the RAS in the practice of the treatment of cardiovascular diseases such as hypertension, atherosclerosis, endothelial dysfunction, and others.

肾素-血管紧张素系统(RAS)是机体、组织和细胞水平上许多重要过程的通用多因子调节器。经典(循环)RAS提供维持动脉压力,水和盐平衡,脂质和葡萄糖稳态。局部组织RAS独立发挥作用,参与代谢过程和保护反应。小肠粘膜的局部RAS实际上是由一系列的成分(肾素、血管紧张素原、血管紧张素转换酶、血管紧张素受体)组成的,主要分布在肠上皮、固有层和肌层粘膜。局部RAS参与小肠大部分活动水平的调节,影响肠道运动、分泌-运输过程、适应和保护反应。本综述中提出的实验数据非常有希望用于检测使用药物时可能的并发症,这些药物改变了这些药物与其潜在靶点相互作用的ras相关未探索效应的活性,这些靶点不仅局限于血管,而且直接作用于胃肠道的牛膜。在高血压、动脉粥样硬化、内皮功能障碍等心血管疾病的治疗实践中,广泛使用调节RAS活性的药物,这一点尤为重要。
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引用次数: 0
THE FUNCTIONAL STATE OF THE SMALL INTESTINE IN THE EARLY STAGES OF GALL STONE FORMATION. 胆囊结石形成初期小肠的功能状态
Ya M Vakhrushev, A Yu Gorbunov, A P Lukashevich, D V Tronina, D R Sharafutdinova, D S Rybin

Complex studying of functional condition of small intestine at bile stone disease and analyzing connection of small intestine functional disorders with formation of lithogenic bile. 123 patients with Bile stone disease were examined at pre-stone stage. Examinations done include ultrasonic exam of gallbladder, biochemical examination of bile, studying of bile acids in the bile by method of mass-spectrometry, morphological examination of duodenal mucous membrane, functional examination of small intestine with loading test.

Results: As the survey showed, a biliary sludge was found at 86,2% of the patients at ultrasonic examination of gallbladder In the patients' bile there were noticed changes of both general pool of bile acids and of ratio of their separate fractions. 82% of patients with bile stone disease at pre-stone stage had disorders of digestive and absorbing functions of small intestine, connected with reducing of general pool of bile acids in bile.

胆汁结石病小肠功能状况的综合研究及分析小肠功能障碍与产石性胆汁形成的关系。本文对123例胆结石病患者进行了结石前期检查。检查包括胆囊超声检查、胆汁生化检查、质谱法测定胆汁中胆汁酸、十二指肠粘膜形态学检查、小肠功能检查及负荷试验。结果:调查显示,86.2%的患者在胆囊超声检查中发现胆道淤渣,患者胆汁中胆汁酸总池及各组分比例均有明显变化。82%的胆结石患者结石前期存在小肠消化吸收功能障碍,与胆汁中胆汁酸总池减少有关。
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引用次数: 0
THE PRIMARY SMALL INTESTINE LYMPHANGIOECTASIA. 原发性小肠淋巴管扩张。
I A Glazunova, N I Kirnus

Lymphangloectasia intestinal Disease (Gordon disease, hypoprotein exudative enteropathy) is a disease in which develops the extension of lymphatic vessels (lymphangioectasia), located in the small intestine, resulting in signi1~cant intestinal protein loss. The article presents a clinical case of primary small intestinal lymphangloectasia in the 17-year old girl, which was admitted to the Morozov hospital Department of gastroenterology and Nephrology with complaints of weakness, widespread swelling on the face, legs and stomach, diarrhea. During a comprehensive clinical and instrumental examinations (including histology) the disease was diagnosed and treatment strategy was developed.

肠淋巴管扩张症(高登氏病,低蛋白渗出性肠病)是一种以位于小肠的淋巴管扩张(淋巴管扩张)为主要表现的疾病,导致肠内大量蛋白质丢失。本文介绍了一个17岁的女孩的原发性小肠淋巴管扩张的临床病例,这是入院的莫罗佐夫医院消化和肾脏科的症状虚弱,广泛的肿胀在脸,腿和胃,腹泻。在全面的临床和仪器检查(包括组织学)期间,诊断出疾病并制定了治疗策略。
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引用次数: 0
METABOLIC DYSBIOSIS OF THE GUT MICROBIOTA AND ITS BIOMARKERS. 肠道菌群代谢失调及其生物标志物。
S I Sitkin, E I Tkachenko, T Y Vakhitov

Existing methods of clustering of gut microbiota (enterotypes, clusters, gradients), as well as the term 'phylogenetic core' do not reflect its functional activity. The authors propose to describe the key microbiora using term 'phylometabolic core of intestinal microbioca which more accurately reflects the functional importance of metabolically active microbiota. Phylometabolic core includes functional groups of microorganisms that perform similar metabolic functions: butyrate-producing bacteria, propionate-producing bacteria, acetate-produc- ing bacteria (acerogens), hydrogenosrophic microorganisms (reductive acetogens, sulfate-reducing bacteria, methanogens), lactate-producing and lactate-utilizing bacteria, bacteria involved in bile acids metabolism, bacteria that metabolize proteins and amino acids, vitamin-producing microorganisms, oxalate-degrading bacteria and others. The hypothesis that disturbance of microbial metabolism is the root of many human diseases is discussed. The microbial dysmexabo- lism leads to the metabolic dysbiosis (a particular form of dysbiosis) that is primarily characterized by metabolic abnormalities (e.g. serum, urinary, fetal or exhaled air). Metabolic dysbiosis is not necessarily accompanied by appreciable quantitative and/or qualitative changes in microbiora composition that called taxonomic dysbiosis. Since in the metabolic dysbiosis metabolic pathways can be switched only, it means the need for completely different approaches to its assessment using metabolomics (metabolic fingerprinting, metabolic profiling, meta-metabolomics). Metabolites concentrations in colon (feces, biopsy samples), blood (serum, plasma), urine or exhaled air, as well as metabolic profiles of examined substrates can serve as biomarkers. The main clinical variants of metabolic dysbiosis are due to the disturbances in microbial synthesis of short-chain fatty acids (primarily butyrate and propionate) and due to increasing bacterial production of hydrogen sulfide, ammonia and secondary bile acids (particularly deoxycholic acid). These kinds of metabolic dysbiosis can eventually lead to inflammatory bowel disease (IBD) or colorectal cancer (CRC). The metabolic dysbiosis due to bacterial choline dysmetabolism followed by overproduction of trimethylamine (TMA), arherogenic precursor of trimethylamine N-oxide (TMAO), is associated with atherogenesis and increased risk of cardiovascular disease. Dysmetabolism of aromatic amino acids leads to changes in the microbial production of phenylalanine and tyrosine derivatives (phenyl carboxylic acid, p-cresol) and tryptophan indole derivatives (indole carboxylic acid, indole) and contributes to pathogenesis in lBS. IBD, CRC, chronic liver and kidney diseases, cardiovascular diseases, autism and schizophrenia. Metabiotics, a new class of therapeutic agents, e.g. based on microbial metabolites, can correct metabolic dysbiosis, prevent diet- and microbiota-relared diseases and increase the effectivenes

现有的肠道微生物群聚类方法(肠型、聚类、梯度)以及术语“系统发育核心”并不能反映其功能活性。作者建议使用“肠微生物群落代谢核心”(phylmetabolic core of intestinal microbioca)一词来描述关键微生物群,以更准确地反映代谢活性微生物群的功能重要性。细胞代谢核心包括执行类似代谢功能的微生物功能群:产丁酸菌、产丙酸菌、产醋酸菌(醋酸原)、氢营养微生物(还原性醋酸菌、硫酸盐还原性细菌、产甲烷菌)、产乳酸菌和利用乳酸菌、胆汁酸代谢菌、蛋白质和氨基酸代谢菌、产维生素菌、草酸降解菌等。讨论了微生物代谢紊乱是人类许多疾病根源的假说。微生物代谢障碍导致代谢失调(一种特殊形式的生态失调),其主要特征是代谢异常(如血清、尿液、胎儿或呼出的空气)。代谢失调不一定伴随着微生物组成的明显的定量和/或定性变化,称为分类学失调。由于在代谢失调中,代谢途径只能被切换,这意味着需要使用代谢组学(代谢指纹、代谢谱、元代谢组学)来评估其完全不同的方法。结肠(粪便、活检样本)、血液(血清、血浆)、尿液或呼出空气中的代谢物浓度,以及所检查底物的代谢谱,都可以作为生物标志物。代谢失调的主要临床变异是由于短链脂肪酸(主要是丁酸盐和丙酸盐)的微生物合成紊乱,以及由于细菌硫化氢、氨和次级胆油酸(特别是脱氧胆酸)的产生增加。这些代谢失调最终会导致炎症性肠病(IBD)或结直肠癌(CRC)。细菌胆碱代谢异常导致的代谢失调伴随着三甲胺(TMA)(三甲胺n -氧化物(TMAO)的动脉粥样硬化前体)的过量产生,与动脉粥样硬化和心血管疾病风险增加有关。芳香氨基酸代谢失调导致微生物产生苯丙氨酸和酪氨酸衍生物(苯基羧酸,对甲酚)和色氨酸吲哚衍生物(吲哚羧酸,吲哚)的变化,并有助于lBS的发病。IBD, CRC,慢性肝肾疾病,心血管疾病,自闭症,精神分裂症。代谢物是一类新的治疗剂,例如基于微生物代谢物,可以纠正代谢失调,预防与饮食和微生物有关的疾病,并提高治疗的有效性。
{"title":"METABOLIC DYSBIOSIS OF THE GUT MICROBIOTA AND ITS BIOMARKERS.","authors":"S I Sitkin,&nbsp;E I Tkachenko,&nbsp;T Y Vakhitov","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Existing methods of clustering of gut microbiota (enterotypes, clusters, gradients), as well as the term 'phylogenetic core' do not reflect its functional activity. The authors propose to describe the key microbiora using term 'phylometabolic core of intestinal microbioca which more accurately reflects the functional importance of metabolically active microbiota. Phylometabolic core includes functional groups of microorganisms that perform similar metabolic functions: butyrate-producing bacteria, propionate-producing bacteria, acetate-produc- ing bacteria (acerogens), hydrogenosrophic microorganisms (reductive acetogens, sulfate-reducing bacteria, methanogens), lactate-producing and lactate-utilizing bacteria, bacteria involved in bile acids metabolism, bacteria that metabolize proteins and amino acids, vitamin-producing microorganisms, oxalate-degrading bacteria and others. The hypothesis that disturbance of microbial metabolism is the root of many human diseases is discussed. The microbial dysmexabo- lism leads to the metabolic dysbiosis (a particular form of dysbiosis) that is primarily characterized by metabolic abnormalities (e.g. serum, urinary, fetal or exhaled air). Metabolic dysbiosis is not necessarily accompanied by appreciable quantitative and/or qualitative changes in microbiora composition that called taxonomic dysbiosis. Since in the metabolic dysbiosis metabolic pathways can be switched only, it means the need for completely different approaches to its assessment using metabolomics (metabolic fingerprinting, metabolic profiling, meta-metabolomics). Metabolites concentrations in colon (feces, biopsy samples), blood (serum, plasma), urine or exhaled air, as well as metabolic profiles of examined substrates can serve as biomarkers. The main clinical variants of metabolic dysbiosis are due to the disturbances in microbial synthesis of short-chain fatty acids (primarily butyrate and propionate) and due to increasing bacterial production of hydrogen sulfide, ammonia and secondary bile acids (particularly deoxycholic acid). These kinds of metabolic dysbiosis can eventually lead to inflammatory bowel disease (IBD) or colorectal cancer (CRC). The metabolic dysbiosis due to bacterial choline dysmetabolism followed by overproduction of trimethylamine (TMA), arherogenic precursor of trimethylamine N-oxide (TMAO), is associated with atherogenesis and increased risk of cardiovascular disease. Dysmetabolism of aromatic amino acids leads to changes in the microbial production of phenylalanine and tyrosine derivatives (phenyl carboxylic acid, p-cresol) and tryptophan indole derivatives (indole carboxylic acid, indole) and contributes to pathogenesis in lBS. IBD, CRC, chronic liver and kidney diseases, cardiovascular diseases, autism and schizophrenia. Metabiotics, a new class of therapeutic agents, e.g. based on microbial metabolites, can correct metabolic dysbiosis, prevent diet- and microbiota-relared diseases and increase the effectivenes","PeriodicalId":11555,"journal":{"name":"Eksperimental'naia i klinicheskaia gastroenterologiia = Experimental & clinical gastroenterology","volume":"12 12","pages":"6-29"},"PeriodicalIF":0.0,"publicationDate":"2016-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36211358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
FUNCTIONAL FOODS ARE CRITICAL COMPONENTS OF TREATMENT OF METABOLIC DISORDERS IN CELIAC DISEASE. 功能性食品是治疗乳糜泻代谢紊乱的关键成分。
E I Tkachenko, L S Oreshko, S I Sitkin, E A Soloveva, A A Shabanova, M S Zhuravleva

Aim: To evaluate the effectiveness of Native-complex functional food to correct nutritional disorders and to normalize gastrointestinal motor activity in celiac disease (CD).

Methods: 20 CD patients with constipation and metabolic disorders were included in the study (age 31.8?9.5 years, male to female ratio 1:5.3). The diagnosis of CD was confirmed by clinical and anamnestic data, endoscopy, histopathology of duodenal biopsy specimens, HLA-DQ2 and HLA-DQS typing. All patients received Native-complex Fucus jelly (Kelp jelly) within 2 months.

Results: At the beginning of the study45% of patients had stools corresponding to the Bristol Stool Form ScaleType 1,40% of patients had Type 2 stools and 15% of patient had Type 3 stools. 15 patients (75%) showed a decrease in fat mass and 13 patients (65%) showed a decrease in fat-free mass indicated by bloimpedance measurement. All patients had low values of total bacterial counts and increased abundance of pathobionts including fungi and viruses in fecal microbiota. Supple- mentary nutrition significantly improved symptoms, intestinal circadian rhythms and stool consistency in CD patients. At the end of the study 70% of patients had daily bowel movements, 30% of patients had stools every other day. The average stool frequency was 5,95 ? 1,80 per week. 80% of patients had Type 4 or Type 5 stools,20% of patients had Type 3 stools according to the Bristol Scale. Supplementary nutrition significantly improved gut microbiota profile.

Conclusion: Long-term gluten-free diet in celiac disease leads to a decrease in dietary fiber and polysaccharides consumption and promotes intestinal dysbiosis. Functional foods improve symptoms; stool consistency and gut microbiota profile in adult celiac patients on gluten-free diet.

目的:评价天然复合功能食品对纠正乳糜泻(CD)患者营养失调和恢复胃肠运动功能的作用。方法:纳入20例伴有便秘和代谢紊乱的CD患者(年龄31.8 ~ 9.5岁,男女比例1:5.3)。经临床和记忆资料、内镜检查、十二指肠活检标本组织病理学检查、HLA-DQ2和HLA-DQS分型证实为CD的诊断。所有患者均在2个月内接受天然复合海带果冻治疗。结果:在研究开始时,45%的患者有符合布里斯托尔粪便量表1型的粪便,40%的患者有2型粪便,15%的患者有3型粪便。15例(75%)患者显示脂肪量减少,13例(65%)患者显示无脂肪量减少。所有患者的总细菌计数均较低,粪便微生物群中包括真菌和病毒在内的病原体丰度增加。补充营养可显著改善乳糜泻患者的症状、肠道昼夜节律和大便一致性。在研究结束时,70%的患者每天排便,30%的患者每隔一天便一次。平均大便次数为5.95 ?每周1,80英镑。根据布里斯托尔量表,80%的患者为4型或5型大便,20%的患者为3型大便。补充营养可显著改善肠道菌群。结论:乳糜泻患者长期无麸质饮食可导致膳食纤维和多糖消耗减少,促进肠道生态失调。功能食品能改善症状;无麸质饮食的成年乳糜泻患者的粪便一致性和肠道微生物群特征。
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引用次数: 0
PATHOGENETIC SIGNIFICANCE OF DYSKINESIA OF THE SPHINCTER OF OKSNER IN THE DEVELOPMENT OF THE SYNDROME OF THE SUPERIOR MESENTERIC ARTERY. 肠系膜上动脉综合征发展过程中oksner括约肌运动障碍的发病意义。
M D Levin

The goal of this study is to investigate the pathological physiology of superior mesenteric artery syndrome (SMAS).

Materials and methods: We selected 35 articles devoted to SMAS, which were published from 1990 to 2014, and performed radiometric analysis of X-rays, CT scans and MRI slices found in these articles. In pictures the narrowing in the third part of the duodenum was measured from the boundary of the expanded segment to the level of the superior mesenteric artery (SMA).

Results: Only in 6 (17%) of. 35 cases the narrowing portion of duodenum was located directly between aorta and SMA, and its length was about 1cm. In the remaining 29 cases, the beginning of the narrow segment was 2.5-4.6 cm (average 3.30 ±0.15 cm) proximal to SMA, ie, most of the narrowed duodenum was out of aortomesenteric angle. Location and length of the narrowed segment of duodenum corresponded to the location and length (3.2 ± 0.15 cm) (P> 0.2) of the functional Ochsner sphincter.

Conclusion: These data indicate that in most cases of SMAS the sphincter Ochsner dyskinesia causes the disease. It is likely that the disease is triggered by heavy stressful conditions that cause a sharp and sustained reduction in the pH of gastric secretions, which in turn leads to the spasms of the sphincter Ochsner. With time this condition progresses to hypertrophy of the contracted wall of the duodenum with subsequent replacement of the muscle fibers by connective tissue. This can lead to the rigidity of the wall.

本研究旨在探讨肠系膜上动脉综合征(SMAS)的病理生理学。材料和方法:我们选取1990 - 2014年发表的35篇关于SMAS的文章,对这些文章中的x射线、CT扫描和MRI切片进行放射学分析。在图片中,从扩张段的边界到肠系膜上动脉(SMA)的水平测量了十二指肠第三部分的狭窄。结果:仅6例(17%)。35例十二指肠狭窄部分位于主动脉与SMA之间,长度约1cm。其余29例中,狭窄段开始于距SMA近2.5 ~ 4.6 cm(平均3.30±0.15 cm)处,即大部分狭窄的十二指肠在主肠系膜角外。十二指肠狭窄段的位置和长度与正常奥氏括约肌的位置和长度(3.2±0.15 cm)一致(P> 0.2)。结论:这些数据表明,在大多数SMAS病例中,括约肌奥克斯纳运动障碍是导致该疾病的原因。这种疾病很可能是由严重的应激条件引发的,这种应激条件导致胃分泌物的pH值急剧和持续下降,这反过来又导致奥克斯纳括约肌痉挛。随着时间的推移,这种情况发展为收缩的十二指肠壁肥大,随后肌纤维被结缔组织取代。这会导致墙体的刚性。
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引用次数: 0
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Eksperimental'naia i klinicheskaia gastroenterologiia = Experimental & clinical gastroenterology
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