甲烷和氢呼气-sim

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甲烷与氢气混合燃烧的理论计算分析

甲烷与氢气混合燃烧的理论计算分析

析。利用计算得到燃气的低位热值、理论空气量、理论烟气量、标况密度、价格、单位热 值 价 格、单 位 热 值 所 需 理 论 空 气 量、
单位热值产生理论烟气量等,对规范建筑陶瓷生产过程能耗实时监控、能源优化调度、能耗数 据 管 理 等 具 有 一 定 的 借 鉴 和
指导作用。
关键词
燃气
燃烧
计算
分析
热值
· 46 ·
陶瓷
(综述) 2023 年 10 月
Ce
r
ami
c
s
甲烷与氢气混合燃烧的理论计算分析
张永伟


艾冬华
袁钧宇
(新明珠集团股份有限公司


梁益斌
郑锴杰
*
伍志良
广东 佛山 528099)
笔者介绍了甲烷与氢气混合燃烧的具体计算方法,对不同混合比的甲烷与氢气混合 燃 料 进 行 了 理 论 计 算 比 较 分
气压,天然气和氢气价格分别按 5 元/Nm3 和 1.
78 元/
Nm3 计算。具体情况如表 2 所示。
表 2 不同比例混合气的重要性能指标
组成成分
低位热值
百分量(% )
燃气
名称
H2 CH4
kJ
/Nm3
kJ
/kg
理论
理论
空气量
烟气量
(
Nm3
(
Nm3
/Nm ) /Nm )
3
3
H2 -0 0
100 35816.
0.
089
3.
87 0.
1505
3.
55 0.
1535
3.
39 0.
1550
3.

氢气甲烷二氧化碳呼气试验 新技术新项目

氢气甲烷二氧化碳呼气试验 新技术新项目

氢气甲烷二氧化碳呼气试验新技术新项目氢气甲烷二氧化碳呼气试验是一项新技术新项目,在现代科学研究和应用领域具有重要的意义。

本文将从背景介绍、技术原理、应用前景和发展趋势等方面进行详细阐述。

**一、背景介绍**随着工业化进程的加快和环境污染问题的日益严重,人们对清洁能源和环保技术的需求日益迫切。

氢气、甲烷和二氧化碳是目前广泛使用的能源和工业原料,它们的燃烧和排放对环境和人类健康造成了严重影响。

因此,如何有效地监测和控制这些气体的排放就成为了当前研究的热点之一。

**二、技术原理**氢气甲烷二氧化碳呼气试验是一种基于气体检测技术的新方法,通过对气体中氢气、甲烷和二氧化碳浓度的监测和分析,实现对工业生产和燃烧过程中这些气体排放的实时监测和控制。

该技术主要包括气体采集、样品预处理、气体分析和数据处理等几个步骤。

首先,需要采集目标气体的样品,并经过一定的预处理使其达到分析要求。

然后,利用气体分析仪器对样品进行定量分析,得出氢气、甲烷和二氧化碳的浓度。

最后,将分析结果进行数据处理和分析,实现对气体排放的监测、预警和控制。

**三、应用前景**氢气甲烷二氧化碳呼气试验技术具有广泛的应用前景。

首先,它可以在环保监测领域得到广泛应用,如在工业废气处理、城市环境监测和生态保护等方面。

其次,该技术也可以应用于石油化工、煤炭化工、电力和环保等领域。

另外,随着新能源、清洁能源和低碳经济的快速发展,氢气甲烷二氧化碳呼气试验技术将在新能源开发、能源转化和能源利用等方面发挥重要作用。

**四、发展趋势**在未来,氢气甲烷二氧化碳呼气试验技术有望在监测、控制和利用氢气、甲烷和二氧化碳排放方面发挥更大的作用。

随着气体分析技术的不断进步和仪器设备的不断更新,该技术将更加精准、快速和可靠。

同时,随着大数据、人工智能和云计算等技术的广泛应用,氢气甲烷二氧化碳呼气试验技术将实现更高程度的自动化、智能化和信息化。

总之,氢气甲烷二氧化碳呼气试验技术作为一种新技术新项目,具有广阔的应用前景和发展空间,将在环保监测、工业生产和清洁能源等领域发挥越来越重要的作用。

甲烷和氢呼气-sim

甲烷和氢呼气-sim

临床意义
• 对肝病患者常伴发的小肠细菌过增长有诊断价值及有效指 导治疗,对国人高达80%以上的乳糖酶缺乏症的测定更是 独一无二。 • 该技术的应用范围涵盖40%-60%的胃肠疾病。
• 消化科、儿科、体检中心、内分泌科、胃肠及肝胆外科等 临床科室都可开展。
• 呼气氢试验在消化系疾病的诊断及治疗中有十分重要的意 义,为消化系疾病的诊治开辟了一条崭新的道路。
中国儿童乳糖不耐受发生率
• 随机选择北京、上海、广州和哈尔滨4大城市的3~13岁健 康儿童1168名,采用乳制品摄入量频率调查、乳糖耐量试验 和氢呼气试验的方法,研究了中国儿童乳糖酶缺乏和乳糖不 耐受的发生率.结果表明:3~5岁,7~8岁和11~13岁组儿童 中,乳糖酶缺乏的发生率分别为38.5%、87.6%和87.8%.乳糖 不耐受发生率分别为12.2%、32.2%和29.0%.中国4大城市儿 童乳糖酶降低或消失发生的年龄在7~8岁.当儿童食用50g 奶粉(含13~14g乳糖)时,吸收不良和不耐受的发生率显著 下降,但学龄儿童中仍有39%~41.7%为吸收不良、牛奶不 耐受症状发生率14%~16.7%.研究未发现乳糖酶缺乏的发 生和儿童的喂养史、乳品摄入史有关。
底物 乳果糖 乳糖 山梨醇 牛奶 试餐
剂量(g/ml) 10 18 15 300
口盲时间(分钟) 73.0±6.5 146.8±65.9 73.9±20.4 113±9 192±16
胃肠通过时间(口盲时间)
结论:1.胃肠通过时间75分钟:正常 2.无小肠细菌过增长 3.回盲瓣功能完好
口盲时间:氢呼气试验
– 李俊娜等,呼气氢试验在消化系疾病诊断治疗中的研究进展。河 南科技大学学报(医学版),2006年12月24卷第4期,314-315.

氢呼气试验 (2)

氢呼气试验 (2)

氢呼气试验(HBT)图1. 氢/甲烷呼气试验基本原理氢呼气试验(hydrogen breath tests)指测定口服某种化合物后呼气中的氢气(hydrogen)浓度变化而诊断胃肠疾病的一类检验方法。

仪器条件许可时,除了氢气还同时作甲烷(methane)浓度测定,故试验有时也称为氢/甲烷呼气试验。

我院目前常规开展的项目有:1.葡萄糖氢呼气试验诊断小肠细菌过生长; 2. 乳果糖氢呼气试验测定口-盲肠通过时间,也可同时诊断小肠细菌过生长。

人和哺乳动物细胞代谢不产生氢气和甲烷,呼气中的氢气和甲烷来源于机体细菌对碳水化合物的发酵。

大肠是身体含细菌最多的地方,而胃和小肠的细菌量是很少的。

所以,餐后一段时间出现的呼气氢和甲烷浓度上升显然就是大肠细菌对食物残渣碳水化合物的发酵的结果。

经过一段时间的禁食,残渣中的可分解碳水化合物耗尽,呼气氢气和甲烷浓度将回复到大气水平。

葡萄糖是一种极易被小肠迅速完全吸收的碳水化合物。

因此,健康人口服一定剂量的葡萄糖后不会出现呼气氢气和甲烷浓度上升的现象,因为几乎没有多余的葡萄糖进入大肠。

相反,小肠细菌过生长的病人,口服的葡萄糖在被小肠吸收的同时也被过量的小肠细菌分解产气。

乳果糖是一种不能消化吸收的人工合成碳水合物。

因此,口服一定剂量的乳果糖后将会出现呼气氢气和甲烷浓度上升的现象,从口服起到呼气氢气和甲烷浓度上升的时间便是药物从口到大肠起点盲肠的运行时间,简称口-盲通过时间,它大致反映了小肠的动力状态。

如果有小肠细菌过生长的存在,口服的乳果糖在到达大肠前就会提前被分解,结果出现两次产气高峰。

基本步骤除白开水外禁食禁饮12h以上采集0时气样口服试验糖餐再次采集气样测定报告注意事项1.严格空腹和饮食控制耗尽食物残渣中碳水化合物,让呼气氢气和甲烷浓度保持在大气水平是氢呼气试验的前提条件。

试验前一天的饮食以清淡易消化为宜,晚餐必须在8点前结束、只能喝白稀饭,餐后禁止白开水以外的一切食物或饮料,空腹时间一定要超过12小时!2.严禁吸烟烟草燃烧产生大量的氢气,吸烟者在试验前至少要禁烟一小时。

甲烷和氢呼气可以检查的项目

甲烷和氢呼气可以检查的项目

甲烷和氢呼气可以检查的项目丁文京博士北美医学教育基金会甲烷和氢呼气检测技术在临床有重要的应用前景,可以广泛应用于以下一些检查。

碳水化合物吸收不良:甲烷和氢呼气试验可以检测各种由于先天性或后天性糖类分解酶分泌不足造成的碳水化合物吸收不良。

中国人常见的先天性糖类分解酶不足有乳糖酶缺乏导致的乳糖不耐受。

不常见,但是传统方法比较难以诊断的果糖酶缺乏导致的果糖不耐受、蔗糖酶缺乏导致的蔗糖不耐受等,以及山梨醇酶缺乏导致的山梨醇不耐受等。

后天性糖类分解酶不足,多由于疾病导致。

常见的有由于腹泻导致的乳糖酶缺乏,慢性胰腺疾病导致的胰淀粉酶缺乏等。

检验时给受试者服用特定的糖(常用50g糖,儿童根据每kg体重1g计算),当肠道缺乏相应的酶时,小肠不能完全吸收这些糖,那些不能被吸收的糖进入结肠后被细菌酵解产生甲烷和氢,由此可以判断是否存在酶缺乏。

对于由于慢性胰腺疾病导致的胰淀粉酶缺乏,可以服用100g淀粉或米粉,胰淀粉酶缺乏导致小肠不能完全吸收淀粉或米粉,在结肠段出现甲烷和氢呼气高峰。

小肠细菌过度生长:正常人体小肠部分细菌很少,当服用糖类后尽产生很少的甲烷和氢,基本在基线水平。

当小肠有细菌后,可以酵解糖产生甲烷和氢,当氢呼气值高于基线值12ppm,或者氢气值加甲烷值高于基线值15ppm时表示小肠内有高于正常数量的细菌,临床上称为小肠细菌过度生长(Small Intestinal Bacteria Overgrowth,简称SIBO,欧洲常用Small Bowel Bacteria Overgrowth,简称SBBO)。

用甲烷和氢呼气检测小肠细菌过度生长,可以帮助了解肠道微生态的变化,在诊断和治疗由于菌群移位和菌群失调导致的疾病方面提供有重要价值的帮助。

国内外有大量研究证明肠道菌群失调可以导致人体多个系统的病变。

通过检测小肠细菌过度生长可以打开了解包括糖尿病、心血管、肝脏等疾病的新思路。

口盲时间:即从糖入口到达盲肠的时间,又称口盲传输时间(Orocecal Transit Time, OCTT),用以反映胃肠蠕动速度,检测多种与胃肠传输速度有关的疾病,或者评估某些疾病状态在胃肠传输的功能。

甲烷氢呼气试验操作流程

甲烷氢呼气试验操作流程

甲烷氢呼气试验操作流程一、试验前准备。

1. 饮食要求。

这个试验啊,对饮食可有要求啦。

在试验前一天呢,咱们可不能吃那些高纤维的食物哦,像什么芹菜啦、韭菜啦,这些都得先放放。

还有豆类,它们容易在肚子里产气,也别吃啦。

另外呢,试验前12小时要禁食禁水,这一点可一定要记住哦,不然会影响试验结果的。

就像你要参加一场很重要的比赛,得遵守规则才能取得好成绩呀。

2. 患者告知。

我们得跟患者好好聊一聊这个试验。

要告诉患者这个试验是怎么做的,大概需要多长时间,让患者心里有个底。

比如说,“亲,这个试验不会很复杂的,就是让您吹吹气,大概要两三个小时呢,您只要放松就好啦。

”还要告诉患者在试验过程中如果有什么不舒服的地方,一定要及时跟我们说哦,我们就像您的小管家,会随时照顾您的。

二、试验过程。

1. 基础呼气采集。

首先呢,让患者安静休息15 30分钟,就像让身体先适应一下这个即将开始的小测试。

然后给患者一个专门用来收集气体的袋子或者容器,让患者正常呼气,把这口气收集起来。

这就像是收集一个小样本,作为基础数据。

这个时候我们可以跟患者开个小玩笑,比如说“亲,您就像吹生日蜡烛一样,轻轻吹就好啦。

”2. 口服底物。

接下来,让患者口服特定的底物,这个底物就像是一个小钥匙,用来打开我们身体里某些反应的大门。

口服底物的时候,要确保患者完全服下,可不能洒出来或者剩下哦。

3. 定时呼气采集。

在口服底物之后呢,就开始按照规定的时间间隔来采集患者呼出的气体啦。

一般是每隔15 30分钟采集一次。

这个时候,我们要温柔地提醒患者,“亲,又到了吹气的时间啦,您感觉怎么样呢?”在采集气体的时候,要保证收集的气体量足够,还要标记好每次采集的时间。

这就像在做一个很有趣的记录游戏一样,每个时间点的气体都很重要呢。

三、试验后注意事项。

1. 患者观察。

试验结束后,可不能马上就让患者走哦。

我们要观察患者一会儿,看看患者有没有什么不舒服的地方。

就像在照顾一个刚做完小冒险的小朋友一样,要确保他一切都好。

氢气甲烷呼气文献 (65)

氢气甲烷呼气文献 (65)

Eur opean Rev iew for Med ical and Pharmacol ogical Sci ences 1328Abstract. –Background and Objectives:Calprotectin is a protein especially expressed in neutrophil cytosol. In the la st few yea rs, Feca l calprotectin (FC) turned out to be a direct mark-er of ga strointestina l infla mma tion. Beca use of the simplicity of the method, it has been studied in several gastroenterologic diseases but no da-ta a re a va ila ble a bout its concentra tion in chil-dren with Sma ll Intestina l Ba cteria l Overgrowth (SIBO), a complex and not well known condition defined by an excessive germs proliferation, es-pecially anaerobic, in the small bowel, and char-acterized by dyspeptic and malabsorption symp-toms. The aim of this study was to evaluate FC va lues in children with SIBO, compa ring to healthy subjects, in order to clarify if an inflam-matory process coexists with SIBO.Materials and Methods:We enrolled fifty-eight children affected by SIBO, as diagnosed by Lactu-lose Breath Test (LBT). They were assessed for FC values on stool samples. We compared them with a control population of 60 healthy children.Results:In SIBO pa tients, a media n va lue of 36.0 mg/kg and a mean value ± SD of 43.0 ± 31.6mg/kg were calculated, while in healthy controls the median value was 29.5 mg/kg and the mean va lue ± SD wa s 35.7 ± 20.7 mg/kg, showing no sta tistica lly significa nt differences between the two groups (p = 0.07).Conclusions:FC va lues a re nega tive in chil-dren a ffected by SIBO, not differing from those obtained in healthy children, suggesting that no subclinica l intestina l infla mma tion involving neutrophils occurs in patients with higher prolif-eration of bacteria in the small bowel. The pres-ence of high FC levels in children affected by SI-BO might not be caused by bacterial overgrowth itself and, in this case, another cause should be investigated.Key Words:Fecal calprotectin, Small intestinal bacterial over-growth, Children, Lactulose breath test.Corresponding Author:Claudia Fantacci, MD; e-mail: claudiafantacci@yahoo.itIntroductionCalprotectin is a 36 kDa Calcium and Zincum binding protein which belongs to the S100 pro-tein family 1and it is mapped on the gene q12-q21 on chromosome 12. The S100 protein family is composed by about twenty proteins which are expressed in various cell types and have in com-mon the skill to bind Calcium ion, a second mes-senger which activates their function. S100 pro-tein family is involved in the complicated mecha-nisms of the intracellular transduction, than it takes part in the regulation of various processes such as protein phosphorylation, transcription,cell differentiation, cell cycle regulation, cell growth and proliferation, cell motility, inflamma-tory and immune response regulation 3. In partic-ular, Calprotectin has been described for the first time in 1980 by Fagerhol et al.4, who isolated it from leukocytes and named it “L1 protein”. Af-terwards, it has been found in cells, tissues and fluids in all parts of human body 5, but its pecu-liarity is to be expecially expressed in neutrophil cytosol. In fact, here its concentration is estimat-ed at 5-15 mg/ml and it constitutes about 5% of total proteins in neutrophil granulocytes 4,6. This entails that in inflammatory reactions, with neu-trophil activation and death, Calprotectin is re-leased and then its concentration in body fluids increases, constituting a marker of those inflam-matory processes in which neutrophil granulo-cytes are involved 7-9. Consequently, concerning gastrointestinal diseases, when there is an in-flammatory process in gastrointestinal mucosa,Calprotectin is released in the gut lumen and then it can be retrieved in feces 10-12. When, in 1992,Røseth et al.13described the method for the ex-traction and the assessment of Calprotectin in fe-ces, to quantify its concentrations in various gas-2011; 15: 1328-1335Fecal Calprotectin concentration in children affected by SIBOC. FUNDARÒ, C. FANTACCI, V . ANSUINI, V . GIORGIO, S. FILONI, F . BARBARO*, A. GASBARRINI*, C. ROSSI**Department of Pediatric; *Department of Gastroenterology and **Clinical Chemistry Laboratory,School of Medicine, Catholic University of the Sacred Heart, Gemelli Hospital, Rome (Italy)trointestinal diseases became possible. Because of the simplicity of the method, in the last few years fecal Calprotectin (FC) has been evaluated in various gastrointestinal disorders14-17and has emerged as a sensible and useful marker of gas-trointestinal inflammation, becoming an impor-tant aid in clinical practice.Small Intestinal Bacterial Overgrowth (SIBO) is a qualitative and quantitative variation of intesti-nal flora characterized by an excessive germs pro-liferation, especially anaerobic, in the small bow-el, exceeding 105Colony Forming Unit (CFU) of organisms per ml of intestinal juice18. This disor-der is not actually well known, and for explaining its pathogenesis several factors have been thought to be involved. A number of conditions which can compromise the delicate equilibrium of the gas-trointestinal tract have been supposed to play a role, such as intestinal dismotility (diabetic neu-ropathy, scleroderma, accelerated gastric empty-ing, chronic renal failure), gastrointestinal anato-my changes (gastric atrophy, small bowel divertic-ulosis, intestinal stenosis, gut surgery, resection of the ileocecal valve), hypo or achlorydria, ageing, immunodeficiency and malnutrition19. With regard to clinical aspects, patients affected by SIBO can suffer from dyspeptic and malabsorption symp-toms, such as bloating, meteorism, abdominal dis-comfort or pain, flatulence, diarrhea, steatorrhea, weight loss and anaemia20. The diagnosis of SIBO can be assessed with different methods. The gold standard is the culture of upper intestinal aspirate but it is an invasive and difficult to perform tech-nique, which requires an expert staff18. Today, one of the most used is the Lactulose Breath Test (LBT)21, which is a more simple and less invasive and expensive methodic. LBT is characterized by high sensitivity and specificity22.At present, no data are available about FC con-centrations in children with SIBO.This prospective study was designed to evalu-ate FC concentrations in children affected by SI-BO, comparing them to a group of healthy con-trols, in order to clarify if an inflammatory process coexists with SIBO.Materials and MethodsWe evaluated fifty-eight consecutive children with SIBO as assessed by LBT. They were re-ferred to the Pediatric Gastroenterology Outpa-tients Unit of Catholic University of the Sacred Heart, Gemelli Hospital of Rome between April 1st2008 and September 1st2009.Children who took Non Steroidal Anti-Inflam-matory Drugs (NSAIDs), antibiotics, gastric acidity inhibitors or drugs influencing gut motili-ty within the previous 2 months were excluded. Children who were affected by other gastroin-testinal disorders, respiratory or urinary infec-tions, or chronic diseases such as rheumatoid arthritis, diabetes, thyroid diseases, connective tissue diseases, or had a history of intestinal surgery were excluded. Children who had nasal or menstrual bleeding in the last three weeks were excluded too.The control population included sixty healthy children, without SIBO (as assessed by negative LBT). They were referred to our General Pedi-atrics Outpatients Unit for routine medical care. All patients affected by SIBO and all healthy controls were assessed for F C values after stool sample measurements.All children were clinically evaluated at three and six months of follow-up.All patients and control subjects were enrolled with parents informed consent, according to the Ethics Committee of our University.Hydrogen/Methane Lactulose Breath TestHydrogen (H2)/methane (CH4) Lactulose Breath Test (LBT) was performed under standard conditions. No patients had received laxatives in the 30 days preceding the test. Subjects were asked to have a carbohydrate-restricted dinner on the day before the test and to fast for at least 12hours to minimize basal H2excretion. On the day of testing, patients received a mouthwash with 20 mL of chlorhexidine 0.05%. Physical exercise was not allowed for 30 minutes before and dur-ing the test. End-alveolar breath samples were collected immediately before lactulose ingestion (lactulose 10 g in solution 20 mL). Samples were taken every 15 minutes for 4 hours with a 2 bag system, consisting of a mouthpiece, a T-valve, and 2 collapsible bags; the first one collects dead space air, the second one collects alveolar air. The breath sample was aspirated from this bag into a 20 mL plastic syringe. Samples were ana-lyzed immediately for H2and CH4with a model DP Quintron gas chromatograph (Quintron In-strument Company, Milwaukee, WI, USA). The results were expressed as parts per million. A normal LBT was defined as the absence of anearly rise in H2or CH4excretion of more of 20 parts per million within the first 90 minutes.1329Fecal Calprotectin concentration in children affected by SIBO1330FC Measurement and RangesOne hundred-eighteen stool samples were col-lected, using a disposable plastic test tube. Speci-mens were returned to the laboratory within 48hours of defecation. The weight of the samples necessary for the test was 40-120 mg. This little amount was collected with a specific device and then diluted with a buffer solution containing cit-rate and urea in a weight per volume ratio 1:50(20 µl of stool sample in 980 µl of buffer solu-tion). If necessary, a second dilution 1:250 (200µl of the first diluted solution in 800 µl of buffer solution) could be performed for very concentrat-ed stool samples. After this procedure, the sam-ple was mixed for 30 seconds by a vortex method, homogenized for 25 minutes and then one milliliter of the homogenate was centrifuged for 20 minutes. The supernatant was collected and kept refrigerated at –20°C. Within seven days, the samples were thawed at room tempera-ture and then Calprotectin concentration was ac-tually measured by the quantitative ELISA test Calprest ®(Eurospital Spa, Trieste, Italy).Laboratory ranges were expressed as mg of Calprotectin/kg of feces. The linearity of the method was 15-500 mg/kg.On the basis of data available in literature concerning the F C cut-off value in the pediatric age, a negative FC concen-tration was defined by a FC value lower than 100mg/kg, while a positive FC concentration was de-fined by a F C value equal or higher than 100mg/kg 16,23.Statistical AnalysisThe statistical analysis was performed with ANOV A test. Student’s t -test was used for data analysis. A p value <0,05 has been considered statistically significant. All results have been pre-sented as median and mean ± standard deviation (SD), or as absolute count numbers when appro-priate.ResultsThe results were reported on Tables I, II and Figures 1, 2.Fifty-eight children affected by SIBO and six-ty healthy subjects were evaluated.The number of males/females was 39/19 in the group of patients affected by SIBO and 36/24 in the group of healthy controls. The age range of the children in the two groups was respectivelyC. Fundarò, C. Fantacci, V . Ansuini, V . Giorgio, S. Filoni, F . Barbaro, A. Gasbarrini, C. Rossi52-202 months and 52-211 months, with a mean age of 121.8 ± 38.9 months and 126.8 ± 46.9months. Concerning demographic data, a p value of 0.26 was calculated, demonstrating that no statistically significant differences for sex and age were observed between the two groups.F ifty-six (96.6%) patients affected by SIBO and sixty (100%) healthy children had a negative F C value. In particular, the range of F C values obtained in the two groups was <15-159 mg/kg and <15-89 mg/kg respectively. In the group of patients affected by SIBO, a median value of 36.0 mg/kg and a mean value ± SD of 43.0 ±31.6 mg/kg were calculated, while in the group of healthy controls the median value was 29.5mg/kg and the mean value ± SD was 35.7 ± 20.7mg/kg. Evaluating these results obtained in the two groups, a p value of 0.07 was calculated,suggesting that no statistically significant differ-ences came out between FC concentrations in pa-tients affected by SIBO in comparison with healthy children.DiscussionFor the first time, our case control study shows that F C levels in children affected by SIBO are not statistically different from those obtained in healthy controls. Our findings are similar to those pointed out by Montalto et al 24, who per-Table I.Demographic characteristics of patients affected by SIBO and healthy controls.*p = 0.26.Table II.Fecal Calprotectin values obtained in patients af-fected by SIBO and in healthy controls.*p = 0.07.1331Fecal Calprotectin concentration in children affected by SIBOformed the only study available in literature about the correlation between SIBO and FC con-centrations. Their study was carried out on an adult population: they evaluated 40 patients af-fected by SIBO and 40 controls, demonstrating no statistically significant differences in FC con-centrations between the two groups.In the last few years, the importance of F C measurement in the management of gastrointesti-nal disorders is becoming more and more evi-dent, and it is settling as an useful marker of gas-trointestinal inflammation which can support the clinical practice 8.In fact, FC concentration increases in a num-ber of organic gastroenterologic conditions such as colorectal cancer, NSAIDs enteropathy, al-choolic enteropathy, active inflammatory bowel diseases (IBD), acute gastroenteritis, allergic col-itis and gastro-esophageal reflux disease 8,25-28.This happens because it is released from neu-trophils in gut lumen during gastrointestinal in-flammation, then it binds Ca 2+, becoming resis-tant against heat and proteolysis. Consequently, it is eliminated intact in feces and there it can re-main stable at room temperature for about 7days 10,11. This allows to measure it by means of a simple and non invasive laboratory test, which requires a little amount of feces. These character-istics make F C measurement a convenient labo-ratory test, easy to be performed by patients, es-pecially in the pediatric age.Furthermore, supporting data that FC can con-stitute a direct marker of those gastrointestinal inflammatory processes in which neutrophils are involved, some studies which compared FC mea-surement with invasive techniques have shown interesting results.Røseth et al 29investigated the correlation be-tween the faecal excretion of the granulocyte marker protein and that of 111-Indium-labelled granulocytes in patients with IBD. In fact, faecal excretion of 111-Indium-labelled neutrophilic granulocytes has been suggested as the gold stan-dard of disease activity, but it is a complex and expensive method which expose patients to ion-izing irradiation. The results obtained in this study suggested that FC reflects the granulocyte migration through the gut wall in patients with IBD and hence could be used as a simple, inex-pensive alternative to the 111-indium technique.Limburg et al 30evaluated 110 subjects with chronic diarrhea who were referred for colonoscopy and observed that increased FC lev-els were significantly associated with the colono-scopic and histological findings of colorectal in-flammation.A recent metanalysis has analyzed 30 prospec-tive studies which compared F C levels against the histological diagnosis in patients with diag-nosis of IBD. It evaluated F C concentrations of 5983 adults and children and demonstrated that FC has a sensitivity of 95% and a specificity of 91% in IBD diagnosis. The same metanalysis shows that the diagnostic precision in childhoodFigure 2.Fecal Calprotectin values obtained in the group of patients affected by SIBO and in healthy controls.F e c a l c a l p r o t e c t i n (m g /k g )Patients ControlsFigure parison between the age of the patients af-fected by SIBO and healthy controls.A g e (m o n t h s )Patients Controlspopulation is higher than in the adult popula-tion23. F urthermore, F C values of children with IBDs in remission turn into normal ranges be-coming non statistically different from those of healthy children16,31, while they increase again in relapses, preceding clinical symptoms32-36. Moreover, FC values in functional symptoms have been demonstrated to be not statistically different from controls16, and this is true in children affected by IBD too. So, FC can help in distinguishing functional pains from relapses in a child affected by IBD, and this is very im-portant for these subjects because they present with an increased frequency bowel movements, urgency and abdominal cramping, and these symptoms can be mistakenly interpreted as a flare-up37.Concerning literature which has examined FC levels specifically in the pediatric age, a remark-able study is that of Berni Canani et al16, who en-rolled 281 children assessed for gastrointestinal symptoms. Among these subjects, those of them affected by a disease characterized by gastroin-testinal mucosal inflammation, such as Crohn’s disease (38 children), ulcerative colitis (45 chil-dren) had increased FC concentrations, while 44 children suffering from functional gastrointesti-nal disorders (F GIDs) showed normal values. Therefore, they pointed out that FC is a sensitive but not disease specific marker to easily detect inflammation throughout the whole gastrointesti-nal tract and may help in identifying an organic disease and in the differential diagnosis of func-tional bowel disorders.All these results impact on clinical practice be-cause suggest that several invasive diagnostic techniques can be avoided, and this is even more important in Pediatrics38.SIBO is a condition characterized by an exces-sive germs proliferation, especially anaerobic, in the small bowel (more than 105CF U/ml of in-testinal juice)18, liable to antibiotic treatment, which improves gastrointestinal symptoms39. Generally, in the intestinal tract there are 103-104CF U/ml of bacteria such Enterococcus and Lactobacillus, and there are a number of factors which permit to restrain bacterial overgrowth. Among these, there are anatomical and function-al factors (such as gastric acidity, ileocecal valve continence, gall and pancreatic secretions and their antibacterial activity), mechanical factors (the peristalsis) and factors which inhibit bacteri-al adhesion to the epithelium (gastric mucus, se-cretory IgA and epithelial desquamation)40,41.Moreover, gut micloflora plays a crucial role in the development of intestinal defences: the colonization with diverse intestinal microbes, in fact, is necessary for the synthesis and the secre-tion of polymeric immunoglobulin A and the generation of a balanced T Helper cell response. By studying germ-free animals, it results that neither function exists in the germ-free state, but rapidly develops after germ colonization42.In-testinal bacteria maintain “a physiological in-flammation” in the human gut which is efficient-ly protective and necessary to have an appropri-ate local immune response, while a disregulation of the mucosal immune response can switch a “controlled” toward an “uncontrolled”intestinal inflammation, paving the way to pathology43. Therefore, when intestinal bacteria exceed, this label equilibrium can be broken. The presence of a higher bacterial number in the small bowel causes a premature and abnormal deconjugation of the bile acids, determining a larger jejunal re-absorption and secondary lipid malabsorption. Moreover, contaminant bacteria can cause a di-rect damage on entherocytes because of their adesivity on epithelial surface and because of their competition with entherocytes for the link with the complex vitamin B12 – intrinsic factor. This results in a reduction of the vitamin B12 ab-sorption. Even if some type of bacteria can pro-duce the vitamin theirselves, finally the subject has reduced levels of bio-availability of vitamin B12 and can have malabsorption symptoms40. Otherwise, patients affected by SIBO often suffer from a nebulouse symptomatology charac-terized by diarrhea, flatulence, abdominal pain or discomfort. Underlying these symptoms, there is the glucidic malabsorption, which causes an ac-centuated fermentation and then higher produc-tion of water, short chain fatty acids and gas such as carbon dioxide, hydrogen and methane44. Whether the presence of SIBO leads to small intestinal mucosal changes is not well known. There are some investigations about the histolog-ical changes caused by SIBO in animal models, where changes of villus and crypt architecture and an increase in chronic inflammatory cells number – mostly lymphocytes of the lamina pro-pria – have been shown45-47.Recently, a retrospective study has been per-formed on 122 subjects who underwent upper gastrointestinal endoscopic examination because of gastrointestinal symptoms. Among these pa-tients, 67 was affected by SIBO (as assessed by duodenal aspirate culture >105CF U/ml), whileC. Fundarò, C. Fantacci, V. Ansuini, V. Giorgio, S. Filoni, F. Barbaro, A. Gasbarrini, C. Rossi133255 had a negative culture (<105CF U/ml) and they were considered controls. F rom these duo-denal biopsy has emerged one feature significant-ly more frequent in SIBO than in controls, which was villous blunting to crypt ratio (<3:1)48.SIBO seems, also, to determine a higher level of IgA in the proximal small intestine particular-ly when the overgrowth is caused by colonic type bacteria 49. Nevertheless, no study performed on patients with SIBO about direct parameters that indicates the number of leucocytes neutrophils in the gut wall are available. Montalto et al 24have published about F C concentrations in adults af-fected by SIBO considering it as an indirect para-meter of intestinal inflammation. Their results suggested that no inflammatory changes involv-ing neutrophils occurs in SIBO. On the edge of this finding, we have evaluated for the first time F C concentrations in a pediatric population af-fected by SIBO, comparing this values with healthy controls. No statistically significant dif-ferences have been found between cases and con-trol subjects (p = 0.07), according to the findings observed in adults. This confirms the hypothesis that no subclinical intestinal inflammation in-volving neutrophils occurs in patients with high-er proliferation of bacteria in the small bowel.The presence of high FC levels in children affect-ed by SIBO might not be caused by bacterial overgrowth itself and, in this case, another cause should be investigated.In conclusion, our study demonstrates for the first time that F ecal Calprotectin values do not increase in children affected by SIBO. Our re-sults are similar to the findings obtained in adults, supporting the hypothesis that no subclin-ical intestinal inflammation involving neutrophils occurs in SIBO.References1)F AGERHOL MK.Nomenclature for proteins: is Calpro-tectin a proper name for the elusive myelomonocyt-ic protein? J Clin Pathol 1996; 49: M74-79.2)D ORIN JR, E MSLIE E, V AN H EYNINGEN V .Related calci-um-bindings proteins map to the same subregion of chromosome 1q and to an extended region of synteny on mouse chromosome 3. Genomics 1990; 8: 420-426.3)S CHÄFER BW , H EIZMANN CW .The S100 family of EF-hand calcium-binding proteins: functions and pathol-ogy . T rends Biochem Sci 1996; 21: 134-140.1333Fecal Calprotectin concentration in children affected by SIBO4)F AGERHOL MK, D ALE I, A NDERSON I . Release andquantitation of a leukocyte derived protein (L 1).Scand J Haematol 1980; 24: 393-398.5)J OHNE B, F AGERHOL MK, L YBERG T, P R YDZ H,B RANDTZAEG P , N AESS -A NDRESEN CF , D ALE I . Functional and clinical aspects of the myelomonocyte protein calprotectin. Mol Pathol 1997; 50: 113-123.6)B ERNTZEN HB, F AGERHOL MK . L I, a major granulo-cyte protein: isolation of high quantities of its sub-units. Scand J Clin Lab Invest 1990; 50: 769-774.7)V OGANATSI A, P ANYUTICH A, M IYASAKI KT, M URTHY RK.Mechanism of extracellular release of human neutrophil calprotectin complex. J L eukoc Biol 2001; 70: 130-134.8)P OULLIS A, F OSTER R, M ENDALL MA, F AGERHOL MK .Emerging role of calprotectin in gastroenterology.J Gastr Hepatol 2003; 18: 756-762.9)B ERNI C ANANI R, R OMANO MT, T ERRIN G, R APACCIUOLOL . Fecal calprotectin is a useful diagnostic tool in pediatric gastroenterology. It J Pediatr 2005; 32:89-94. 10)N AESS -A NDRESEN CF , E NGELANDSDAL B, F AGERHOL MK .Calcium binding and concomitant changes in the structure and heat stability of calprotectin (L1 pro-tein). Clin Mol Pathol 1995; 48: M278-284.11)R ØSETH AG.Determination of fecal calprotectin, anovel marker of organic gastrointestinal disor-ders. Dig Liver Dis 2003; 35: 607-609.12)A ADLAND E, F AGERHOL MK.Fecal calprotectin: amarker of inflammation throughout the intestinal tract. 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Dig Liver Dis 2004; 36: 467-470.17)C ARROCCIO A, I ACONO G, C OTTONE M, D I P RIMA L,C ARTABELLOTTA F , C AVATAIO F , S CALICI C, M ONTALTO G,D I F EDE G, R INI G, N OTARBARTOLO A, A VERNA MR . Di-C. Fundarò, C. Fantacci, V. Ansuini, V. Giorgio, S. Filoni, F. Barbaro, A. Gasbarrini, C. Rossiagnostic accuracy of fecal calprotectin assay in distinguishing organic causes of chronic diarrhea from irritable bowel syndrome: a prospective study in adults and children. Clin Chem 2003; 49: 861-867.18)B AYELI PF, M ARIOTTINI M, L ISI L, F ERRARI P, T EDONE F.Guidelines on intestinal dysmicrobism (SIBO Small Intestine Bacterial Overgrowth). Minerva Gastroenterol Dietol 1999; 45: 297-308.19)R ANA SV, B HARDWAJ SB.Small intestinal bacterialovergrowth. Scand J Gastroenterol 2008; 43: 1030-1037.20)S INGH VV, T OSKES PP.Small bowel bacterial over-growth: presentation, diagnosis, and treatment.Curr Treat Options Gastroenterol 2004; 7: 19-28.21)R HODES JM, M IDDLETON P, J EWELL DP. 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Dig Dis 2008; 26: 183-186.25)B UNN SK, B ISSET WM, M AIN MJC, G RAY ES, O LSON S,G OLDEN BE.Fecal Calprotectin: validation as anoninvasive measure of bowel inflammation in childhood inflammatory bowel disease. J Pediatr Gastr Nutr 2001; 33: 14-22.26)L EACH ST, Y ANG Z, M ESSINA I, S ONG C, G ECZY CL,C UNNINGHAM AM,D AY AS.Serum and mucosalS100 proteins, calprotectin (S100A8/S100A9) and S100A12, are elevated at diagnosis in chil-dren with inflammatory bowel disease. Scand J Gastroenterol 2007; 42: 1321-1331.27)D E J ONG NS, L EACH ST, D AY AS.Fecal S100A12: anovel noninvasive marker in children with Crohn’s disease. Inflamm Bowel Dis 2006; 12: 566-572.28)F AGERBERG U L, LÖÖF L, M YRDAL U, H ANSSON LO,F INKEL Y.Colorectal inflammation is well predictedby fecal calprotectin in children with gastrointesti-nal symptoms. 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氢气甲烷二氧化碳呼气试验 新技术新项目

氢气甲烷二氧化碳呼气试验 新技术新项目

氢气甲烷二氧化碳呼气试验新技术新项目氢气甲烷二氧化碳呼气试验是一项新技术新项目,通过呼气气体的分析,在临床和科研领域提供了一种便捷、无创、可重复性高的评估方法,用于监测和诊断患者的肺功能和代谢情况。

本文将从技术原理、应用领域、优势和挑战等方面进行介绍。

技术原理:氢气甲烷二氧化碳呼气试验基于肺部气体交换和代谢过程,通过分析呼气气体中的气体成分,了解患者的肺功能和代谢情况。

这些气体成分包括氢气、甲烷和二氧化碳。

通常在测试前,患者会被要求采取一些准备措施,如禁食、禁止吸烟和饮酒等。

在实际测试中,患者通过呼吸进入的空气含有不同浓度的这些气体,通过呼吸将其排出体外。

然后这些呼气气体被采集和分析,从而得到相关指标。

应用领域:氢气甲烷二氧化碳呼气试验广泛应用于临床和科研领域,可用于以下方面:1.消化系统疾病:氢气甲烷呼气试验可用于检测乳糖不耐受、蔗糖不耐受和细菌过度生长等消化系统疾病。

通过分析呼气中的氢气和甲烷含量,可以评估患者对乳糖和蔗糖的消化和吸收情况,并诊断细菌过度生长引起的消化问题。

2.肝功能评估:氢气呼气试验还可用于评估肝功能。

在肝疾病患者中,由于肝脏代谢能力的降低,氢气的清除能力也会受到影响。

通过分析呼气中的氢气浓度,可以间接评估肝功能的状况。

3.肺功能评估:二氧化碳呼气试验可用于评估肺功能,如慢性阻塞性肺疾病、哮喘等。

患者在测试过程中需吸入含有不同浓度二氧化碳的气体,然后呼气时二氧化碳的浓度会被测量和分析,从而评估肺功能的情况。

优势:氢气甲烷二氧化碳呼气试验具有以下优势:1.无创性:呼气试验不需要穿刺和取样,对患者没有任何伤害,非常适合临床应用。

2.便捷性:呼气试验操作简便,无需特殊仪器和复杂的操作。

通常只需要在测试前作一些准备措施即可进行。

3.可重复性:呼气试验结果可重复性高,多次测试的结果具有较好的一致性。

这使得呼气试验成为一种可靠的监测和评估方法。

挑战:尽管氢气甲烷二氧化碳呼气试验在临床和科研领域有广泛应用,但也面临一些挑战:1.结果解读:呼气试验结果的解读需要专业医生进行,对于一般人来说可能较难理解。

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传统检查方法的缺点
• 正常情况下,小肠内是相对无菌的,但在胃大部切除术后 污染综合症、盲肠综合症及肝硬化腹水等情况下进入小肠 的细菌过多超出清除能力,引起小肠内细菌过度生长。以 往是以小肠液培养为诊断的金标准,此法要求具有较高的 操作技术和设备条件,同时给患者带来较大的痛苦,难以 在临床推广,(1)不能完全避免口轻污染的影响,(2) 直接培养从复性仅38%,(3)培养标本仅限于小肠上断。 口服糖类物质和口服乳果糖作BHT,两种方法有高度显著 相关性,说明BHT是一种测定小肠细菌过度生长比较准确 可靠的方法。 • 乳糖不耐受因先天性酶表达异常或肠道损伤引起酶活性降 低所致。BHT诊断该病优于乳糖耐受试验或空肠活检。
市场有多大
Quitron甲烷氢呼气产品特点 • Safe 安全 • Simple 简便 • Special 独特 • Sensitive 灵敏 • Specificity 特异 • Speed 快速
Quintron技术特点
• • • • • 采用固态传感器 有流量控制设计,可以排除外界干扰,确保数据的准确性 有样品除湿装置,防止湿气对结果的干扰。 有双重除尘装置,防止空气污染的影响。 有排气泵,在每次检测后,可以有效地排出设备中的残余样品, 确保每次检测的样品都在同样的基础。 • 有独特设计的样品采集器,不测量死腔的气体,确保检测的是 真正肺泡中的气体。 • 可靠性强,优秀的可重复性。不受外界环境和病人呼气方式的 影响。不受检测次数的影响。 • 还有校正因素,可以确保校正和测量的准确性,可以明确诊断 处于边缘结果的病人。
乳糖不耐受检测的重要性
• 乳糖酶缺乏(LD)所引起的乳糖吸收不良(LM)和乳糖 不耐受(LI)极为常见,多年来临床对儿童认识不足, 小儿腹泻常引起继发性乳糖不耐受症(SLI),对因LI 腹泻病患儿仍鼓励进食含乳糖丰富的母乳及奶制 品,导致部分患儿腹泻加重或迁延。 • 小儿腹泻尤其是轮状病毒性肠炎时,应常规进行 乳糖不耐受试验的检测,及早发现 ,避免滥用抗 生素并及时指导治疗,有利于患儿早日康复。 • 腹泻婴幼儿应及早做乳糖不耐受试验,避免因腹 泻而滥用抗生素,引起菌群失调,延误病情,加 重经济负担。
甲烷和氢呼气试验
E-mail: abs94555@ bjabs2011@
北美医学教育基金会
目录
• • • • • 前言 Quitron甲烷氢呼气产品特点 甲烷和氢呼气试验原理 甲烷和氢呼气试验的临床用途 甲烷呼气试验的重要性
好产品
深圳大学核技术应用联合研究所所长、研究员。
Lanzkowsky P, et a1. Disaccharidase values in Iron—deficient infants[J].Journal of Pediatrics, 1981,123(99):605—608. Sadowitz PD, Oski FA. Iron Status and infant feeding practices in an urban ambulatory center[J]. Pediatrics,1983,72 (1):33—36.
– 李俊娜等,呼气氢试验在消化系疾病诊断治疗中的研究进展。河 南科技大学学报(医学版),2006年12月24卷第4期,314-315.
临床意义
• 填补国际胰腺功能检查的盲区,诊断胰腺炎后的胰 腺损伤程度可评价糖尿病的病因和预后。 • 诊断和治疗不明原因的长期腹泻及腹胀、消化不良 综合症、儿童和成人的乳糖酶缺乏症、小肠细菌过 度生长。 • 慢性便秘的病因测定肠道通过时间和回盲瓣功能障 碍。 • 诊断糖尿病患者自主神经节病变所致的胃肠动力异 常。 • 对慢性结肠炎合并碳水化合物吸收不良,确定其肠 道感染状况及是否有吸收不良暨严重程度。 • 评价亚健康状况常伴有小肠细菌过度生长
• 呼气氢试验诊断乳糖吸收不良症时,假阳性结果较少见, 如发生,可能与操作因素,包括试验前抽烟、睡眠状态或 膳食中纤维素过量等有关。
儿童乳糖不耐受症与营养吸收
• P Lanzkowsky等发现,儿童乳糖不耐受与严重铁缺乏性贫血(血红蛋白 <7.2 g/L)有一定的联系。1O名贫血婴儿(8~20月,平均14.6月)血红蛋 白平均仅为6.4g/L(5.2~7.1g/L),血细胞比容平均21.8(17.5 ~24.3 ), 血清中铁的含量平均24.3~g/L(12~35~g/L)。而这1O名儿童中有6名 乳糖不耐受。 • PD Sadowitz等同样发现9~12个月的婴儿喂养牛奶会造成33.3 的铁缺 乏。牛奶中的铁含量非常少,而且乳糖不耐受和乳糖吸收不良会造成 铁吸收障碍,某种意义上牛奶成为了儿童和青少年铁缺乏的一种病原
底物 乳果糖 乳糖 山梨醇 牛奶 试餐口盲时间(分钟) 73.0±6.5 146.8±65.9 73.9±20.4 113±9 192±16
胃肠通过时间(口盲时间)
结论:1.胃肠通过时间75分钟:正常 2.无小肠细菌过增长 3.回盲瓣功能完好
口盲时间:氢呼气试验
杨月欣等,中国儿童乳糖不耐受发生率的调查研究,卫生研究,第28卷,第1期,44-46页。
果糖不耐受症
• 遗传性果糖不耐受症,又称果糖-1,6-二磷酸醛缩酶缺陷病,是婴儿饮食中开 始含有果糖时出现的一种严重疾病,它是由于肝、肾、小肠中醛缩酶B活性缺 乏所致。果糖-1,6-二磷酸醛缩酶催化果糖-1,6-二磷酸水解生成磷酸丙糖和磷 酸甘油醛。此酶活性缺乏导致患者吸收果糖后,体内果糖-1-磷酸迅速聚集, 引起 遗传性果糖不耐症患者在吸收果糖或者蔗糖(通常从水果、果汁或者糖化的 谷类摄取)前无任何临床症状。若新生儿出生后即服用含这些糖类的食物或 者配方奶粉,患儿会很快出现症状。 早期临床表现类似半乳糖血症,包括黄疸、肝大、呕吐、萎靡、易激惹和惊 厥。实验室检查包括凝血时间延长、低白蛋白血症、胆红素转氨酶升高和近 端肾小管功能障碍。急性果糖摄入导致患者出现低血糖症状;长期摄入果糖 ,患者会出现生长迟缓和肝脏病变。若持续摄入果糖,低血糖症状反复发作 ,肝肾功能衰竭进展,最终患者死亡。严重的毒性症状。


果糖不耐受
没有果糖不耐受:果糖氢呼气试验 结果阴性。
果糖不耐受:果糖氢呼气试验结果 阳性。
同一个人:糖不耐受试验
胃肠通过时间(口盲时间)
• 口服小肠不吸收性糖如乳果糖后,呼气中H2排出升高所需的时间,即 代表口至盲肠传递时间,即小肠传递时间,正常为60~120分钟。 • 由于乳果糖可保留肠腔内水分,并可增加肠动力,因此一般以小剂量 (10g)作为标准剂量。 • 如果受检者为不产生氢气者(可高达25%),则可测定口服乳果糖后 呼气中CH4。
• 呼气氢试验最早被用于乳糖吸收不良症的诊断。 • 当肠道吸收细胞病变或缺乏膜结合性双糖酶,如乳糖酶、 蔗糖-异麦芽糖酶或麦芽糖酶等时,相应的糖摄入后均可 直接进入结肠并产生氢气,并被检测出,而明确诊断。
• 与诊断乳糖吸收不良症的其它方法,如空肠粘膜活检标本 乳糖酶活性直接测定,或间接的乳糖耐受试验等相比,结 果极为一致,而具有非侵入性及简便等优点。
利用呼气氢方法进行小肠传递时间测定,对小肠动力学研究具有重要价值,已被广泛地应 用于药代动力学、生理学、营养学以及临床多种疾病状态时的研究,并证明呼气氢试验是 一种简易、灵敏及重复性好的口至盲肠传递时间的测定方法。
碳水化合物吸收不良
• • • • • • • • 乳糖、乳果糖酶缺乏症 山梨醇吸收不良症 海藻糖酶缺乏症 木糖吸收不良症 果糖吸收不良症 葡萄糖吸收不良症 蔗糖吸收不良症 其它碳水化合物
• 当肠道吸收细胞病变或缺乏膜结合性双糖酶,如乳糖酶、 蔗糖-异麦芽糖酶或麦芽糖酶等时,相应的糖摄入后均可 直接进入结肠并产生甲烷和氢气,并被检测出,而明确诊 断。
甲烷和氢呼气试验的机制
正常人呼出气中氢气浓度变化
呼气氢仪器技术原理
• 气相色谱法:采用氢离子探头或以氢气为载 体的热导气相色谱仪,近年采用以空气为 载体的固相探头检测; • 电化学检测法:采用电化学法使呼出气标本 中H2氧化生成水,以百万分之一浓度10xl06/L或ppm表示H2含量。 • 固态传感器检测法:
呼气试验的优点
• 高灵敏性和特异性
– 几乎都达到100%
• 可以检测整个小肠
– 明显优于传统活检方法
• 检查项目多
– 根据不同底物
传统的诊断碳水化合物吸收不良症的方法需抽血或粘膜活检,操作需一定的专业 技术,且给患者带来一定的痛苦。
甲烷和氢呼气原理
• 正常人体平静状况下是不产生甲烷和氢的,其唯一来源只能是与人体 相伴的肠道内的细菌。 • 厌氧菌偏好代谢的糖类分子,糖分子作为发酵反应最初的阶段,被分 解成短链脂肪酸(SCFA),二氧化碳、甲烷和氢气。
甲烷和氢呼气试验原理
什么是呼气试验
• 给受检者口服一定量的试验底物,通过检 测呼出气中的二氧化碳(CO2)、氢气(H2)、 甲烷(CH4)等浓度的变化,进行生理及或疾 病研究的方法。 • 是一种重要的无创检查胃肠与肝、胰功能 的手段。在消化病临床与科研领域被有广 泛应用价值。 • 具有无创、方便、灵敏、准确、可靠等优 点。
甲烷和氢呼气的临床应用
• • • • • • • • • • • • 碳水化合物不耐受:吸收不良、过敏 胃肠通过时间 判断小肠粘膜完整性 小肠细菌过度生长 胃酸分泌 胰腺功能测定 消化系统肿瘤胃肠功能评估 肝病胃肠功能评估 用于食品营养学 消化道微生态学 结肠镜检查前肠道清洁程度评估等 药理学研究
判断小肠粘膜完整性
• 口服微量的且正常吸收量不大的碳水化合 物(如山梨醇、木糖)后出现明显呼气氢 浓度升高,提示广泛小肠粘膜损伤。用于 乳糜泻等弥漫性小肠疾病早期筛查。
传统方法的问题
• 以往临床上缺乏简便有效的诊断方法,通常以小肠液细菌 培养作为诊断的金标准。但此法需插管,给患者带来极大 痛苦,且现已证明直接细菌培养诊断小肠细菌过生长并不 可靠,不能作为评价其它诊断方法的参照标准。 • 首先,抽吸小肠液标本时无法避免口腔细菌的污染, • 其次,实验证实直接细菌培养的重复性仅为38%, • 并且小肠细菌过生长,标本培养仅限于小肠上段,而大多 数小肠细菌过生长的发生是结肠型菌群向近段小肠移行。 此时,远段小肠的细菌量显然是极度增多,然而要取得远 段小肠液标本培养几乎是不可能的。
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