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氢气和甲烷呼气试验 (25)

SUBJECTS AND METHODS
Subjects Fifteen patients with IBS (8 women and 7 men; age (mean 2 SD), 49 2 12 years) and 24 healthy subjects (19 women and 5 men; age, 38 2 16 years), who acted as a control group, participated in the study. Healthy subjects had n o significant gastrointestinal symptoms, were not taking reg-
Fructose-Sorbitol In Gastroenterol Downloaded from by Francis A Countway Library of Medicine on 12/25/12 For personal use only.
different from that in healthy volunteers. Even though symptom provocation was more prevalent in the IBS group than in controls, the authors concluded that fructose-sorbitol malabsorption was not important in the aetiology of IBS, ascribing their findings to the previously identified tendency of IBS patients to react to various intestinal stimuli (11). We therefore felt it appropriate to define further, in IBS patients and controls, the responses to ingestion of combinations of fructose and sorbitol. Two different mixtures of fructose and sorbitol were thus administered to compare, in the same subject, differences in symptom provocation and to relate differences in the extent of intestinal hydrogen production to such symptom provocation.

氢气和甲烷呼气试验 (39)

J oseph H. S ellin , M DA Breath of Fresh AirB ratten J R, Spanier J , Jones M P: L actulosebreath testing does not discriminate patients with irritable bowel syndrome from healthy controls. A m J Gastroenterol 2008, 103: 958–963. R ating: •Of importance.I ntroduction: O ver the past few years, the hypothesis that irritable bowel syndrome (IBS) is commonly associated with small intestinal bacterial overgrowth (SIBO) has gained considerable currency. The SIBO associated with IBS has been characterized as distal, involving the ileum, rather than proximal. A presumptive diagnosis has been obtained with a positive lactulose hydrogen breath test (LHBT). Proof of principle has been established by antibiotic treatment, which both improves symptoms and normalizes the LHBT. Despite some clinical acceptance of this hypothesis, there have been concerns about the accuracy of the LHBT for SIBO.A positive H 2breath test occurs when a test sugar is not absorbed in the small intestine and is subject to colonic bacterial metabolism or, alternatively, when the presence of an abnormal amount of bacteria in the small intestine results in metabolism of the test sugar proximal to the ileocecal valve.L actulose, a nonabsorbable disaccharide, would be expected to pass into the colon and produce an H 2signal. In fact, the initial use of the LHBT was as a measure of orocecal transit time. However, if lactulose were to pro-vide an “early” signal or a double peak resulting from fi rst SIBO and then colonic metabolism, then the LHBT could serve as a useful and convenient test for SIBO.U sing the LHBT, Pimentel and colleagues [ 1 , 2 ] have observed that most patients with IBS have concomitant SIBO. However, concerns about the criteria used for the diagnosis of SIBO gave rise to questions about the accu-racy of the diagnosis.A ims: T o determine the incidence of abnormal LHBTs in a well-defi ned population of IBS patients and healthy con-trols and to fi nd out whether there is a specifi c correlation between symptoms and patterns observed on breath tests.M ethods: B reath testing was performed on 224 patients meeting Rome II diagnostic criteria for IBS and 40 healthy controls. Serial collections of H 2and methane were obtained every 20 minutes for 180 minutes after inges-tion of 10 g of lactulose mixed in 240 mL of water. Three criteria previously used to diagnose SIBO were used:• breath H 2> 20 ppm before 180 minutes • dual breath H 2peaks • increase in breath H 2in < 90 minutes R esults: U sing these criteria, there was no signifi cant dif-ference between IBS patients and healthy controls in the percentage of abnormal studies. A substantial majority (74%) of IBS patients had an abnormal study, similar to the results in the literature. However, 85% of healthy controls also had an abnormal LHBT. The double-peak pattern was least commonly observed, but it was found in 15% of patients and 20% of controls. Not surprisingly, there was a positive H 2signal by 180 minutes in 78% of patients and 70% of controls. In the shorter period of 90 minutes, there still was a large number of positive tests, 35% in patients and 45% in controls. The proportion of methane producers in the IBS group (20%) was not dif-ferent from that in the control group (15%); in the IBS group, methane producers were more likely than nonpro-ducers to complain of constipation.D iscussion: T he rate of abnormal lactulose breath tests was similarly high in healthy normal controls and patients with IBS. Theoretically, the normal controls could have occult SIBO, but this seems improbable. It is more likely that the diagnostic criteria for a positive test are not specifi c enough, resulting in unacceptably high false posi-tivity. The rate of positive LHBTs in normal controls in this study is much higher than the rate seen by Pimentel et al. [ 1 , 2 ] but is similar to rates seen by others [ 3 , 4 ]. The present study included the largest number of healthy con-trols and therefore provides insight into the patterns of response that might reasonably be expected in a normal population.E ditor’s comments diagnostic studies, and treatment of IBS has been a chal-lenging and elusive goal. The hypothesis that SIBO is a common factor in IBS provides an opportunity to rethink some of the basics of the disease and ask some pertinentquestions: Are the proposed etiology and pathophysiology plausible? How accurate are the diagnostic tests used? How effective and targeted is the therapy? T he new article by Bratten et al. addresses the sec-ond of these issues—how do we establish a diagnosis of SIBO? What’s a good test for SIBO? Unfortunately, there442 Small Intestineis none. Culturing the small bowel is arduous and rarelydone outside a research setting. The 14Ccholylglycine breath test was an ingenious attempt to take advantage of the physiology of bile salts. Bacterial overgrowth would lead to deconjugation and early absorption of luminal bile salts, whereas ileal disease would lead to an increase in colonic bile salts and, thus, a later signal. Unfortunately, the ability to separate out “early” and “late” limited the usefulness of the test. This problem will be a recurring theme in the limitations of breath tests.T he 14C-D-xylose breath test has proved to be fairly specifi c and sensitive but is not widely available. The lure of hydrogen breath testing is that it is relatively simple, inexpensive, noninvasive, and can be obtained in aca-demic and community hospitals. Unfortunately, to put it simply, breath tests are not that good.G iven the catechism that glucose is rapidly and effi -ciently absorbed in the upper small bowel, a positive glucose H 2breath test is assumed to represent small bowel bacterial overgrowth in the duodenum or jejunum. Similarly, lactu-lose may be a reasonable test sugar to examine overgrowth in the ileum, but numerous studies document the lack of sensitivity and specifi city of these breath tests [ 5 , 6 ].T he major factor that accounts for this problem is the unpredictability of small bowel transit time. The period that can be considered normal orocecal transit time varies widely. Diarrhea from any cause may alter transit time, and lactulose itself has been shown to accelerate intestinal transit.T he specifi city of breath testing can be improved con-siderably if it is combined with an intestinal transit scan obtained with nuclear scintigraphy. This approach, fi rst used with glucose H 2 breath testing [ 7 ] and subsequently with lactulose [ 8 ], makes it possible to determine how the timing of an H 2signal correlates with transit along the intestine. Surprisingly, it is possible to observe a posi-tive glucose H 2 signal in individuals with rapid intestinal transit [ 7 ]. A more accurate diagnosis of SIBO or, alter-natively, of rapid intestinal transit would permit a more focused treatment strategy.T he new study by Bratten et al. does not necessarily refute the hypothesis of SIBO but points out signifi cant problems with the accuracy of the tests involved. What about the documented symptom improvement and “nor-malization” of breath tests after the use of antibiotics? It is important to note that the most commonly used antibi-otic for SIBO, rifaximin, is given at a dose considerablyhigher than that used to treat infectious diarrhea, lead-ing to the interesting speculation that the improvement observed in patients with IBS is a result of unintended or unexpected consequences. High-dose antibiotics may alter the number and/or type of colonic fl ora and thereby decrease symptoms. This effect may result in changes in the pattern of breath tests and certainly could account for the decrease in bloating, the symptom that appears to improve most consistently in these studies. Measurement of the area under the curve for overall H 2production may provide an opportunity to test this hypothesis.T he study should serve to move the fi eld forward. More specifi c testing for SIBO (combined H 2and scintig-raphy testing) can give us a more accurate diagnosis. A greater focus on the role of colonic fl ora may provide an opportunity to rethink (once again) the role of intestinal bacteria in IBS.D isclosure N o potential confl ict of interest relevant to this article was reported.R eferences 1. P imentel M , C how E J, L in H C:E radication of small intesti-nal bacterial overgrowth reduces symptoms of irritable bowel syndrome. A m J Gastroenterol 2000, 95: 3503– 3506. 2. P imentel M , C how E J, L in H C: N ormalization of lactulosebreath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study. A m J Gastroenterol 2003, 98: 412– 419. 3. P osserud I , S totzer P O, B jornsson E S, e t al. : S mall intesti-nal bacterial overgrowth in patients with irritable bowelsyndrome. G ut 2007, 56: 802– 808. 4. W alters B , V anner S J: D etection of bacterial overgrowth inIBS using the lactulose H2 breath test: comparison with 14C-D-xylose and healthy controls. A m J Gastroenterol 2005, 100: 1566– 1570. 5. K erlin P , W ong L :B reath hydrogen testing in bacterial overgrowth of the small intestine. G astroenterology 1988, 95: 982– 988. 6. M ac Mahon M , G ibbons N , M ullins E , e t al. : A re breathhydrogen tests valid in the elderly? G erontology 1996, 42: 40– 45. 7. S ellin J H, H art R :.G lucose malabsorption associated with rapid intestinal transit. A m J Gastroenterol 1992, 87: 584– 589. 8. R iordan S M, M cIver C J, W alker B M, e t al. : T he lactulosebreath test and small intestinal bacterial overgrowth. A m J Gastroenterol 1996, 91: 1795– 1803.。

甲烷和氢呼气sim

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。
肠内甲烷和氢气产生的机制
• 适量的糖类物质摄入后，一般均能被小肠吸收。但一些在小肠内吸收较差的糖，如D-木糖，或小肠内不能消化的糖，如乳果糖、棉子糖及纤维素等，摄入后即直接进入结肠，并被结肠菌株分解或发酵产生氢气。所产甲烷和氢气除大部分被排出外，约14％～21％吸收后从肺呼出。 • 正常呼气中仅含极微量的甲烷和氢气，但肠内只要有2g以上的糖类物质发酵，呼气中的甲烷和氢气含量即可以明显增高，并可被准确检出。
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．

甲烷氢呼气试验

检测步骤--数据分析
将测量数据填入“检查结果记录单”，并将其输入分析软件（Quintron，北美医学教育基金会推荐），系统将生成图形，通过分析各种气体浓度开始升高的时间，即峰型和丰度来判断有无糖类吸收不良及小肠细菌过度生长等。
北京大学第三医院
检查结果记录单
底物选择：乳果糖
标本袋编号 1
2
北京大学第三医院
使用技术
气相色谱技术电化学技术固态传感器技术
北京大学第三医院
呼气氢测试仪
北京大学第三医院
甲烷-氢气呼出气体分析仪
QuinTron家庭式呼吸测试仪正在迅速成为采集乳糖不耐受/吸收不良，果糖不耐受/吸收不良，小肠细菌过度生长(SIBO)和蔗糖不耐受/缺乏患者呼气样本的首选方法。
标本袋编号 1
2
3
4
5
6
7
8
9 10
时间间隔
0 20 40 60 80 100 120 140 160 180
呼气时间
北京大学第三医院
气体收集
4.全部呼气结束后，将这10个标本袋、检查记录单和呼气装置放在运输袋中，24小时内送至化验室进行测量分析。
北京大学第三医院
甲烷和氢呼气试验原理
北京大学第三医院
需要记录数据，按归零键，屏幕上的数字消失后，方可重新注气，
进行下一次测量。
北京大学第三医院
检测结果的判读
北京大学第三医院
小肠细菌过度生长诊断标准
H2 ≧ 12 H2 + CH4 ≧ 15 CH4 ≧ 20
北京大学第三医院
临床应用
碳水化合物不耐受：吸收不良、过敏小肠细菌过度生长胃肠通过时间判断小肠粘膜完整性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

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。

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. Eur J Gastroenterol Hepatol 2002; 14: 823-825.13)R ØSETH AG, F AGERHOL MK, A ADLAND E, S CHJØNSBY H.Assessment of the neutrophil dominating protein calprotectin in feces. A methodologic study.Scand J Gastroenterol 1992; 27: 793-798.14)O LAFSDOTTIR E, A KSNES L, F LUGE G, B ERSTAD A . Faecalcalprotectin levels in infants with infantile colic,healthy infants, children with inflammatory bowel disease, children with recurrent abdominal pain and healthy children. Acta Paediatr 2002; 91: 45-50.15)K AISER T, L ANGHORST J, W ITTKOWSKI H, B ECKER K,F RIEDRICH AW , R UEFFER A, D OBOS GJ, R OTH J, F OELL D.Faecal S100A12 as a non-invasive marker dis-tinguishing inflammatory bowel disease from irri-table bowel syndrome. Gut 2007; 56: 1706-1713.16)B ERNI C ANANI R, R APACCIUOLO L, R OMANO MT, T ANTUR -RI DE H ORATIO L, T ERRIN G, M ANGUSO F , C IRILLO P , P A -PARO F , T RONCONE R.Diagnostic value of faecal cal-protectin in pediatric gastroenterology clinical practice. 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. The lactulosehydrogen breath test as a diagnostic test for small-bowel bacterial overgrowth. Scand J Gas-troenterol 1979; 14: 333-336.22)M ENDOZA E, C RISMATT C, M ATOS R, S ABAGH O, C AMPOM, C EPEDA J, V ILLANUEVA D. Diagnosis of small in-testinal bacterial overgrowth in children: the use of lactulose in the breath hydrogen test as a screening test. Biomedica 2007; 27: 325-332. 23)V ON R OON AC, K ARAMOUNTZOS L, P URKAYASTHA S,R EESE GE, D ARZI AW, T EARE JP, T EARE JP, P ARASKEVA P, T EKKIS PP.Diagnostic precision of fecal calprotectin for inflammatory bowel diseases and colorectal malignancy. Am J Gastroenterol 2007; 102: 803-813.24)M ONTALTO M, S ANTORO L, D ALVAI S, C URIGLIANO V,D’O NOFRIO F, S CARPELLINI E, C AMMAROTA G, P ANUNZI S,G ALLO A, G ASBARRINI A, G ASBARRINI G. Fecal calpro-tectin concentrations in patients with small intesti-nal bacterial overgrowth. 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. J Pediatr Gastr Nutr 2005; 40: 450-455.29)RØSETH AG, S CHMIDT PN, F AGERHOL MK.Correlationbetween faecal excretion of Indium-111-labelledgranulocytes and Calprotectin, a granulocytemarker protein, in patients with inflammatorybowel disease. Scand J Gastroenterol 1999; 34:50-54.30)L IMBURG PJ, A HLQUIST DA, S ANDBORN WJ, M AHONEYDW, D EVENS ME, H ARRINGTON JJ, Z INSMEISTER AR. Fe-cal Calprotectin levels predict colorectal inflam-mation among patients with chronic diarrhea re-ferred for colonscopy. Am J Gastroenterol 2000;95: 2831-2837.31)RØSETH AG, A ADLAND E, G RZYB K. Normalization ofFecal Calprotectin: a predictor of mucosal healingin patients with inflammatory bowel diseases.Scand J Gastroenterol 2004; 39: 1017-1020. 32)RØSETH AG, A ADLAND E, J AHNSEN J, R AKNERUD N. As-sessment of disease activity in ulcerative colitisby faecal calprotectin, a novel granulocyte markerprotein. Digestion 1997; 58: 176-180.33)H O GT, L EE HM, B RYDON G, T ING T, H ARE N, D RUM-MOND H, S HAND AG, B ARTOLO DC, W ILSON RG, D UN-LOP MG, A RNOTT ID, S ATSANGI J. Fecal calprotectin predicts the clinical course of acute severe ulcer-ative colitis. Am J Gastroenterol 2009; 104: 673-678.34)D IAMANTI A, C OLISTRO F, B ASSO MS, P APADATOU B,F RANCALANCI P, B RACCI F, M URACA M, K NAFELZ D, D EA NGELIS P, C ASTRO M. Clinical role of calprotectinassay in determining histological relapses in chil-dren affected by inflammatory bowel diseases. In-flamm Bowel Dis 2008; 14: 1229-1235.35)T IBBLE JA, S IGTHORSSON G, B RIDGER S, F AGERHOL MK,B JARNASON I.Surrogate markers of intestinal in-flammation are predictive of relapse in patientswith inflammatory bowel disease. Gastroenterolo-gy 2000; 119: 15-22.36)P ARDI DS, S ANDBORN WJ.Predicting relapse in pa-tients with inflammatory bowel disease: what isthe role of biomarkers? Gut 2005; 54: 321-322. 37)S APS M, D I L ORENZO C. 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甲烷氢呼气试验

甲烷氢呼气试验
北京大学第三医院
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Байду номын сангаас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。
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。
北京大学第三医院
临床意义
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。
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。
判定标准:
•胰腺外分泌功能轻度低：[H2]数据高于本底值10-20ppm，伴相关临床症状： •胰腺外分泌功能中度低下：[H2]数据高于本底值20-30ppm，伴相关临床症状： •胰腺外分泌功能重度低下：[H2]数据高于本底值30ppm及以上，伴相关临床症状：
北京大学第三医院
胰腺外分泌功能测定
有小肠细菌过度生长：葡萄糖氢呼气试验结果阳性。
北京大学第三医院
葡萄糖氢呼气检测SIBO
空肠细菌过度生长
回肠细菌过度生长
灵敏性：62%；特异性：83%
北京大学第三医院 Simrenetal.Gut2006;55:300-301
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。
判断小肠粘膜完整性

甲烷氢呼气试验ppt课件

甲烷氢呼气试验
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。
试验机制
适应症
·
腹泻、腹胀、腹痛、嗳气、恶心、呕吐
·
肠易激综合症（ IBS ）
·
碳水化合物吸收不良
使用技术

检测结果的判读
小肠细菌过度生长诊断标准
H2 ≧ 12 H2 + CH4 ≧ 15 CH4 ≧ 20

临床应用
碳水化合物不耐受：吸收不
良、过敏小肠细菌过度生长胃肠通过时间判断小肠粘膜完整性胃酸分泌胰腺功能测定
Байду номын сангаас
乳糖吸收不良
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，
验证，国际标准采用。 2、唯一采用固态传感器，性能稳定。 3、无创、无痛、即时、准确。 4、可同时测量氢气、甲烷和 CO2，世界独家。
操作步骤
患者准备
1.呼气前24小时内禁食乳制
品、豆制品、麦面制品和高纤维蔬菜等产氢食物，可进食米饭、肉、蛋类，避免过饱。 2.呼气前至少空腹12小时，除可以饮少量白开水之外，严禁一切饮料，严禁嚼口香糖，
患者准备
气体收集
1.按要求准备完善后进行呼
气检查，按顺序排列好110号气体收集标本袋。注意：不要打乱顺序或搞混，否则影
响结果判读。
气体收集
2.收集空腹呼气标本：先不
要喝任何东西，将“标本袋” 1安装在呼吸管上，用口含住滤嘴，平静呼气（不要深吸气或深呼气），将标本袋吹满，取下后立即旋紧封口。注意：标本袋要装满，不要漏气。

氢气甲烷呼气实验报告

一、实验目的1. 掌握氢气和甲烷呼气实验的操作方法。

2. 了解氢气和甲烷的性质，观察其燃烧现象。

3. 通过实验验证质量守恒定律，分析实验结果。

二、实验原理1. 氢气（H2）的性质：无色、无味、密度小于空气，熔点-259.2℃，沸点-252.77℃，难溶于水。

氢气具有可燃性，燃烧时产生淡蓝色火焰，生成水。

2. 甲烷（CH4）的性质：无色、无味、密度小于空气，熔点-182.5℃，沸点-161.5℃，难溶于水。

甲烷具有可燃性，燃烧时产生蓝色火焰，生成二氧化碳和水。

三、实验用品1. 火柴2. 氢气瓶3. 甲烷瓶4. 干燥的小烧杯5. 澄清石灰水6. 玻璃棒7. 烧杯8. 玻璃片9. 集气瓶四、实验步骤1. 准备工作a. 将氢气瓶和甲烷瓶分别置于干燥的桌面上。

b. 检查集气瓶、烧杯、玻璃棒等实验用品是否干燥。

2. 氢气呼气实验a. 点燃火柴，将火焰靠近氢气瓶口，观察氢气燃烧现象。

b. 将干燥的小烧杯罩在火焰上方，观察烧杯内壁是否有水珠生成。

c. 将蘸有澄清石灰水的小烧杯罩在火焰上方，观察石灰水是否变浑浊。

3. 甲烷呼气实验a. 点燃火柴，将火焰靠近甲烷瓶口，观察甲烷燃烧现象。

b. 将干燥的小烧杯罩在火焰上方，观察烧杯内壁是否有水珠生成。

c. 将蘸有澄清石灰水的小烧杯罩在火焰上方，观察石灰水是否变浑浊。

五、实验现象及分析1. 氢气呼气实验a. 氢气燃烧时产生淡蓝色火焰。

b. 烧杯内壁有水珠生成，证明氢气燃烧生成水。

c. 澄清石灰水无变化，证明氢气燃烧不生成二氧化碳。

2. 甲烷呼气实验a. 甲烷燃烧时产生蓝色火焰。

b. 烧杯内壁有水珠生成，证明甲烷燃烧生成水。

c. 澄清石灰水变浑浊，证明甲烷燃烧生成二氧化碳。

六、实验结论1. 氢气燃烧时只生成水，不生成二氧化碳。

2. 甲烷燃烧时生成二氧化碳和水。

3. 通过实验验证了质量守恒定律。

七、注意事项1. 实验过程中注意安全，避免火灾和爆炸事故。

2. 实验用品需保持干燥，以免影响实验结果。

氢气和甲烷呼气试验 (36)

Small-Intestinal Bacterial Overgrowth in Patients with Liver Cirrhosis,Diagnosed with Glucose H 2or CH 4Breath TestsC.-Y.YANG,C.-S.CHANG &G.-H.CHENDivision of Gastroenterology,Dept.of Internal Medicine,Taichung Veterans General Hospital,Taichung,TaiwanYang C-Y,Chang C-S,Chen G-H.Small-intestinal bacterial overgrowth in patients with liver cirrhosis,diagnosed with glucose H 2or CH 4breath tests.Scand J Gastroenterol 1998;33:867–871.Background:Small-intestinal bacterial overgrowth (SIBO)has been considered a predisposing factor of spontaneous bacterial peritonitis in cirrhotic patients by bacterial translocation or hematogenous spread during spontaneous bacteremia.We investigated 45cirrhotic patients and 28healthy subjects to assess the prevalence of SIBO and its relationship with the severity of liver dysfunction and the presence of ascites.Methods:Bacterial overgrowth was measured by the glucose hydrogen and methane breath test.Results:SIBO was documented in 16(35.6%)of the 45cirrhotic patients and in 1(3.6%)of the 28healthy controls.The prevalence of SIBO was signiﬁcantly higher in patients with Child–Pugh class B or C (50%)than in those with class A (19%)and had no relationship with the presence or absence of ascites.Conclusions:We conclude that the prevalence of SIBO in cirrhotic patients is approximately 35.6%and that it is related to the severity of liver disease.There was no difference among various causes of cirrhosis,such as viral,alcoholic,or idiopathic.Key words:Hydrogen;hydrogen breath test;liver cirrhosis;methane;small-intestinal bacterial over-growthGran-Hum Chen,M.D.,Division of Gastroenterology,Dept.of Internal Medicine,Taichung Veterans General Hospital,No.160,Sec.3,Chung-Kung Rd.,Taichung,Taiwan 40705(fax: 8864-3741318)Spontaneous bacterial peritonitis is a major and serious complication of liver cirrhosis,which may lead to deterio-rated liver function and even death.Gram-negative enteric bacilli have been documented in most of these infections.Although the precise mechanism is still obscure,bacterial translocation from the intestinal tract to the ascites is considered the possible mechanism (1).Small-intestinal bacterial overgrowth can increase the incidence of bacterial translocation (1).Morencos et al.(2)found the prevalence of small-intestinal bacterial overgrowth to be approximately one-third of patients with alcoholic cirrhosis.We have now designed this study to evaluate the prevalence of small-intestinal bacterial overgrowth among various causes of cirrhosis and included methane measurement to investigate the possible bias of ignoring the problem of non-hydrogen producers in hydrogen breath tests (3–5).MATERIALS AND METHODSForty-ﬁve patients with liver cirrhosis (34men,11women;mean age,57years;range,33–76years)and 28healthy controls with normal liver function and without signiﬁcant gastrointestinal symptoms (19men,9women;mean age,51years;range,34–76years)were included in this study.Cirrhosis was related to hepatitis B virus (HBV)in 22patients,to hepatitis C virus (HCV)in 14patients,and to alcohol intake in 6patients,and the etiology remained unknown in 3patients.The diagnosis was conﬁrmed by means of appropriate investigations,including clinical chem-istry,radiology,endoscopy,and liver biopsy.In accordance with the Child–Pugh criteria (6),21patients were classiﬁed as stage A,14patients as stage B,and 10patients as stage C.All subjects with diabetes mellitus,marked serum electrolyte imbalance disturbance,previous gastric surgery,scleroderma,hypothyroidism,use of drugs that suppress gastric acidity (such as histamine-2receptor antagonists,proton pump inhibitors)or inﬂuence gastrointestinal motility (such as anticholinergics,antidepressants,opioids,metoclopramide,and cisapride),or use of antibiotics in the month preceding the study were excluded.Bacterial overgrowth was measured by means of a glucose breath test (7).Breath samples were collected after an overnight fast (12h),and all the subjects were asked to avoid eating bread,pasta,and ﬁbers the previous evening because these foods may cause prolonged excretion of hydrogen (8,9).Cigarette smoking and exercise were not allowed for at least 2h before and during the test (10).End-expiratory breath samples were measured before and at 15-min intervals for 2h after the ingestion of 50g glucose in 200ml water by using a gas chromatograph (Microlyzer Model SC;Quintron,Wisc.,USA)(11).Results were expressed in parts per million (ppm).All values are expressed as mean values 6standard deviation (s )from the mean.On the basis of the results from the controls,the abnormalities of fasting breath concentrationS c a n d J G a s t r o e n t e r o l D o w n l o a d e d f r o m i n f o r m a h e a l t h c a r e .c o m b y F r a n c i s A C o u n t w a y L i b r a r y o f M e d i c i n e o n 12/29/12F o r p e r s o n a l u s e o n l y .were deﬁned as mean 2s .Small-intestinal bacterial over-growth was diagnosed as an increase in breath hydrogen or methane concentration mean 2s ppm above the basal value after glucose ingestion (7).Without adequate increase in hydrogen or methane concentration after glucose ingestion,high fasting breath hydrogen or methane levels were considered negative results.The unpaired Student’s t test was used to compare age,hydrogen level,and methane level in the control group and the patient group.The unpaired Student’s t test was also used to compare age,prothrombin time,albumin level,and bilirubin level between the positive group and the negative group of patients.The chi-square test or Fisher’s exact probability test was used for statistical analysis of the sex ratio,age more or less than 70years,presence or absence of ascites,Child classiﬁcation,and various causes of cirrhosis in the positive group and the negative group of patients.The chi-square test was also used to compare the sex ratio between the control group and the patient group.The level of signiﬁcance was taken as P <0.05.RESULTSThere was no statistically signiﬁcant difference in mean age or sex between the control group and the cirrhotic group (P >0.1and 0.3,respectively).For the 28controls the fasting H 2and CH 4levels were 5.8665.07ppm (range,2–26ppm)and 1.9663.16ppm (range,0–13ppm),respectively.The increase in the H 2and CH 4levels in the breath test after glucose intake in the control group was 3.2564.52ppm (range,0–23ppm)and 4.7164.92ppm (range,0–14ppm),respectively (Figs.1and 2).On the basis of results from the controls,the abnormalities of fasting breath H 2and CH 4concentration were deﬁned as 16and 9ppm,respec-tively.Small-intestinal bacterial overgrowth was diagnosed as an increase in breath hydrogen concentration of 13ppm or in methane concentrations of 15ppm above the basal value after glucose ingestion.Glucose hydrogen breath testThe fasting hydrogen levels in the controls andpatientsTable I.Characteristics of the cirrhotic patients with or without small-intestinal bacterial overgrowth (SIBO)VariablesSIBO ( )(n =16)SIBO (ÿ)(n =29)P value Mean age (years)59612556130.44*Age more/less than 70years 4:128:210.57*Sex,male/female ratio 12:422:70.61*Albumin (g/dl) 2.860.7 3.160.60.10*Bilirubin (mg/dl)3.162.94.166.30.54*Prothrombin time (sec)14.961.414.162.00.16*Ascites ( /ÿ)9:711:180.20**Nosigniﬁcance.S c a n d J G a s t r o e n t e r o l D o w n l o a d e d f r o m i n f o r m a h e a l t h c a r e .c o m b y F r a n c i s A C o u n t w a y L i b r a r y o f M e d i c i n e o n 12/29/12F o r p e r s o n a l u s e o n l y .were 5.865.1ppm and 13.6625.4ppm,respectively (P >0.05).Abnormal fasting hydrogen levels ( 16ppm)were noted in 10patients,and only 3of them had adequate in-crease in breath hydrogen to meet the criterion of small-intestinal bacterial overgrowth;the other 7patients,lacking adequate increase in breath hydrogen level after glucose ingestion,were considered to have negative results.The average increase in hydrogen level after glucose ingestion for the controls and the patients were 3.364.5ppm and 14.0633.5ppm,respectively (chi-square =6.208,P <0.05)(Fig.1).The fasting hydrogen levels did not differ signiﬁcantly between patients with and without evidence of small-bowel bacterial overgrowth (P >0.1).Glucose methane breath testThe fasting methane levels in the controls and the patients were 2.063.1ppm and 2.563.7ppm,respectively (P >0.5).Abnormal fasting methane levels ( 9ppm)were found in two patients and controls who did not meet the increased criterion for the diagnosis of small-bowel bacterial over-growth and were considered to have negative results.The average increased methane levels after glucose ingestion for the controls and the patients were 4.764.9ppm and 3.967.0ppm,respectively (P >0.5)(Fig.2).The fasting methane levels did not differ signiﬁcantly between patients with and without evidence of small-bowel bacterial overgrowth (P >0.6).All the controls except one had negative results for small-intestinal bacterial overgrowth.The positive one was diag-nosed by an increase in breath hydrogen level (23ppm)after glucose ingestion,with normal values of basal hydrogen and methane.Furthermore,intestinal bacterial overgrowth was documented in 16(35.6%)of the 45cirrhotic patients.Ten patients (22.2%)were diagnosed on the basis of increased hydrogen,and 6(13.3%)on the basis of increased methane after glucose intake.No subject had increased levels of both hydrogen and methane.There were no statistically signiﬁcant differences between patients with and without evidence of bacterial overgrowth with regard to the male to female ratio (12:4versus 22:7),age (59612versus 55613,age more than 70versus less than 70years (4:12versus 8:21),albumin level (2.860.7versus 3.160.6g/dl),presence or absence of ascites (9:7versus 11:18),bilirubin level (3.162.9versus 4.166.3mg/dl),or prothrombin time (14.961.4versus 14.162.0sec)(Table I).Furthermore,there were nosigniﬁcant differences among various causes of cirrhosis.The positive ratios were 8:22(36.4%)with HBV-related,4:14(31.1%)with HCV-related,3:6(50.0%)with alcohol-related,and 1:3(33.3%)with idiopathic-related cirrhosis (Table II).Small-intestinal bacterial overgrowth was signiﬁ-cantly more frequent among patients with Pugh–Child class B or C (12:24;50%)than in patients with class A (4:17;19%)(P <0.05)(Fig.3).DISCUSSIONSmall-intestinal bacterial overgrowth may be diagnosed by several methods,such as jejunal ﬂuid culture (7,12,13),the 14C-labeled bile acid breath test (14),the 14C-D -xylose breath test (14,15),the lactulose-H 2breath test (12,16),and the glucose-H 2breath test (7,17).Direct bacterial culture is considered the gold standard for the diagnosis of small-bowel bacterial overgrowth (13),but it is invasive and uncomfor-table,and the sampling techniques have problems with contamination from the oral cavity or upper gastrointestinal tract (12,18).The 14C-D -xylose breath test provides an excellent means for diagnosis of small-bowel bacterial overgrowth,with a sensitivity range of 85%–100%(12,19)and a speciﬁcity of 40%–100%(19–21).The hazard of radioactivity restricts its widespread application,however,as it does that of the 14C-labeled bile acid breath test.The glucose hydrogen breath test is a simple,indirect,non-invasive,diagnostic tool with a sensitivity range of 62%–93%(7,12)and a speciﬁcity range of 78%–100%(7,12,17).Unfortunately,many investigators have proven that the group of non-hydrogen producers ranges from 15%to 27%of the general population (3–5,22).Both hydrogen and methane are produced by intestinal ﬂora (5,23),and methane measure-ment can provide useful information in non-hydrogen-producing subjects (3).When ignoring the methane informa-tion,physicians relying on breath tests may underestimate the exact positive result (3,5).Our study includes the methane measurement for the diagnosis of small-bowel bacterial overgrowth and corrects this bias.If we exclude the methane data from our study,the prevalence of small-bowel bacterial overgrowth in cirrhosis decreases from 35.6%to 22.2%.According to Morencos et al.(2),the prevalence of small-bowel bacterial overgrowth in alcoholic cirrhosis was approximately one third and is related to the severity of liver dysfunction and the presence of ascites.There were twoTable II.The positive ratios of small-intestinal bacterial overgrowth (SIBO)among various causes of cirrhosisEtiology of cirrhosis (no.of patients)SIBO HBV HCV Alcohol Idiopathic P valuePositive 81431Negative141032Positive ratios36.4%31.1%50.0%33.3%0.84**No signiﬁcance.Small-Intestinal Overgrowth in Cirrhosis869S c a n d J G a s t r o e n t e r o l D o w n l o a d e d f r o m i n f o r m a h e a l t h c a r e .c o m b y F r a n c i s A C o u n t w a y L i b r a r y o f M e d i c i n e o n 12/29/12F o r p e r s o n a l u s e o n l y .possible biases,however,that might lead to incorrect results.The ﬁrst is underestimating the group of non-hydrogen producers,as mentioned previously,and the second is that Morencos et ed a high fasting hydrogen level ( 20ppm)as a positive result for the diagnostic criterion,without mentioning whether these subjects had increased hydrogen levels from the base line after glucose ingestion.As we know,a high fasting breath level could result from either bacterial overgrowth or poor diet restriction (9).Therefore,their results may have shown a possible false positive from poor diet restriction.Fortunately,the two biases in the study of Morencos et al.were in the opposite direction,and this might be the reason why the ﬁnal prevalence of small-intestinal bacterial overgrowth in cirrhotic patients in their study was nearly the same as that in our study despite the biases.Other investigators have shown that true small-bowel bacterial overgrowth will increase hydrogen level after test glucose intake,and this will not happen in the case of poor diet control,even though both conditions show a high fasting breath hydrogen level (7,9).If combined with a high fasting hydrogen level and a signiﬁcantly increased hydrogen level from the base line after glucose ingestion,the diagnostic speciﬁcity could reach nearly 100%,despite its sensitivity of only 41%(7).If we also include a high fasting hydrogen level as a positive diagnostic criterion,the positive rate would increase from 16:45(35.6%)to 23:45(51.1%).Both these factors might cause a great difference.Our study excluded both of these biases and further conﬁrmed the signiﬁcantly increased prevalence of small-bowel bacterial overgrowth in cirrhotic patients.A false-positive breath test would be expected in patients without bacterial overgrowth if there were accelerated gastric emptying and rapid transit ofsubstrate to the cecum (7,11).This might be rare in patients with cirrhosis,because cirrhotic patients have been shown to have delayed oral–cecal time (24–26).Furthermore,we also showed that there was no difference in the prevalence of small-bowel bacterial overgrowth among various causes of cirrhosis,whether viral,alcoholic,or idiopathic (P >0.8).The etiology of the increased prevalence of small-bowel bacterial overgrowth in cirrhotic patients most likely results from impairment of the intestinal motility function (27).The concept of impaired motility in cirrhosis predisposing to bacterial overgrowth might also explain why the increase in hydrogen level after the glucose test was higher in the cirrhotic group than in the control group (P <0.05)(Fig.1).Our result further conﬁrmed that there is a higher incidence of bacterial overgrowth in cases of more advanced liver dysfunction (P <0.05),as Morencos et al.(2)had shown.Many investigators have shown that bacterial overgrowth may lead to hepatic injury through endotoxins (28),pepti-doglycan-polysaccharide polymers (29),lithocholic acid (30,31),or a systemic inﬂammatory response (29,32).When rats with bacterial overgrowth in the small intestine were treated with antibiotics,hepatic function and survival rate improved after clearance of the bacteria (29).These results have been shown only in animals,and no similar results have ever been reported in humans so far.Madrid et al.(33)showed alterations in cyclic activity during fasting and the appearance of prominent clustered contractions in cirrhosis with MMC recording.They also showed more intense abnormalities of small-intestinal motility in patients with more advanced disease.This observation might explain a higher prevalence of small-bowel bacterial overgrowth in more advanced cirrhosis,as Morencos et al.(2)and this report have shown.However,we have also shown that small-bowel bacterial overgrowth in cirrhosis is not related to albumin or bilirubin level or to prothombin time.Our cirrhotic patients had a tendency towards increased age (mean,57years;range,33–76years),which has been described as a signiﬁcant higher prevalence factor (34–37),but we did not ﬁnd a signiﬁcant difference in bacterial overgrowth between the groups of patients younger or older than 70years (P >0.5).In conclusion,we have conﬁrmed the previous report of a high prevalence of small-bowel bacterial overgrowth in cirrhosis and that a higher prevalence is related to greater severity of liver dysfunction.There is no statistically signiﬁcant difference among various causes of cirrhosis and the presence or absence of ascites.We have corrected the possible biases of the previous report and included methane measurement for the diagnosis of small-bowel bacterial overgrowth to reduce the possibility of the false positive in non-hydrogen producers.Even though there is no previous report speciﬁcally comparing the breath hydrogen test with the gold standard of small-bowel bacterial culture in the cirrhotic patients for the diagnosis of small-intestinalbacterialS c a n d J G a s t r o e n t e r o l D o w n l o a d e d f r o m i n f o r m a h e a l t h c a r e .c o m b y F r a n c i s A C o u n t w a y L i b r a r y o f M e d i c i n e o n 12/29/12F o r p e r 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overgrowth.Gastroenter-ology 1986;91:1447–51.King CE,Toskes PP.Breath tests in the diagnosis of smallintestinal bacterial overgrowth.CRC Crit Rev Clin Lab Sci 1984;21:269–81.23.Bond JH,Levitt e of pulmonary hydrogen [H 2]measurements to quantitate carbohydrate absorption.Study of partially gastrectomized patients.J Clin Invest 1972;51:1219–25.24.Huppe D,Tonissen R,Hoﬁus M,Kuntz HD,May B.Inﬂuenceof chronic alcoholism and liver cirrhosis on oro-cecal transit (H2breath test).Z Gastoenterol 1989;27:624–8.25.Chesta J,Lillo R,Deﬁlippi C,Jouanne F,Massone MA,MaulenM,et al.Mouth to caecum transit time and solid meal gastric emptying in patients with liver cirrhosis.Rev Med Chile 1991;119:1284.26.Galati JS,Holdeman KP,Dalrymple GV,Harrison KA,QuigleyEM.Delayed gastric emptying of both the liquid and solid components of a meal in chronic liver disease.Am J Gastro-enterol 1994;89:708–11.Husebye E.Gastrointestinal motility disorders and bacterialovergrowth.J Intern Med 1995;237:419–27.28.Nolan JP.Intestinal endotoxins as mediators of hepatic injury:an idea whose time is coming again.Hepatology 1989;10:887–91.29.Lichtman SN,Keku J,Schwab JH,Sartor RB.Hepatic injuryassociated with small bowel bacterial overgrowth in rates is prevented by metronidazole and tetracycline.Gastroenterology 1990;100:513–9.30.Miyazaki K,Nakayama F,Koga A.Effect of chenodeoxycholicand ursodeoxycholic acids on isolated adult human hepatocytes.Dig Dis Sci 1984;29:1123–30.31.Gustafsson J,Anderson S,Sjovall J.Bile acid metabolismduring development:metabolism of lithocholic acid in human fetal liver.Pediatr Res 1987;21:99–103.32.Lichtman SN,Sartor RB,Keku J,Schwab JH.Hepaticinﬂammation in rats with experimental small intestinal bacterial overgrowth.Gastroenterology 1990;98:414–23.33.Madrid AM,Cumsille F,Deﬁllippi C.Altered small bowelmotility in patients with liver cirrhosis depends on severity of liver disease.Dig Dis Sci 1997;42:738–42.34.MacMahon M,Lynch M,Mullins E,O’Moore RR,Walsh JB,Keane CT,et al.Small intestinal bacterial overgrowth–an incidental ﬁnding?J Am Geriatr Soc 1994;42:146–9.35.Roberts SH,James O,Javis EH.Bacterial overgrowth syndromewithout ‘blind loop’:a cause for malnutrition in the ncet 1977;2:1193–5.36.McEvoy A,Dutton J,James OFW.Bacterial contamination ofthe small intestine is an important cause of occult malabsorption in the elderly.Br Med J 1983;287:789–93.37.Riordan SM,McIver CJ,Wakeﬁeld D,Bolin TD,DuncombeVM,Thoms MC.Small intestinal bacterial overgrowth in the symptomatic elderly.Am J Gastroenterol 1997;92:47–51.Received 24March 1998Accepted 25May 1998Small-Intestinal Overgrowth in Cirrhosis 871S c a n d J G a s t r o e n t e r o l D o w n l o a d e d f r o m i n f o r m a h e a l t h c a r e .c o m b y F r a n c i s A C o u n t w a y L i b r a r y o f M e d i c i n e o n 12/29/12F o r p e r s o n a l u s e o n l y .。

北京斯达恒通CJR4-5甲烷二氧化碳测定器使用说明书

仪器关机
只过专业训的技术人员才能从测定器的调校工作
1 调甲烷零点
仪器开机在清空气中工作 5 分钟在显示气体浓度状态按 DOWN 键 2 仪器
入调校状态 “CH4” 符闪动按一 POWER 键行显示“P 1” 符最按一 POWER 键确
认仪器自动把当前状态调烷零
调校状态返回到实时检测状态
±0.1 %CO2 ± 0.05 真值的5%
2
测定器的烷部分显示稳定性 0.00～4.00 ％CH4 显示范围内当烷浓度保持稳定时显示值
变
超过 0.03 %CH4
在0.00～5.00% CO2 范围内当氧碳浓度保持恒定时测定器的显示值的变
超过0.04 % CO2
2.3 测定器的警能
1
仓
目录
一概述仓………………………………………………………………………………………1仓结构特仓…………………………………………………………………………………1仓要性能和技术参数……………………………………………………………………2仓仓仓
四工作原理仓…………………………………………………………………………………2仓操作使用仓…………………………………………………………………………………3仓使用维注意项仓………………………………………………………………………5仓
绝缘套防短路
限流能限流电阻保板和充电型单节 1500mAh 锰酸锂矿灯用锂离子蓄电池
浇封在一起,浇封选用酚 A 型氧树脂浇封的厚度小于 3mm
电池型 PL123450
容 1500m Ah 锰酸锂矿灯用锂离子蓄电池
最高开路电压 U0 4.3V

甲烷和氢呼气使用手册

甲烷和氢呼气使用手册甲烷和氢呼气试验解决了很多其它试验难以检查的项目以及一些无法完成的检测盲区，譬如胰腺功能检查、小肠细菌过增长、肠道通过时间以及乳糖酶缺乏症，都是其它检查方法都不能完成的“盲区”。

呼气检测方法是一种无创、无痛、准确、环保、快捷技术，具有广泛的临床应用价值。

检测前需要做好准备工作。

∙禁食12小时∙头天晚餐不吃不易消化的食物。

∙晚饭后至测试前不喝含糖的饮料。

∙清晨清洁口腔。

∙不吸烟、不喝酒。

∙避免剧烈运动。

空腹基础值的解释：H2 <10ppm：正常H2 10-20ppm：禁食不充分或晚餐进食不宜消化食物。

H2 >20ppm：考虑小肠细菌过度生长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。

1填补国内外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。

2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。

3慢性便秘的病因测定肠道通过时间和回盲瓣功能障碍。

4诊断糖尿病患者自主神经节病变所致的胃肠动力异常。

5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。

6评价亚健康状况常伴有小肠细菌过度生长最常用的几种氢呼气试验1、支链淀粉呼气试验(测定胰腺外分泌功能)用一定负荷量的支链淀粉作试验餐，可诊断胰腺损伤程度，这个试验填补目前国内外胰腺功能无法检测的盲区。

评估胰腺炎后胰腺功能损伤和糖尿病患者的病因和预后。

2、乳果糖呼气试验(用于小肠细菌过量增长、口盲通过时间、回盲瓣功能不良)适应症：慢性腹泻或慢性结肠炎功能性肠病，消化不良综合症、慢性肝病或肝硬化糖尿病患者的胃肠动力异常慢性便秘亚健康状态3、乳糖呼气试验(测定乳糖酶缺乏症、小肠细菌过增长、胃肠通过时间)适应症：乳糖酶缺乏症或不耐症各种功能性肠病慢性腹泻或慢性肠炎肠道预激综合症的诊断胃肠或肝胆外科手术后肠道功能恢复的评估。

甲烷和氢呼气检测设备

甲烷和氢呼气检测设备丁文京博士北美医学教育基金会前言甲烷和氢呼气检测是了解人体胃肠功能和代谢的一个重要无创检查方法，也是了解由于肠道微生态变化所导致的疾病的一个有实用价值的方法。

甲烷和氢呼气检测的原理甲烷和氢呼气检测之所以可以用于临床检验的基本是基于以下几个基本要素：第一、人体的新陈代谢虽然可以产生氢离子，但是不产生分子状态的氢气和也不能产生甲烷气体。

我们呼出气中的甲烷和氢气全部来自于胃肠道的细菌在酵解碳水化合物过程中产生的代谢产物。

第二、胃肠道产生甲烷和氢气必须基于两个最基本的条件，即胃肠道要有碳水化合和可以酵解碳水化合物的细菌，这两个因素缺一不可。

所以可以认为甲烷和氢呼气主要是反映与胃肠道细菌和胃肠道对碳水化合物消化吸收有关的疾病。

第三、正常情况下，胃肠道细菌酵解碳水化合物后产生包括甲烷和氢在内的气体，其中大约有14-21%的气体可以通过肠粘膜屏障进入血液循环，经血液循环到达肺泡，通过气体交换呼出体外。

呼出气中的甲烷和氢含量很低，在ppm水平。

ppm是英文Parts Per Million的缩写，称百万分率，表示百万分之几。

在某些疾病情况时，肠粘膜的通透性变化，甲烷好氢通过率增加，有报导肠道甲烷和氢的通过率可以达到50%。

第四、正常情况下小肠内的细菌非常少，所以在甲烷和氢呼气曲线在小肠段呼出的量很少，当小肠内细菌增加时，临床上称为小肠细菌过度生长，在小肠段代谢产生的甲烷好氢就会增加，甲烷和氢呼气曲线会明显上升。

第五、某些肠道细菌可以利用氢，使2个氢分子与1个碳原子结合生产甲烷。

不同的文献报道，大约有15-35%的人群由于上述原因，在疾病时呼出气中氢的浓度没有变化，会出现假阴性结果。

中国人大约有65%左右的人群没有产甲烷的细菌，或只有很少产甲烷的细菌，其呼出其中或者没有甲烷，或者只有很少量的甲烷。

鉴于这两个因素，现在临床日益认识到有必要同时测量呼出气中的甲烷和氢，整合这两个参数的变化以减少假阴性。

氢气甲烷呼气文献 (194)

Irritable bowel syndrome is widely regarded as a disorder of colonce suggests that it may encompass abnormalities in the motor activity of other parts of the gastrointestinal tract.4 It may be difficult to show such disorders by measuring intraluminal pressure or myoelectrical activity because of the wide range of normal motor activity and because symptoms in irritable bowel syndrome are usually related to the presence of food in the gut, while measurements of motor activity are more easy to interpret with the bowel empty. We have investigated the effects of abnormal motor activity in patients with irritable bowel syndrome by relating the time taken for a meal to pass through the stomach, small intestine, and colon to the patients' symptoms. An important advantage of this 'meal transit test' is that it does not involve the subject swallowing an intestinal tube. Intubation is poorly tolerated by irritable bowel syndrome patients and

(精选文档)新版甲烷安全技术说明书

化学品安全技术说明书（甲烷）xxxxxxxxxxxxxx有限公司二O一二年六月一日化学品安全技术说明书第一部分化学品及企业标识化学品中文名称：甲烷化学品俗名或商品名：甲烷化学品英文名称：Methane企业名称：地址：邮编：电子邮件地址：电话/传真号码：企业应急电话：技术说明书编码：生效日期：国家应急电话：化学品推荐用途和限制用途：燃料、也应用在石油化工等领域。

如改做其他用途，请及时与厂家联系，擅自使用导致不良后果的厂家概不负责。

第二部分危险性概述主要物化危险性：与空气混合能形成爆炸性混合物，遇明火高热能引起燃烧爆炸。

与氟等能发生剧烈的化学反应。

若遇高热，容器内压增大，有开烈和爆炸的危险。

GHS危险性类别：压力下气体：压缩气体（GB20580）易燃气体：1类（GB20577）标签要素和象形图：防范说明：远离热源、火源，避免野蛮作业，佩戴好安全附件。

使用过程应穿戴防静电工服，使用防火花工具。

危险信息：极易燃烧气体。

压缩气体，遇热超压可能会引起爆炸。

气体大量泄漏可导致人员窒息，警示词：危险极易燃气体，遇热可能爆炸。

侵入途径：吸入健康危害：深度暴露可引起缺氧窒息。

环境危害：甲烷也是一种温室气体.燃爆危险：易燃，遇空气可形成爆炸混合物，遇明火、高热有燃烧爆炸危险。

第三部分成分/组成信息混合物化学品名称：甲烷分子式：CH4有害物甲烷组分浓度＞99.0% CAS No.74-82-8第四部分急救措施皮肤接触：无意义眼睛接触：无意义吸入：万一发生吸入性事故，将患者移至新鲜空气处并保持安静。

如呼吸困难，给输氧。

如呼吸停止，立即进行人工呼吸。

就医。

食入：无资料第五部分消防措施危险特性：易燃，与空气混合能形成爆炸性混合物，遇热源和明火有燃烧爆炸的危险，与五氧化溴、氯气、次氯酸、三氟化氮、液氧、二氟化氧及其它强氧化剂接触剧烈反应。

有害燃烧产物：无灭火方法及灭火剂：切断气源。

喷水冷却容器，或将容器从火场移至空旷处，雾状水，泡沫、二氧化碳、磷酸铵干粉。

甲烷和氢呼气检测的原理

甲烷和氢呼气检测的原理丁文京博士，北美医学教育基金会甲烷和氢呼气检测是了解人体胃肠功能和代谢的一个重要的无创检查方法，也是了解由于肠道微生态变化所导致的疾病的一个有实用价值的方法。

甲烷和氢呼气检测用于临床检验的基本是主要是基于以下几个基本要点：第一、人体的新陈代谢虽然可以产生氢离子，但是不产生分子状态的氢和也不能产生分子状态的甲烷这两种气体。

我们呼出气中的甲烷和氢气唯一的来源是胃肠道的细菌在酵解碳水化合物过程中产生的代谢产物。

第二、胃肠道产生甲烷和氢气必须基于两个最基本的条件，即胃肠道要有碳水化合和可以酵解碳水化合物的细菌，这两个因素缺一不可。

所以可以认为甲烷和氢呼气主要是反映与胃肠道细菌和胃肠道对碳水化合物消化吸收有关的疾病。

呼出气中的甲烷和氢含量很低，在ppm水平。

ppm是英文Parts Per Million的缩写，称百万分率，表示百万分之几。

在某些疾病情况时，肠粘膜的通透性变化，甲烷好氢通过率增加，有报导肠道甲烷和氢的通过率可以达到50%。

第五、某些肠道细菌可以利用氢，使2个氢分子与1个碳原子结合生产甲烷。

不同的文献报道，大约有15-35%的人群由于上述原因，在疾病时呼出气中氢的浓度没有变化，会出现假阴性结果。

中国人大约有65%左右的人群没有产甲烷的细菌，或只有很少产甲烷的细菌，其呼出其中或者没有甲烷，或者只有很少量的甲烷。

鉴于这两个因素，现在临床日益认识到有必要同时测量呼出气中的甲烷和氢，整合这两个参数的变化以减少假阴性。

作者联系方式： abs94555@。

CH4和CO2操作

CH4与CO2使用注意事项一、工作环境应尽量选择无尘洁净的环境对设备进行维护和配置。

二、换膜1.拆外塑料壳用2.5mm六角螺丝刀（内附）拆掉最外层塑料壳（共4个螺丝，轮流给螺丝松劲儿，保持塑料壳受力均匀。

切忌完全松掉一个螺丝，再松下一个）。

2.拆内部法兰用3mm六角（内附），拆卸方法同上，拆开后如下图，注意其内的熔结金属板容易掉出。

建议将设备探头朝上，竖直放置设备，以防内部部件掉出。

图1 传感器头组成:1:螺丝；2；法兰盘；3：密封环；4：膜；5：熔结金属板；6：传感器室头3.更换膜首先放入熔结金属板，粗糙面面对传感器室，光滑面面对外侧。

然后，放入膜，光滑面面对外侧，粗糙面面对熔结金属板。

将密封环用手伸展，（如图2）再放到膜上，否则密封环太小。

安装法兰（同拆卸，轮流给螺丝加劲）。

最后检查，如图3，图4。

图 2 用手伸展密封环图 3 检查法兰是否安装好，如左图，有间隙，则重新放置密封环，再次检查。

图 4 最后检查法兰与膜间应有0.2mm左右的空隙，否则膜与密封环的压力则过大，或者损坏。

在此过程中一定注意，1.不能涂硅油。

2.不可以碰到膜的表面，只可以抓边缘，膜只要损坏，测量完全错误！如图5:图 5 不可碰到膜表面三、安装泵1.安装泵安装好连接泵的卡环，将垂直于泵的出水口插入传感器塑料外壳的缺口，将过滤器安置于与泵同向的入水口，见图6。

用一字型改刀旋紧过滤器与泵的连接处的螺丝（不必很紧），见图7。

注意旋紧线缆接头保护盖。

用绑带绑住连接泵的架子的卡扣，见图8。

图6 泵的安装图7 安装过滤器。

图8 用绑带绑住泵连接架卡扣2.连接线如图6，B 为连接泵的接口。

连接线的另一头是两针插口，一粗一细。

连接线必须与线路同向插拔，不可扭动。

注意旋紧线缆接头保护盖。

图 9 传感器接口四、连接电脑紧固此处螺丝，固定过滤器用绑带绑住此处如图6，A为连接电脑线的接口，用带有串口的线缆与该口对应插入，插拔必须直上直下，不可扭动。