甲烷和氢呼气使用手册
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. Diagnosis and managingfunctional symptoms in the child with inflammato-ry bowel disease. J Pediatr Gastr Nutr 2004; 39:S760-762.38)B JARNASON I, S HERWOOD R. Fecal Calprotectin: asignificant step in the noninvasive assessment ofintestinal inflammation. J Pediatr Gastr Nutr 2001;33: 11-13.39)S CARPELLINI E, G ABRIELLI M, L AURITANO CE, L UPASCU A,M ERRA G, C AMMAROTA G.High dosage rifaximin for the treatment of small intestinal bacterial over-growth. Aliment Pharm Ther 2007; 25: 781-786.40)G REGG CR. Enteric bacterial flora and bacterialovergrowth syndrome. Semin Gastrointest Dis2002; 13: 200-209.41)J ONES MP, B RATTEN JR. Small intestinal motility. CurrOpin Gastroenterol 2008; 24: 164-172.42)S HI HN, W ALKER A.Bacterial colonization and thedevelopment of intestinal defences. Can J Gas-troenterol 2004; 18: 493-500.1334。
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
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。
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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检测名称检测指标和目的检测方法适应症乳糖呼气试验乳糖酶缺乏症1、先测空腹基础值乳糖酶缺乏症或不耐症小肠细菌过度生长2、口服乳糖，1g/Kg体重，各种功能性肠病总量不超过25g 慢性腹泻或慢性肠炎口盲通过时间3、每30分钟至60分钟采气肠道预激综合症的诊断一次胃肠或肝胆外科手术后肠道功能恢复的(如不考虑小肠细菌过度生评估。
长，可以每60分钟取气一次)检测名称检测指标和目的检测方法适应症乳果糖呼气试验小肠细菌过度生长1、先测空腹基础值慢性腹泻或慢性结肠炎2、口服乳果糖0.5g/Kg体口盲通过时间功能性肠病重，总量不超过10g 回盲瓣功能不良消化不良综合症溶于180-250ml水慢性肝病或肝硬化 3、每20分钟至30分钟采气糖尿病患者的胃肠动力异常一次慢性便秘阳性:2小时内H2上亚健康状态升>12ppm 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。
检测名称检测指标和目的检测方法适应症葡萄糖呼气试验小肠细菌过度生长 1、先测空腹基础值2、口服葡萄糖，1g/Kg体重，总量不超过100g溶于250ml水3、每20分钟至30分钟采气一次阳性:2小时内H2上升>12ppm检测名称检测指标和目的检测方法适应症果糖呼气试验果糖不耐受检测名称检测指标和目的检测方法适应症蔗糖呼气试验蔗糖不耐受检测名称检测指标和目的检测方法适应症山梨醇呼气试验山梨醇不耐受检测名称检测指标和目的检测方法适应症支链淀粉呼气试胰腺外分泌功能评估胰腺炎后胰腺功能损伤验糖尿病患者的病因和预后检测名称检测指标和目的检测方法适应症金属镁呼气试验胃酸含量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。
氢呼气试验一(氢呼气试验的原理、应用范围及方法1.肠道感染.肠道菌群移位或小肠细菌过增长:1)正常人体小肠内无细菌生长，但在肝患者尤其是肝硬化患者，由于门脉高压、肠道粘膜水肿及免疫功能下降等诸多原因导致大肠内细菌向上移位到小肠。
2)普通成人或更多见的儿童肠道感染病例。
3)亚健康状态上述病理状况即可以氢呼气试验的方法获得诊断。
通常使用的底物为乳果糖:受检者口服乳果糖10g，若小肠内有细菌存在，则通常在30分钟内会出现第一个H2呼出峰值，(是为小肠峰，是乳果糖在小肠内遭遇细菌产生的H2峰值)，之后在一个小时左右时间再出现第二个H2呼出峰值(是为盲肠峰，是乳果糖遭遇更大量的细菌时产生大量H2的波峰)，有时上述两波峰也会融合。
2.胃肠道通过时间(口盲时间)，用于胃肠道动力的测定:采用氢呼气试验可以很简便地测定受检者的肠道通过时间，使用的底物一般是乳果糖，但限于无肠道感染的受检者，原理同上，服用10g乳糖后，实时检测患者H2产生量，直至发现患者盲肠波峰为止，自口服乳果糖开始计时，直至盲肠波峰出现的这个时段即是肠道通过时间。
3.乳糖酶缺乏症及其他针对糖类吸收障碍的检测适应症及原理:包括:乳糖、蔗糖、果糖、山梨醇、木糖等吸收障碍或吸收不良。
首先让患者口服上述某一种糖类水溶液，如果该种糖类能被患者肠道粘膜所吸收，则不会有氢气产生，如果吸收不良或完全不被吸收，则服下的上述糖类会随肠蠕动进入大肠，此时因为大肠内的细菌可以快速地分解上述糖类，且分解后会产生大量的氢气，并弥散入血，经肺呼出，故检测氢气的呼出量即可了解糖类吸收障碍的程度。
最广泛使用的氢呼气试验之一是检测乳糖酶缺乏症，或称乳糖酶不耐症。
该类患者的最主要的症状是不能喝牛奶，喝牛奶后感胃肠严重不适，且肠鸣不断，且大多很快排出稀便，原因是患者肠道内缺乏能分解乳糖的乳糖酶，而牛奶中除3?%的脂肪和3?%蛋白外，唯一的糖类即是含量高达5%的乳糖，乳糖吸收不良则会加速肠道蠕动并将未分解吸收的乳糖排入大肠，遇大肠细菌后则产生大量氢气，经呼气试验即可检出。
该试验方案使用的底物为25g乳糖，溶于250ml水中口服。
4(胃泌酸功能测定:口服金属镁后，它在胃内可与盐酸反应而产生H2，并经胃粘膜弥散入血而随呼气排出。
呼气中H2排出量与胃内盐酸量呈正相关。
因此，检测呼气中H2浓度即可反映其胃泌酸功能。
采用该法与五肽胃泌素刺激试验、99mTc 胃γ照相法比较，表明无论在正常人或胃与十二指肠疾病患者中三种试验均呈显著的相关性。
呼气氢胃泌酸功能测定方法具有不需要插入鼻胃管而引起患者不适的优点。
二、氢呼气试验的适应症:1.糖类吸收障碍患者，如可疑有果糖、蔗糖、乳糖、木糖等糖类吸收障碍的患者都可以做H2呼气试验。
2.肝病患者可疑有小肠细菌过增长，儿童或成人可疑有肠道感染的情况，亚健康状态等。
3.功能性消化不良患者或胃肠神经官能症或肝病患者测定肠道通过时间以帮助诊察肠道功能状况。
4(功能性便秘5.胃泌酸功能测定。
6.亚健康状态7.肠道预激综合症的诊断8(外科手术后肠道功能恢复的评估。
三、结果评判:1.肠道感染.小肠细菌过增长:基础H2测定高于20PPM，或有有典型的小肠峰及盲肠峰或二者融合形成的"高平台"现象，均可确诊。
如口服乳果糖(10g)后出现小肠峰、呼气中氢浓度升高?12ppm时，即可诊断为小肠细菌过度生长。
如果空腹时呼气中氢浓度,20ppm，且服用乳果糖后进一步升高,12时，更可确诊。
2.胃肠通过时间:正常值在60-110分钟范围内，少于60分钟为肠道通过时间过快，高于110分钟则为胃肠通过时间延迟。
3.乳糖或其它糖类吸收障碍:如H2峰值大于本底值20ppm以上，即可判定有糖类吸收障碍或糖类分解酶缺乏。
20-40ppm为轻度、40-80ppm为中度、>80ppm为重度四、氢呼气试验的优点:1.无创、无痛、准确、及时:受检者只需按要求口服少量底物，再吹口气即可获得诊断，譬如乳糖酶缺乏症、不必用咬检肠道粘膜的方法进行诊断。
2.解决了其它试验根本无法完成的检测"盲区"，譬如小肠细菌过增长、和肠道通过时间以及乳糖酶缺乏症、无创胃酸测定，都是其它检查方法都不能或不便完成的"盲区"。
五、氢呼气试验的注意事项:1.刷牙漱口，空腹接受检查。
2.晨起后禁止吸烟，因为烟草燃烧会产生大量的氢气。
3.服用底物后要再漱口，以防止口腔内少量细菌对试验的干扰。
4.试验过程中要静坐，不做剧烈运动。
5(肠道感染患者在感染控制前，不要做肠道通过时间这项检查。
结语:无创、即时的现场诊断技术是医疗发展的大方向、大趋势。
必将人类的疾病诊治过程舒适化、人性化、简便化～目前呼气试验诊断技术已发展为所有无创诊断技术分支中最成熟、最具使用性、也最舒适化的趋于完善的独立学科。
随着研究的进展和多学科技术的综合应用，呼气试验将不仅仅提升为一个独立学科或独立学会的学术高度，更将会将其技术延伸扩展并贯穿到医学诊断的各个领域。
以其准确、简捷、舒适、人性的科学神奇服务于人类。
Hydrogen and Methane Breath Testing for Gastrointestinal Disorders Hydrogen and methane breath testing at Gastrolab is carried out in accordance with guidelines established by the RomeConsensus Conference, a meeting of world experts in breath testing and sugar malabsorption in Rome 2007. Our medical directors continuously review the latest medical literature to guarantee that the policies and protocols adopted by Gastrolabreflect current best practice, so that Gastrolab continues todeliver diagnostic services of the highest standard.Hydrogen & Methane Breath TestsA Hydrogen / Methane Breath Test is a painless and non-invasive test which helps to diagnose the following gastrointestinal disorders., Lactose Breath test for lactose intolerance (lactase deficiency) , Fructose Breath test for fructose malabsorption, Glucose Breath test for small bowel/intestinal bacterial overgrowth, Lactulose Breath test for Hydrogen production and intestinal transit time, Sucrose Breath test for sucrose malabsorption (sucrase-isomaltase deficiency), Sorbitol Breath test for sorbitol malabsorption, Mannitol Breath test for mannitol malabsorptionHow does the breath test work?A wide range of sugars we ingest everyday, such as lactose and fructose, are usually absorbed within the small bowel. A large proportion of people absorb these sugars poorly, allowing the sugars to pass into the colon, or large bowel. Fermentation of incompletely absorbed sugars within the colon may result in the symptoms typical of irritable bowel syndrome (IBS), such as bloating, abdominal pain, excessive wind, diarrhoea, constipation, or a mixture of both.The breath test is based upon the fact that bacteria within thelarge bowel produce either hydrogen or methane gas (or a combination of both) when ingested sugars are not completely absorbed by the small intestine. The gas is absorbed into the bloodstream from the bowel and travels to the lungs where it is breathed out, allowing detection by hydrogen or methane breath testing. Malabsorption of an orally ingested sugar such as lactose or fructose is indicated by a signi,cant increase above baseline levels in breath hydrogen or methane.In patients suspected of having small bowel bacterial overgrowth,gas producing bacteria are also found in the small intestine.In this case orally-ingested sugars such as glucose are fermented by bacteria in the small intestine before they can be absorbed leading to an increase in breath hydrogen or methane.The lactulose control testSome patients are thought not to produce hydrogen in large amounts, so called “low-hydrogen producers,” and may insteadproduce other gases such as methane. In addition, some patients may produce sufficient amounts of hydrogen, but it is quickly metabolised to produce methane. Both of these situations may result in a patient with true sugar malabsorption having a “false-negative” hydrogen breath test, that is, being told they don’t have sugar malabsorption when in fact they do. The rate of low-hydrogen producers quoted in the medical literature ranges from 5-43%.In order to maximise the accuracy and information obtained from a breath test, we believe it is important to have a baseline lactulose hydrogen breath test. This test will enable our gastroenterologists to determine whether the bacteria within your bowel predominantly produce either hydrogen or methane gas, thereby allowing us to perform subsequent tests measuring the most appropriate gas for you. In addition to this, the lactulose control test allows us to accurately measure the oro-caecal transit time, that is the time taken for the sugar to pass from your mouth to large bowel. As this time varies significantly between different people, knowing your personal transit time allows us to tailor the duration of subsequent tests specifically for you. As way of quality control, Gastrolab continues to monitor the latest research developments and as such procedures andprotocols reflect current best practice and are subject to change over time.佛学经典励志语录，一、人之所以痛苦，在于追求错误的东西。