甲烷氢呼气试验ppt课件
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.
甲烷完整PPT课件(2024)
实验操作规范流程介绍
实验前准备
检查实验器材完好性，阅读实验指导手册，了解实验步骤和注意 事项。
实验操作过程
按照实验指导手册逐步进行，记录实验数据，注意观察实验现象。
实验后处理
清理实验现场，处理废弃物，关闭实验器材，提交实验报告。
危险源识别及风险评估方法
危险源识别
甲烷易燃易爆，实验中可能产生泄漏、静电火花等危险因素。
甲烷燃料电池汽车
甲烷可作为燃料电池汽车的燃料，通过化学反应产生电能驱动汽 车行驶，具有零排放、高效率等优点。
甲烷重整制氢
甲烷可通过重整反应得到氢气，氢气是一种清洁能源，可用于氢燃 料电池汽车等领域。
甲烷直接利用
甲烷在高压下可液化为液态甲烷，可作为汽车燃料直接使用，具有 燃烧效率高、污染小等优点。
06
3
国际化合作
随着全球化进程的加速推进，国内外甲烷产业将 加强合作与交流，共同推动全球甲烷产业的健康 发展。
05
甲烷在工业生产和生活中应用案例
化工原料生产中应用
合成氨原料
甲烷是合成氨的主要原料之一，通过甲烷化反应 可得到合成气，进而生产氨。
生产甲醇
甲烷可通过氧化反应转化为甲醇，甲醇是一种重 要的化工原料和燃料。
工艺流程
生物质预处理、发酵反应 、气体净化与收集等步骤 。
工艺流程简介及关键设备
工艺流程简介
根据不同的制备方法，甲烷的生产工艺流程包括原料准备、反应过程、产品分 离与提纯等环节。
关键设备
包括反应器、分离器、压缩机、冷却器等设备，用于实现原料的转化、产品的 分离与提纯以及工艺过程的控制。
03
甲烷燃烧反应与能量转换原理
甲烷和氢呼气使用标准手册
甲烷和氢呼气使用手册
甲烷和氢呼气实验解决了诸多其他实验难以检查旳项目以及某些无法完毕旳检测盲区，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少症，都是其他检查措施都不能完毕旳“盲区”。
呼气检测措施是一种无创、无痛、精确、环保、快捷技术，具有广泛旳临床应用价值。
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旳食物。
•晚饭后至测试前不喝含糖旳饮料。
•清晨清洁口腔。
•不吸烟、不喝酒。
•避免剧烈运动。
空腹基本值旳解释：
H2 <10ppm：正常
H2 10-20ppm：禁食不充足或晚餐进食不适宜消化食物。
H2 >20ppm：考虑小肠细菌过度生长。
氢呼气试验 (2)
氢呼气试验（HBT）图1. 氢/甲烷呼气试验基本原理氢呼气试验（hydrogen breath tests）指测定口服某种化合物后呼气中的氢气（hydrogen）浓度变化而诊断胃肠疾病的一类检验方法。
仪器条件许可时，除了氢气还同时作甲烷(methane)浓度测定，故试验有时也称为氢/甲烷呼气试验。
我院目前常规开展的项目有：1.葡萄糖氢呼气试验诊断小肠细菌过生长; 2. 乳果糖氢呼气试验测定口-盲肠通过时间，也可同时诊断小肠细菌过生长。
人和哺乳动物细胞代谢不产生氢气和甲烷，呼气中的氢气和甲烷来源于机体细菌对碳水化合物的发酵。
大肠是身体含细菌最多的地方，而胃和小肠的细菌量是很少的。
所以，餐后一段时间出现的呼气氢和甲烷浓度上升显然就是大肠细菌对食物残渣碳水化合物的发酵的结果。
经过一段时间的禁食，残渣中的可分解碳水化合物耗尽，呼气氢气和甲烷浓度将回复到大气水平。
葡萄糖是一种极易被小肠迅速完全吸收的碳水化合物。
因此，健康人口服一定剂量的葡萄糖后不会出现呼气氢气和甲烷浓度上升的现象，因为几乎没有多余的葡萄糖进入大肠。
相反，小肠细菌过生长的病人，口服的葡萄糖在被小肠吸收的同时也被过量的小肠细菌分解产气。
乳果糖是一种不能消化吸收的人工合成碳水合物。
因此，口服一定剂量的乳果糖后将会出现呼气氢气和甲烷浓度上升的现象，从口服起到呼气氢气和甲烷浓度上升的时间便是药物从口到大肠起点盲肠的运行时间，简称口-盲通过时间，它大致反映了小肠的动力状态。
如果有小肠细菌过生长的存在，口服的乳果糖在到达大肠前就会提前被分解，结果出现两次产气高峰。
基本步骤除白开水外禁食禁饮12h以上采集0时气样口服试验糖餐再次采集气样测定报告注意事项1．严格空腹和饮食控制耗尽食物残渣中碳水化合物，让呼气氢气和甲烷浓度保持在大气水平是氢呼气试验的前提条件。
试验前一天的饮食以清淡易消化为宜，晚餐必须在8点前结束、只能喝白稀饭，餐后禁止白开水以外的一切食物或饮料，空腹时间一定要超过12小时！2．严禁吸烟烟草燃烧产生大量的氢气，吸烟者在试验前至少要禁烟一小时。
氢气和甲烷呼气试验 (46)
post-transplant group.Paired pre and post-operative data wereavailable for eight patients:function scores improved significantlyfor general health(p0.04**).Improvements in physical function,social functioning,emotional role limitations,energy/fatigue,emotional well-being and pain were seen but this did not reachstatistical significance.Physical role limitation was the only func-tion to decline.Of the eight pairs,two patients had significantlybetter overall scores post transplant(p¼0.02,p¼0.01**)and fourhad improved overall scores not reaching statistical significance.*independent T test**Wilcoxon signed rank.Conclusion In this small experience there was an overall trend forbetter quality of life after transplantation,but certain QOLparameters appear to improve more than others.If quality of life isto be an indication for transplantation it will be important to selectpatients on the basis of quality of life parameters that are known toimprove after transplantation.Longer term and larger studies arerequired.Competing interests None declared.SMALL BOWEL ULTRASOUND:DIAGNOSTIC YIELD INESTABLISHED SMALL BOWEL CROHN’S DISEASEdoi:10.1136/gutjnl-2012-302514c.1511D S Pearl,*2A Higginson,1A Quine.1Gastroenterology,Portsmouth Hospitals NHSTrust,Portsmouth,UK;2Radiology,Portsmouth Hospitals NHS Trust,Portsmouth,UKIntroduction Crohn’s disease is an intestinal inflammatory disorderwhich frequently involves the small intestine.Accurate localisationof disease is important to direct targeted therapy.Video capsuleendoscopy(VCE)has revolutionised clinical assessment of smallintestinal Crohn’s disease.Small bowel ultrasound(SB USS)is arapid,inexpensive,interactive and non-invasive alternative methodfor assessing small bowel Crohn’s disease,which is in routine useonly at selected UK institutions.We evaluated the diagnostic yieldof SB USS in VCE determined Crohn’s disease.Methods A retrospective assessment of patients who had undergoneVCE in2008e2010was carried out.Patients investigated forsuspected small bowel Crohn’s disease,or who hadfindings of smallbowel Crohn’s on VCE were included,if they had also had a SB USSwithin12months.VCEfindings were graded as mild(aphthousulcers only),moderate(aphthous ulcers with mucosal distortion)orsevere(aphthous ulcers with mucosal distortion and strictures/stenosis).SB USS was graded positive or negative for small bowelCrohn’s disease.Both assessments were single operator.Eitherinvestigation could predate the other.Results were expressed assensitivity,specificity,positive and negative predictive value(PPVand NPV)of SB USS compared with VCE for detection of smallbowel Crohn’s.Sub-analysis of SB USSfindings for VCE-definedseverity of small bowel Crohn’s disease was carried out.Results196VCE procedures were reviewed,of which22fulfilled theinclusion criteria.10patients had SB Crohn’s on VCE;this wasdetected in four patients by SB USS(sensitivity40%).12patientshad no evidence of SB Crohn’s on VCE;none of these had SB USSfindings of Crohn’s disease(specificity100%).Of18patients withno evidence of SB Crohn’s on SB USS,VCEfindings of Crohn’sdisease were apparent in6patients(negative predictive value67%);however,all patients with positivefindings of Crohn’s disease on SBUSS had evidence of SB Crohn’s on VCE(positive predictive value100%).Sub-analysis for severity of inflammation on VCE wascarried out.Of four patients with positivefindings at SB USS,3were severe and one moderate on VCE.One patient with severeCrohn’s on VCE was missed by SB USS;however,the patient’s bodyhabitus was unfavourable.Conclusion SB USS has excellent positive predictive value(100%)and specificity(100%)for detection of SB Crohn’s disease,with onlymoderate negative predictive value(67%).In addition,all detectedcases were moderate or severe,which may complicate VCE.Ittherefore seems a safe,quick,relatively cheap initial investigation inexpert hands,which may obviate more costly,invasive inves-tigations.A prospective evaluation of these diagnostic modalitiesshould be carried out.Competing interests None declared.SIGNIFICANT IMPROVEMENTS IN ABDOMINAL PAINAND BOWEL SYMPTOMS IN A PHASE3TRIAL OFLINACLOTIDE IN PATIENTS WITH IRRITABLE BOWELSYNDROME WITH CONSTIPATION(IBS-C):A EUROPEANPERSPECTIVEdoi:10.1136/gutjnl-2012-302514c.1521E M Quigley,*2A J Lembo,3C Diaz,3J Fortea,3M Falques,4S Shiff,4K Shi,4H A Schneier,5J M Johnston.1University College Cork,Cork,Ireland;2Beth IsraelDeaconess Medical Center,Boston,Massachusetts,USA;3Almirall,Barcelona,Spain;4Forest Research Institute,Jersey City,New Jersey,USA;5Ironwood Pharmaceuticals,Cambridge,Massachusetts,USAIntroduction Linaclotide,a minimally absorbed guanylate cyclase-Cagonist,was evaluated in a Phase3trial.T o fulfil EMA submissionrequirements,the efficacy,safety and effects of withdrawal oflinaclotide290m g in patients with IBS-C were assessed.Methods In a randomised,double-blind,placebo(PBO)-controlledtrial,IBS-C patients(modified Rome II criteria),with an average of<3complete spontaneous bowel movements(CSBM)/week(wk),#5spontaneous bowel movements(SBM)/wk and abdominal pain$3(0e10scale)during a2-wk baseline period,received oral,once-daily linaclotide or PBO for a12-wk treatment period(TP).In a4-wk randomised withdrawal period(RWP),linaclotide-treatedpatients were re-randomised to receive linaclotide or PBO,andPBO-treated patients to receive linaclotide.Results800patients(median age44;female90.5%)received lina-clotide(n¼405)or PBO(n¼395).For thefirst co-primary parameter($30%reduction from baseline in mean abdominal pain ordiscomfort score for$6of the1st12wks with neither scoreworsening),54.8%of linaclotide-treated patients and41.8%of PBO-treated patients responded(p¼0.0002).For the second co-primaryparameter(patients“considerably relieved”/“completely relieved”onthe weekly degree-of-relief of IBS symptoms question for$6of the1st12wks),37.0%of linaclotide-treated patients and18.5%of PBO-treated patients responded(p<0.0001).Linaclotide significantlyimproved all secondary parameters(including CSBM frequency rate,stool consistency,bloating and severity of straining)vs PBO(exceptwk12EQ-5D VAS;p¼0.06).Improvements occurred in wk1andwere sustained throughout the TP.During the RWP,patientscontinuing linaclotide had sustained efficacy in abdominal pain/discomfort response and IBS degree-of-relief response,and patientsswitched to PBO had symptom recurrence to the level of PBOduring treatment.In patients initially treated with PBO andswitched to linaclotide,abdominal pain improved to the level oflinaclotide patients during the TP.Similar trends were seen in otherabdominal/bowel parameters.Diarrhoea was the most common AE,causing discontinuation in5.7%of linaclotide-treated patients and0.3%of PBO-treated patients.Conclusion In patients with IBS-C,linaclotide significantlyimproved all primary and secondary abdominal pain and bowelsymptom parameters with no evidence of rebound on stoppingtreatment.Competing interests E M Quigley Consultant for:Ironwood Pharmaceuticals,A JLembo Grant/Research Support from:Ironwood Pharmaceuticals,Consultant for:Ironwood Pharmaceuticals/Salix/Prometheus/Alkermes/Ardelyx/GSK/Theravance,Conflict with:Lecture fees from Ironwood Pharmaceuticals,C Diaz Employee of:Almirall,J Fortea Shareholder with:Almirall,Employee of:Almirall,M FalquesEmployee of:Almirall,S Shiff Employee of:Forest Research Institute,K Shi Employee of:Forest Research Institute,H A Schneier Employee of:Forest Research Institute,J M Johnston Employee of:Ironwood Pharmaceuticals.CAN A 10YEAR FRACTURE RISK SCORE (FRAX)BE USED TO AVOID DUAL ENERGY X-RAYABSORPTIOMETRY (DEXA)SCANS IN PATIENTS WITH COELIAC DISEASE?doi:10.1136/gutjnl-2012-302514c.153E Derbyshire,*A Dhar.Gastroenterology,County Durham &Darlington NHS Foundation Trust,Bishop Auckland,UKIntroduction The BSG Guidelines for Osteoporosis in In flammatory Bowel Disease and Coeliac state there is a de finite increased risk of fracture in these conditions and recommend DEXA scanning after introduction of gluten free diet in subgroups of patients where the risk of osteoporotic fracture is high.A 10-year risk of major osteo-porotic and hip fracture using the WHO Fracture Risk Assessment Score (FRAX)can be calculated in patients with coeliac disease and this score mapped to the National Osteoporosis Guideline Group (NOGG)assessment tool may be better to decide the need for a DEXA scan.Methods The aim of this study was to determine if the WHO FRAX can be used to screen patients with Coeliac disease to decide who needed a DEXA scan,and make pathways more cost effective.A retrospective analysis of all duodenal biopsies in our T rust between June 2010and April 2011was undertaken and 50de finitive patho-logical diagnoses of coeliac disease that is,Marsh stage 1to 4were identi fied.The notes of these patients were reviewed to see if a DEXA scan had been requested and to calculate their FRAX score with and without a BMD measurement.Results Of 50patients with a de finitive pathological diagnosis of coeliac disease,33were female and 17male.The median age at diagnosis was 45,with 30(60%)of patients aged between 42and 71yrs,making them eligible for the FRAX score.Documentation of smoking status,alcohol history,use of corticosteroids,past medical history and family history of fracture was done for most patients.Of the 30patients,13had already had a DEXA scan;in two pts a FRAX score was unable to be calculated due to information not being documented.17had not had a DEXA scan;seven of these were unable to be FRAX scored due to information not being docu-mented.11patients had both FRAX scores and DEXA scores:4had T scores <À2.5,indicating eligibility for treatment of osteoporosis.In these patients FRAX scores,without a BMD measurement,ranged from 6.1%to 13%for a major osteoporotic fracture and 0.9%to 6.6%for a hip fracture.In the seven patients with Tscores >À2.5,FRAX scores,without a BMD measurement,ranged from 3.1%>9.5%for a major osteoporotic fracture and 0.2%>1.8%for a hip fracture.Conclusion The majority of coeliac patients in this study were females,over the age of 40.Coeliac patients,over the age of 40,with FRAX scores for a major osteoporotic fracture >9.5%and for a hip fracture >1.8%may need DEXA scans and be offered osteoporosis treatment.A cost effectiveness analysis of this strategy is needed to change the current guidance.Competing interests E Derbyshire:None Declared,A Dhar Speaker bureau with:Several Pharmaceutical Companies,Conflict with:Honoraria from Pharmaceutical and endoscopy industry.REFERENCES1./FRAX2.Scott EM ,Gaywood I,Scott BB,et al.BSG Guidelines for Osteoporosis in Coeliac Disease and Inflammatory Bowel Disease .2000.INVESTIGATION OF THE OPTIMAL DURATION OF THE GLUCOSE HYDROGEN METHANE BREATH TESTdoi:10.1136/gutjnl-2012-302514c.1541,2E Grace,*3K Thomas,3S Gupta,2A Lalji,1K Whelan,4C Shaw,2J Andreyev.1Nutritional Sciences,King’s College London,London,UK;2GI Unit,London,UK;3Research Data Management &Statistics Unit,London,UK;4Dietetics Department,The Royal Marsden NHS Foundation Trust,London,UKIntroduction Historically,the glucose hydrogen breath test has been popular for diagnosing small intestinal bacterial overgrowth (SIBO).Lately the glucose hydrogen methane breath test has become available.It is non-invasive and simple to carry out.This test is used as a part of standard clinical practice in patients suspected of having SIBO in our hospital.There are limited published data on the optimal test duration,with 3h being the longest reported.This study aimed to determine if there is a signi ficant difference in the number of patients who would be considered positive for SIBO depending on test duration.Methods Patients in whom the gastroenterologist suspected SIBO underwent a breath test performed by endoscopy nurses using the QuinTron BreathT racker DP Digitial Microlyzer that measures hydrogen (H 2)and methane (CH 4)concentrations in parts per million (ppm).Pre-test preparation included avoiding slowly absorbed carbohydrates,fibre and large meals and limiting dairy intake and carbonated drinks for 24h,a 12h fast and avoiding exercise and cigarette smoking for 2h.Breath H 2and CH 4concen-trations were noted at baseline.Subjects then consumed 75g (or 50g if weight was <50kg)in 100ml of water.Thereafter,breath H 2and CH 4values were recorded every 20min for 3h (or less if posi-tive).Positive test was de fined as fasting H 2$20or CH 4$10ppm or a rise in H 2$12or CH 4$6ppm.Results 98males and 95females,median age 63years (range 28e 86)underwent a breath test.Of these,67(35%)had a positive result for one or both gases:18(32%)at baseline,39(60%)by 40min,56(84%)by 100min,60(90%)by 140min,67(100%)by 160min.126patients had negative breath tests;n ¼75had the test performed for a full 3h,26(20%)had the test performed for 100min only.In patients where the test was performed for 3h the 95%CI for a false negative result at 100min is 0.003to 0.10.Conclusion Most patients with SIBO will have a positive result by 100min.This suggests that a reduction in the duration of the test can be achieved without compromising the number of true positives being diagnosed with SIBO.Competing interests None declared.IS THE GLUCOSE HYDROGEN METHANE BREATH TEST AN ACCURATE DIAGNOSTIC TOOL FOR SMALL INTESTINAL BACTERIAL OVERGROWTH?doi:10.1136/gutjnl-2012-302514c.1551R I Rusu,1,2E Grace,*3K Thomas,2K Whelan,4C Shaw,1H J N Andreyev.1The GI Unit,Royal Marsden NHS Foundation Trust,London,UK;2Diabetes and Nutritional Sciences Division,King’s College London,London,UK;3Department of Computing,Royal Marsden NHS Foundation Trust,London,UK;4Department of Dietetics,Royal Marsden NHS Foundation Trust,London,UKIntroduction Small intestinal bacterial overgrowth (SIBO)is prob-ably the most common cause for chronic gastrointestinal (GI)symptoms following cancer treatments.There is no diagnostic gold standard.We assessed whether the glucose hydrogen methane breath test has greater value than the hydrogen breath test alone and whether a duodenal (D2)aspirate improves the diagnostic yield.Methods Patients in a cancer centre referred for potential SIBO.Breath hydrogen (H2)and methane (CH4)were measured in parts/doi: 10.1136/gutjnl-2012-302514c.1522012 61: A247-A248GutE M Quigley, A J Lembo, C Diaz, et al.(IBS-C): a European perspectiveirritable bowel syndrome with constipation phase 3 trial of linaclotide in patients with abdominal pain and bowel symptoms in a Significant improvements inPTU-152/content/61/Suppl_2/A247.2Updated information and services can be found at: These include:serviceEmail alertingthe box at the top right corner of the online article.Receive free email alerts when new articles cite this article. Sign up in Notes/group/rights-licensing/permissions To request permissions go to:/cgi/reprintform To order reprints go to:/subscribe/To subscribe to BMJ go to:。
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 ppt课件
活动探究三 甲烷能与氯气反应吗？
CH4与Cl2的反应
现象： 试管内气体颜色变浅，液面上升，内
壁出现油状液滴，试管中出现少量白雾。
学一学
H
· · H C × H + Cl Cl
H
H
·Байду номын сангаас· H C Cl + H × Cl
H
H
· H C × H
H
Cl ··Cl
学一学
H
H
H C H + Cl Cl 光 H C Cl + H Cl
NaOH溶液
稀硫酸
（滴有石蕊溶液）（滴有石蕊溶液）
活动探究二 甲烷能与高锰酸钾、强酸和强碱反应吗？
通常情况下，甲烷比较稳定，不与 高锰酸钾、强酸和强碱反应。
化学性质
一、甲烷的燃烧
产生淡蓝色火焰， 并放出大量的热
点燃
CH4+2O2
CO2+2H2O
活动探究三 甲烷能与氯气反应吗？
注意：观察实验现象并记录
第三章 有机化合物
最简单的有机化合物 甲烷
观察甲烷——物理性质
自无色无味的气体沼） 密度比空气小(标况 下0.717g/L)） 极难溶于水
温故知新 甲烷的分子结构 电子式： 结构式：
甲烷的分子结构模型
球棍模型
比例模型
验证实验——CH4的稳定性
CH4
验证实验——CH4的稳定性
尾气 收集
酸性KMnO4溶液
H
H
CH4+Cl2 光 CH3Cl+HCl
一氯甲烷（难溶于水的气体）
写一写
H
H
Cl C H + Cl Cl 光 Cl C Cl + H Cl
最简单的有机化合物甲烷课件
HCБайду номын сангаасOH + NaOH → CH4 + NaHCO3
3
实验条件
催化剂的选择和反应温度对甲烷的制
实验操作
4
备有重要影响。
详细的实验操作指导可以根据具体实 验方案进行说明。
甲烷的用途
热力学能源
甲烷是一种重要的 燃料，在能源领域 发挥着重要作用。
工业原料
甲烷被用于合成多 种重要有机化学品， 如甲醇、氨、乙炔 等。
物理性质
甲烷是一种无色、无味、无毒的气体，高压 下可液化。
结构式
甲烷的结构式是一个碳原子中心，四个氢原 子朝向碳原子四面八方。
化学性质
甲烷不易燃烧，但在适当的条件下可以产生 明亮的火焰。
甲烷的制备
1
学名：阿克曼反应
甲烷的主要制备方法是通过阿克曼反
反应方程式
2
应，其中甲酸和碱类催化剂反应生成 甲烷。
家庭燃料
甲烷被广泛用于家 庭的烹饪、供暖和 照明。
甲烷水合物
甲烷水合物是一种 在深海沉积物中存 在的天然气体储存 形式。
总结
1 有机化合物的定义
2 甲烷基本信息
有机化合物由碳和氢（以及其他元素）构 成，是多种天然和合成材料的基础。
甲烷是由一个碳原子和四个氢原子组成的 无色气体。
3 甲烷的制备过程
4 甲烷的多种用途
甲烷主要通过阿克曼反应制备，反应方程 式为H C O O H + N aO H → CH 4 + N aH C O 3。
甲烷被广泛应用于热力学能源、工业原料、 家庭燃料和甲烷水合物等领域。
最简单的有机化合物甲烷 ppt课件
有机化合物是由碳和氢（以及其他元素）构成的化合物，是多种天然和合成 材料的基础，在生活中无处不在。
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
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 气中的二氧化碳(CO2)、氢气(H2)、甲烷(CH4)等浓 度的变化，进行生理及或疾病研究的方法。
是一种重要的无创检查胃肠与肝、胰功能的手段。 在消化病临床与科研领域被有广泛应用价值。
具有无创、方便、灵敏、准确、可靠等优点。
北京大学第三医院
气体收集
3.第一次呼气结束后，将10g乳果糖口服液混在250ml水中 （约一纸杯），30秒内喝完，并开始计时，每20分钟按前述 方法收集一次，逐次将“标本袋2-10”装满，前后共持续 180分钟，并在“检查记录单”上填写各标本袋的时间点。
北京大学第三医院
检查记录单
底物选择：乳果糖口服溶液10g
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
1. 当前一次测量结束后，显示屏上红灯亮起以后代表测量结束，机器
将自动关闭进气通道，此时方可拔出注射器，抽取下一个标本袋中的 气体；
2. 将装有待测气体的注射器插入过滤管，若此时橙色灯频繁闪动，说
明机器内部正在测量和计算数据，此时不可向机器内注气；
3. 等到显示屏上的数字固定不变，且绿灯亮起后代表测量完毕，此时
3
4
5
6
7
8
9 10
时间间隔
0 20 40 60 80 100 120 140 160 180
H2 CH4 CO2
北京大学第三医院
结果曲线图
北京大学第三医院
注意事项
医师应根据不同的检查目的合理选择底物，并可适当调整 患者的准备和集气方法，最终对检测结果作出合理解释。
北京大学第三医院
规范操作的细节步骤
北京大学第三医院
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，并被检测出，而明确诊断。
北京大学第三医院
患者准备
北京大学第三医院
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1-10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。
北京大学第三医院
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。
甲烷和氢呼气试验原理
正常人体平静状况下是不产生甲烷和氢的，其唯一来源只能是与人体 相伴的肠道内的细菌。
厌氧菌偏好代谢的糖类分子，糖分子作为发酵反应最初的阶段，被分 解成短链脂肪酸(SCFA)，二氧化碳、甲烷和氢气。
北京大学第三医院
检测步骤
北京大学第三医院
检测步骤--准备阶段
1.排出残余气体：开机，空跑几分钟，排出机器内残存 气体； 2.调试机器：检查机器各项指标，如气流Flow保持在60 左右； 3.安装过滤管：将装有新鲜干燥剂的过滤管与机器相连 ； 4.标准气体校准：用注射器抽取20ml“标准气体”通过 过滤管注入机器进行校准；
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
北京大学第三医院
试验机制
北京大学第三医院
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 · 乳糖不耐受症 · 诊断乳糖酶缺乏和牛奶过敏 · 细菌过度生长（ SIBO ） · 肠道传递时间（ ITT ）和肠道动力 · 其他因乳糖等吸收不良导致的症状如；肌纤维痛等
北京大学第三医院 各指标的校正参数分别为 H2: 150，CH4: 76，CO2: 6.1
检测步骤--正式测量
用注射器抽取20ml标本袋1中的气体，通过过滤管注入机器 进行测量；
北京大学第三医院
检测步骤--正式测量
测量结束后记录显示屏上的数据，以此源自推，测量标本袋210中的气体。北京大学第三医院
北京大学第三医院
产品信息
1、世界第一品牌，50年历史验证，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。 5、特有CO2浓度校正和肺泡气体测量，确保结果精确。
北京大学第三医院
操作步骤
北京大学第三医院
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，禁止吸烟（包括避免二手烟） ，检查当日空腹并先行刷牙漱口。 3.呼气过程中保持清醒、安静，禁饮、禁食、禁止睡觉， 不得剧烈运动，以免影响肠道蠕动和肺通气量变化。
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。