甲烷氢呼气试验的临床应用进展

近年兴起的甲烷氢呼气试验是一种诊断胃肠疾病及相关疾病的非侵入性方法。现回顾性分析甲烷氢呼气试验的相关文献,归纳其在临床应用方面的情况。总结甲烷氢呼气试验在诊断小肠细菌过度生长(small intestinal bacterial overgrowth,SIBO)、乳糖不耐受,以及大肠癌筛查中的作用。     

慢性腹泻患者乳糖氢呼吸试验结果分析

利用呼气氢方法进行小肠传递时间测定，对小肠动力学研究具有重要价值，已被广泛应用于药代动力学、生理学、营养学以及临床多种疾病状态时的研究［１］。本文用美国贝克曼公司的ＣＭ型氢气微分析仪，对６２例慢性腹泻患者以１８９乳糖为基质作氢呼吸试验。比较不同病因的慢性腹泻患者乳糖吸收不良的发生率，同时观察肺泡呼气的含氢量峰值及峰值出现的时间。其目的是了解对乳糖吸收不良的严重程度及肠道运动功能。对象与方法从门诊中选择慢性腹泻病人６２例，男性４２例，女性２０例。年龄２１～７６岁，平均４２．４４岁。其中慢性结肠炎３…     

氢气结合甲烷气呼气试验检测肠易激综合征患者小肠细菌过度生长

目的通过乳果糖氢气结合甲烷气呼气试验检测肠易激综合征(irritable bowel syndrome,IBS)患者小肠细菌过度生长(small intestinal bacterial overgrowth,SIBO)的发生率,判断SIBO与IBS症状的关系,探讨甲烷呼气试验在不产氢气患者的临床应用价值。方法纳入符合罗马Ⅲ诊断标准的IBS患者和年龄、性别匹配的健康人(对照组),进行乳果糖氢气结合甲烷气呼气试验,计算SIBO阳性发生率,对比各时间点呼气氢与甲烷浓度;将IBS患者分为SIBO阳性组和SIBO阴性组,比较其症状评分。结果共纳入70例IBS患者(IBS组,92.86%为腹泻型和混合型)和30名健康人(对照组)。两组SIBO阳性率分别为71.43%和36.67%(P0.05)。两组甲烷呼气试验结果与氢呼气试验结果均呈显著线性相关(IBS组:r=0.999,P=0.000;对照组:r=0.745,P=0.003),仅1例腹泻型IBS患者氢呼气试验阴性而甲烷呼气试验阳性。SIBO阳性(n=50)与SIBO阴性(n=20)IBS患者症状评分比较,差异无统计学意义(P0.05)。结论 IBS患者SIBO阳性率明显高于健康人,提示SIBO与IBS有关,但SIBO并不加重IBS患者的症状;在乳果糖呼气试验中,甲烷气与氢气浓度呈显著线性相关,甲烷气对不产氢气的IBS患者合并SIBO的补充检测作用有限。     

老年入及慢性非器质性腹泻患者的乳糖酶缺乏症

用乳糖氢呼吸试验检测了18例20～65岁正常人基础氢值均在30PPM以下,平均22.5±3.8PPM,服乳糖后氢上升≥20PPM者13例(72.2％),平均升高62.9±64.4MMP。基本健康的70～87岁老人共17例,基础氢值19.7±4.0PPM,乳糖试验异常者7例(41.1％),呼气中氢平均升高42.4±23.6PPM。21例非器质性慢性腹泻患者基础氢平均22.7±9.0PPM,有2例>30PPM,服乳糖后异常者18例(85.7％),平均升高60.4±34.5PPM。说明我国正常人中乳糖酶缺乏的阳性率约为72.2％。高龄老人中阳性率41.1％,有随年龄增高逐渐适应的趋势。非器质性腹泻组乳糖酶缺乏的阳性率85.7％,且有2例空腹氢含量升高,提示乳糖酶缺乏可能与部份慢性腹泻患者的病因有关,这类病人在症状发作期间限制乳类制品是值得推荐的。     

补充乳糖酶对改善乳糖不耐受的效果研究

乳糖酶是一种由小肠细胞分泌的消化酶,功能是消化乳糖,乳糖需经乳糖酶分解才能吸收.乳糖酶缺乏会引起乳糖消化吸收障碍,其中部分患者会出现以腹胀、腹痛、腹泻为主的一系列临床症状,称为乳糖不耐受(lactose intolerance,LI).乳糖主要存在于牛奶及其制品中.乳糖酶缺乏在北欧人中占15%,黑人及拉美人占80%,而美国印第安人和亚洲人可高达100%[1].     

乳糖酶缺乏者饮乳糖酶处理过的牛奶其吸收和耐受性观察

60例健康人饮500ml鲜牛奶后，经氢气呼吸试验测定，49例（81．67％）有牛奶乳糖吸收不良，后者改饮经乳糖酶处理的500ml低乳糖牛奶后，37例（75．51％）转为吸收正常，其余12例中10例有不同程度好转，总有效率达95．91％。49例出现胃肠道症状，牛奶乳糖不耐受率为79．59％；改饮低乳糖牛奶后，不耐受率降低至10．20％（P＜0．01）。故低乳糖牛奶能有效地减少正常人群对牛奶乳糖的吸收不良及不耐受性。     

呼气氢试验临床应用与研究近展

呼气氢试验(BHT)作为一种非侵入性胃肠功能检查方法,1984年起在国内广泛开展。近年该试验得到进一步扩大应用。本文就近年来国内外应用与研究进展作一简介如下。 碳水化合物吸收不良 BHT最早用于乳糖吸收不良症的诊断。其原理为摄入后在小肠内未被吸收的乳糖被结肠内细菌发酵产生氢气,其中一部分(14％～21％)恒定地经血循环由肺呼出。该方法与诊断乳糖吸收不     

根治小肠细菌过度生长能减轻肠易激综合征的症状

本研究应用乳果糖氢呼气试验旨在验证肠易激综合征(ＩＢＳ)患者小肠细菌过度生长(ＳＩＢＯ)发生率较高,使用抗生素根治ＳＩＢＯ能改善ＩＢＳ的症状。方法 在Ｃｅｄａｒｓ＿Ｓｉｎａｉ医疗中心行乳果糖氢呼气试验(ＬＨＢＴ)的病人均进行问卷调查,包     

氢呼气试验的临床应用

氢呼气试验是指受试者口服产氢性基质后测定呼气中氢含量以反映消化道生理病理变化的试验,具有简便、迅速、无创伤等优点,可用于多种胃肠道功能或疾病的诊断。近年来,采用较为简单的收集、贮存与分析呼气中氢含量的方法使其临床应用得到进一步发展。     

营养与代谢疾病

8了092了24氢呼气试验对乳糖酶缺乏的研 ·究一了98名健康人调查/贝谦…刀中华内科 杂志一1987,‘26(3)一131~133 ,被测者基础氢值为19.92士13·49 ppm‘(X士1.965一)。乳糖氢呼气试验(HBT) 阳性(乳葡酶缺乏)者169人(85 .4肠), 其末段呼气中氢气浓度峰值与基础氢值之差 (△ppm)为54 .12士Zo.17ppm(X+SD); HBT阴性29人(14.6帕),△ pPrn为6.34士 8.56ppm,两者P<0.02。HBT阳性者中 88.2肠呼氢峰值在服乳糖后第2、3小时出 现,3.5肠在第一小时,8.3肠在第四小时出 现。性别与各年龄组无显著差别。试前晚吃 面食者比吃米食者明显升高;平时常…     

Lactose malabsorption and intolerance: What should be the best clinical management?

Lactose malabsorption (LM) is the incomplete hydrolysis of lactose due to lactase deficiency, which may occur as a primary disorder or secondary to other intestinal diseases. Primary adult-type hypolactasia is an autosomal recessive condition resulting from the physiological decline of lactase activity. Different methods have been used to diagnose LM. Lactose breath test represents the most reliable technique. A recent consensus conference has proposed the more physiological dosage of 25 g of lactose and a standardized procedure for breath testing. Recently a new genetic test, based on C/T13910 polymorphism, has been proposed for the diagnosis of adult-type hypolactasia, complementing the role of breath testing. LM represents a wellknown cause of abdominal symptoms although only some lactose malabsorbers are also intolerants. Diagnosing lactose intolerance is not straightforward. Many non-malabsorber subjects diagnose themselves as being lactose intolerant. Blind lactose challenge studies should be recommended to obtain objective results. Besides several studies indicate that subjects with lactose intolerance can ingest up to 15 g of lactose with no or minor symptoms. Therefore a therapeutic strategy consists of a lactose restricted diet avoiding the nutritional disadvantages of reduced calcium and vitamin intake. Various pharmacological options are also available. Unfortunately there is insufficient evidence that these therapies are effective. Further double-blind studies are needed to demonstrate treatment effectiveness in lactose intolerance.     

Lactose malabsorption

Opinion statement Lactose malabsorption is a syndrome producing constellation of symptoms, including abdominal pain, bloating, flatulence, diarrhea, and sometimes nausea and/or vomiting. Primary causes of lactose malabsorption due to loss of intestinal lactase activity include genetic/racial lactase nonpersistence, congenital lactase deficiency, and developmental lactase deficiency. Secondary lactose malabsorption can be caused by any disorder that injures the small intestinal mucosa, such as viral gastroenteritis, celiac disease, allergic (eosinophilic) gastroenteritis, and radiation enteritis. The diagnosis depends on careful clinical evaluation and is customarily confirmed with a lactose breath hydrogen test. As the symptoms are nonspecific, many adults diagnosed with lactose malabsorption actually have irritable bowel syndrome. Treatment consists of a trial of eliminating lactose-containing dairy foods, with supplementation of alternative calcium and protein sources. Commercial enzyme products containing β-galactosidases can be prescribed to help patients digest dietary lactose. Long-term lactose restriction usually is not necessary and can lead to reduced bone mineral density.     

High prevalence of celiac disease in patients with lactose intolerance

BACKGROUND/AIMS: Acquired lactase deficiency is a common cause of gastrointestinal symptoms but its etiology remains unclear. Celiac disease could lead to lactase deficiency and is much more common than previously suspected. Several studies have highlighted the prevalence of lactose intolerance in celiac disease, but studies assessing the prevalence of celiac disease in lactose intolerance are lacking. We evaluated the prevalence of celiac disease in patients with a positive H2-lactose breath test compared to a control group. METHODS: This retrospective study included 54 patients (15 males/39 females; mean age 37.8 +/- 7 years) from southern Italy, referred to the Gastroenterology Unit for bloating and diarrhea after the introduction of milk or dietary lactose. They had a positive H2-lactose breath test and a negative H2-glucose breath test. 50 blood donors were drawn from a similar population, matched for sex and age, and enrolled as a control group. All patients were screened for possible celiac disease by measuring the serum level of IgA antibodies to endomysium, anti-transglutaminase and total IgA. Patients positive for at least one of these markers were submitted to upper gastrointestinal endoscopy. RESULTS: None of the patients had a IgA deficiency. 24% of the patients showed positivity of celiac disease antibodies compared to 2% in the control group (p < 0.001). Histologic samples of these patients showed villous atrophy (53.8% Marsh type IIIa, 38.4% Marsh IIIb, and 7.6% with Marsh type IIIc) confirming the celiac disease, while in the control subjects duodenal biopsies were normal. CONCLUSIONS: A high prevalence of celiac disease was observed in patients with a positive H2-lactose breath test compared to healthy controls. In these subjects lactase deficiency seems to be the only manifestation of celiac disease. We suggest serologic screening for celiac disease in all patients with a positive H2-lactose breath test before beginning a milk-exclusion diet.     

Lactase deficiency: a common genetic trait of the American Indian

Intestinal lactase activity was assessed indirectly in 156 American Indians by measuring breath hydrogen after an oral lactose load. Lactase deficiency was present in 66% of subjects and correlated highly with the percentage of Indian blood. Lactase deficiency was present by the age of 5 years and was unrelated to sex. Most lactase-deficient subjects (81%), but only a minority (23%) of lactase-sufficient subjects, developed symptoms after the oral lactose load, and among lactase-deficient subjects, symptoms occurred more frequently in adults than in children (P = 0.05). Indeed, by history, 53% of lactase-deficient adults, but only 10% of lactase-deficient children under 18 years of age, were aware of milk intolerance. Despite these differences, milk consumption was only slightly less (19 g) in the lactase-deficient subjects than in those with normal lactase activity (25 g) (P less than 0.05). The results indicate that lactase deficiency is a common autosomal genetic trait in the American Indian that becomes manifest in early childhood. Tolerance to dietary lactose appears to decline in the American Indian as he reaches adulthood, but in this population the decline in tolerance had only minor influence on lactose intake.     

Management and treatment of lactose malabsorption

Lactose malabsorption is a very common condition characterized by intestinal lactase deficiency. Primary lactose malabsorption is an inherited deficit present in the majority of the world's population, while secondary hypolactasia can be the consequence of an intestinal disease. The presence of malabsorbed lactose in the colonic lumen causes gastrointestinal symptoms. The condition is known as lactose intolerance. In patients with lactase nonpersistence, treatment should be considered exclusively if intolerance symptoms are present. In the absence of guidelines, the common therapeutic approach tends to exclude milk and dairy products from the diet. However, this strategy may have serious nutritional disadvantages. Several studies have been carried out to find alternative approaches, such as exogenousβ-galactosidase, yogurt and probiotics for their bacterial lactase activity, pharmacological and non pharmacological strategies that can prolong contact time between enzyme and substrate delaying gastrointestinal transit time, and chronic lactose ingestion to enhance colonic adaptation. In this review the usefulness of these approaches is discussed and a therapeutic management with a flow chart is proposed.     

Lactose intolerance in active Crohn's disease: clinical value of duodenal lactase analysis.

BACKGROUND: Patients with active Crohn's disease (CD) often report having abdominal symptoms after ingestion of milk products, but the pathomechanism for lactose malabsorption seems to be complex. GOALS: To investigate the prevalence of clinical milk intolerance and to objectify symptoms with hydrogen (H 2 ) breath testing, analysis of lactase protein, and enzyme activity in the duodenal mucosa in patients with CD and in healthy controls. STUDY: In 49 patients with CD and 24 controls, H 2 breath testing was performed. All individuals underwent endoscopy of the upper gastrointestinal tract, in which multiple pinch samples were taken from the distal duodenum. Lactase activity was measured using the method of Dahlquist. The lactase protein expression was analyzed by gel electrophoresis using the monoclonal antibody mlac 10 and by immunochemistry using the monoclonal antibody mlac 4. RESULTS: Prevalence of milk intolerance in healthy controls was 16.6% versus 46.9% in patients with CD, with a high frequency (83.3%) in patients with active disease (CD activity index >150). Milk intolerance was correlated to the duration of inflammatory bowel disease ( p = 0.023) but not to the location or previous bowel resection. Hydrogen breath testing had a moderate sensitivity in detecting lactose maldigestion (70.4%) and a high specificity (95.6%). Duodenal lactase levels were also correlated to disease activity, whereas correlations to clinical symptoms remained poor. Patients with milk intolerance had a significantly reduced bone density at the lumbar spine (z-score, -1.33 +/- 0.92 vs. -0.19 +/- 0.95 [mean +/- SD]; p = 0.002) CONCLUSIONS: Milk intolerance is a frequent problem in active CD, which can be objectified accurately by H 2 lactose breath testing. Decreased lactase levels in the duodenal mucosa may be found during an acute flare but are not the predominant cause of milk intolerance in CD.     

Lactose intolerance in Jewish patients with ulcerative colitis

Seventy patients with ulcerative colitis had lactose tolerance tests. Of 51 non-Jewish patients, 12 (23.5%) had lactose intolerance, whereas of 19 Jewish patients, 16 (84.2%) had lactose intolerance. This difference is significant (P<0.001). The control group of 41 Jews without ulcerative colitis had a 71% incidence of lactose intolerance, whereas of 53 non-Jewish controls, only 20.7% had such intolerance. These results are also statistically valid (P<0.001). This suggested that segregation of the genes for ulcerative colitis as well as for lactase deficiency in Jews is a possible reason for the high incidence of lactase deficiency found in patients with ulcerative colitis.Supported by a grant from The Hartford Foundation.     

Lactose intolerance in adults with chronic unspecific abdominal complaints

77 hospitalized patients with chronic unspecific abdominal complaints, in whom any other organic disease had been previously excluded, were investigated for lactose malabsorption; they were subdivided into two groups: 46 patients complaining primarily of colicky abdominal pain and/or intermittent diarrhoea (group 1) and 31 patients presenting with dyspepsia as the predominant symptom (group 2). To establish the exact prevalence of isolated lactase deficiency in the healthy adult population served by our hospital, 40 Italian adult healthy subjects were also studied. The prevalence of lactose malabsorption was significantly higher (p less than 0.005) in patients of the 1st group than in patients of the 2nd group, and in the healthy adult population seen at our hospital (74% vs 35.5% and 37.5%, respectively). Furthermore a high prevalence of lactose intolerance, determined by means of a three-week diet trial (lactose free-diet versus normal diet), was documented among lactose malabsorbers of the 1st group. We concluded therefore that lactose intolerance is a factor in some Italian adult patients who suffer from long-standing aspecific abdominal discomfort, and it should be always considered in these patients, especially when colicky abdominal pain and diarrhoea are present, before the diagnosis of irritable bowel syndrome is made.     

Intestinal lactase deficiency in an apparently normal Peruvian population

The prevalence of milk and lactose intolerance and intestinal lactase deficiency was studied in 30 apparently healthy Peruvian individuals. At the same time, 20 milk-intolerant persons were included in the study. According to the results of lactose-tolerance tests and intestinal lactase assays, one-third of the 30 were considered normal and were used as controls. The other two-thirds were found to be abnormal and were referred to asasymptomatics; they tolerated well small amounts of milk consumed daily. Upon lactose load, they developed gastro-intestinal symptoms, and maximal rise of blood glucose was below normal limits. Enzymatic assay indicated that they were deficient in intestinal lactase. The remaining 20 were intolerant to milk and the results of their tests were abnormal. Sucrase activity was similar in the 3 groups. This high incidence of lactase deficiency in apparently normal individuals seems to be acquired.     

The Role of Colonic Microbiota in Lactose Intolerance

In a previous study we observed a clear difference in lactose intolerance symptoms after a 25-g lactose load in two groups of persons with lactase nonpersistence and similar small intestinal lactase activity. From this observation we hypothesized a colon resistance factor. To identify this factor, the microbial composition of fecal samples of the two lactose intolerant groups (one with mild symptoms, n = 16, and one with diarrhea-predominant symptoms, n = 11) was compared using the fluorescent in situ hybridization technique. Large interindividual differences were found in the numbers of total bacteria and main groups of bacteria (CV: 0.65 and 0.64-0.82 respectively). The bacterial numbers were not significantly different between the two groups. A significant negative correlation, however, was found between the individual symptom scores of the intolerant persons and the numbers of total hybridizable bacteria (r(s) = -0.42, P = 0.03). The results suggest that an increased number of bacteria might contribute--by means of a higher fermentative capacity--to the reduction of lactose intolerance symptoms.