Brain-Gut Research Group, Gastroenterology Group Practice, Bern, Switzerland.
Mech-Sense, Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark.
Gastroenterology. 2018 Oct;155(4):1034-1044.e6. doi: 10.1053/j.gastro.2018.07.013. Epub 2018 Sep 3.
BACKGROUND & AIMS: Functional gastrointestinal disorders (FGID) are defined by broad phenotypic descriptions and exclusion of recognizable disease. FGIDs cause multi-organ symptoms and abnormal results in a wide range of laboratory tests, indicating broad mechanisms of pathogenesis. Many patients with FGID develop symptoms following ingestion of fermentable sugars; we investigated the associations between symptoms and intestinal gas production following sugar provocation tests to elucidate mechanisms of FGID.
We performed fructose and lactose breath tests in 2042 patients with a diagnosis of FGID (based on Rome III criteria), referred to a gastroenterology practice from January 2008 through December 2011. Medical and diet histories were collected from all subjects. Breath samples were collected before and each hour after, for 5 hours, subjects ingested fructose (35 g) and lactose (50 g) dissolved in 300 mL water. Hydrogen and methane gas concentrations were measured and GI and non-GI symptoms were registered for 5 hours following sugar ingestion. Symptom and gas time profiles were compared, treelet transforms were used to derive data-related symptom clusters, and the symptom severity of the clusters were analyzed for their association with breath gas characteristics.
We identified 11 GI and central nervous system (CNS) symptom profiles and hydrogen and methane breath concentrations that changed significantly with time following sugar ingestion. Treelet transform analysis identified 2 distinct clusters, based on GI and CNS symptoms. The severity scores for the GI and CNS symptoms correlated following ingestion of sugars (all, P < .0001). However, only the GI symptoms associated with hydrogen and methane gas production (all, P < .0001).
In an analysis of breath test results from more than 2000 patients with FGIDs, we identified clusters of GI and CNS symptoms in response to fructose of lactose ingestion. The association between specific symptoms and breath gas concentrations indicate distinct mechanisms of FGID pathogenesis, such as changes in the microbiome or mechanical and chemical sensitization. ClinicalTrials.gov ID: NCT02085889.
功能性胃肠病（FGID）的定义是基于广泛的表型描述和排除可识别的疾病。FGID 引起多器官症状和广泛的实验室检查异常结果，表明发病机制广泛。许多 FGID 患者在摄入可发酵糖后出现症状；我们研究了糖激发试验后症状与肠道气体产生之间的关系，以阐明 FGID 的发病机制。
我们对 2042 例 FGID 患者（基于 Rome III 标准）进行了果糖和乳糖呼气试验，这些患者于 2008 年 1 月至 2011 年 12 月被转诊至胃肠病学诊所。所有受试者均采集了病史和饮食史。受试者在 300 毫升水中溶解 35 克果糖和 50 克乳糖后，分别在 5 小时内每小时采集一次呼吸样本。测量氢和甲烷气体浓度，并在糖摄入后 5 小时内记录胃肠道和非胃肠道症状。比较症状和气体时间曲线，使用树状变换来推导与数据相关的症状聚类，并分析聚类的症状严重程度与呼吸气体特征的关系。
我们确定了 11 种胃肠道和中枢神经系统（CNS）症状谱，以及在摄入糖后随时间变化的氢和甲烷呼气浓度。树状变换分析基于胃肠道和中枢神经系统症状确定了 2 个不同的聚类。糖摄入后，胃肠道和中枢神经系统症状的严重程度评分呈正相关（均 P < 0.0001）。然而，只有与氢和甲烷气体产生相关的胃肠道症状（均 P < 0.0001）。
在对 2000 多名 FGID 患者的呼气试验结果进行分析后，我们确定了对果糖和乳糖摄入的胃肠道和中枢神经系统症状聚类。特定症状与呼吸气体浓度之间的关联表明 FGID 发病机制存在不同的机制，例如微生物组的变化或机械和化学致敏。ClinicalTrials.gov ID：NCT02085889。
