Chelimsky Gisela, Conant Lisa, Simpson Pippa, Zhang Liyun, Marchand Serge, Hillard Cecilia, Chelimsky Thomas
Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Virginia Commonwealth University, Richmond, VA, USA.
Department of Neurology, Medical College of Wisconsin, Milwaukee, WI, USA.
Pain Rep. 2025 Jun 16;10(4):e1273. doi: 10.1097/PR9.0000000000001273. eCollection 2025 Aug.
Pain constitutes the chief complaint of some functional gastrointestinal disorders (FGIDs). The endocannabinoid (EC) and peroxisome proliferator-activated receptors (PPARs) agonist systems have not been explored as possible contributors.
To determine if EC and PPAR agonist abnormalities occur in adolescents with FGID.
Institutional Review Board approved study compared 33 children (12-18 years) with a FGID to 18 healthy controls (HC). Clinical measures: functional disability inventory and pediatric pain questionnaire (PPQ). Endocannabinoid and PPAR agonist concentrations were determined in serum from blood. Data were analyzed using Mann-Whitney and Fisher exact tests (2-sided < 0.05 considered significant).
When compared to HC, FGID subjects used different terms to describe their pain, which also occurred in more body areas. Functional gastrointestinal disorder subjects exhibited higher palmitoylethanolamide (PEA) and -oleoylethanolamide, while EC did not differ. Interestingly, PEA correlated significantly with PPQ "worst pain the week before" in the HC group with Spearman ρ = 0.519, = 0.003, but not in the FGID group (ρ = 0.079, = 0.66).
Children with FGID exhibit significant pain in nongastrointestinal regions. The higher concentrations of PEA found in the FGID subjects, also occurring in other chronic pain conditions, could reflect a compensatory response due to feedback loops from a downregulated or nonresponsive PPAR system, while the absence of the expected relationship between pain intensity and PEA levels in the FGID group suggests that the PPAR system may not be functioning normally.
疼痛是一些功能性胃肠疾病（FGID）的主要症状。内源性大麻素（EC）和过氧化物酶体增殖物激活受体（PPAR）激动剂系统尚未被探讨是否可能是导致这些疾病的因素。
确定FGID青少年中是否存在EC和PPAR激动剂异常。
经机构审查委员会批准的研究，将33名患有FGID的儿童（12 - 18岁）与18名健康对照者（HC）进行比较。临床测量指标：功能残疾量表和儿童疼痛问卷（PPQ）。测定血液中血清内的内源性大麻素和PPAR激动剂浓度。数据采用曼 - 惠特尼检验和费舍尔精确检验进行分析（双侧 < 0.05认为具有显著性）。
与HC相比，FGID受试者用不同术语描述他们的疼痛，且疼痛发生在更多身体部位。功能性胃肠疾病受试者表现出较高的棕榈酰乙醇胺（PEA）和油酰乙醇胺，而EC无差异。有趣的是，在HC组中，PEA与PPQ“前一周最严重疼痛”显著相关，斯皮尔曼ρ = 0.519， = 0.003，但在FGID组中无相关性（ρ = 0.079， = 0.66）。
FGID儿童在非胃肠道区域存在明显疼痛。在FGID受试者中发现的较高浓度的PEA，在其他慢性疼痛病症中也存在，这可能反映了由于PPAR系统下调或无反应的反馈回路引起的代偿反应，而FGID组中疼痛强度与PEA水平之间缺乏预期关系表明PPAR系统可能未正常发挥作用。
