Walecka-Kapica Ewa, Klupińska Grazyna, Harasiuk Agnieszka, Felicka Ewa, Foryś Sebastian, Chojnacki Cezary
Uniwersytet Medyczy w Łodzi, Klinika Gastroenterologii i Chorób Wewngtrznych.
Pol Merkur Lekarski. 2007 May;22(131):332-5.
The pathogenesis of functional dyspepsia is very complicated and its etiology is still not clear. One of the supposed pathophysiological mechanisms is the deficiency of melatonin. The deficiency of melatonin leads to increase the oxide reactive form's concentration as nitric oxide metabolites and to decrease of antyoxidative enzymes activity. This last factor seems to be very important in correct digestive tract function. The aim of our study was answer the question if is the difference between NO metabolites concentraction in gastric juice in patients with functional dyspepsia and in healthy subjects and wheather the treatment with melatonin plays the role in normal digestive tract function.
The study included 60 subjects between of 18 to 48 years with diagnosed functional dyspepsia (according to the Rome III Criteria). The study group was divided into two subgroups: group I--30 subjects with Epigastric Pain Syndrome-EPS and group II--30 subjects with Postprandial Disorders Syndrome-PDS. Control group comprised 25 healthy subjects (without any clinical or morphological symptoms of digestive tract disease). In each patient the gastroscopy was performed. During gastroscopy 5 ml gastric juice was collected. The juice was centrifuged for 15 min (4500 rotations). The undiluted supernatant was frozen in the temperature -70 degrees C. The concentration of nitric oxide metabolites in gastric juice was determined with spectrophotometric based on ELISA test (540 nm wavelength) using a microplates reader (Multiscan, Labsystems). In patients with functional dyspepsja the investigations were performer twice before and after 6 weeks treatment with melatonin. Melatonin was applied in dose 5 mg daily, in the evening.
The concentration of nitric oxide metabolites in gastric juice in healthy subjects was 6.81 +/- 2.23 microM. In patients with functional dyspepsia was significantly higher; in patients with Epigastric Pain Syndrome--10.99 +/- 2.46 microM (p < 0.05), in patients with Postprandial Disorders Syndrome--9.28 +/- 2.18 microM (p < 0.05). After treatment with melatonin the concentration of nitric oxide metabolites in gastric juice in both groups decreased and were 8.21 +/- 1.83 microM in patients with Epigastric Pain Syndrome and 6.93 +/- 1.61 microM in patients with Postprandial Disorders Syndrome.
In patients with functional dyspepsia the concentration of nitric oxide metabolites in gastric juice was significantly higher than in control group. After treatment with melatonin the concentration of nitric oxide metabolites in gastric juice in both groups decreased--in patients with Epigastric Pain Syndrome as well as in patients with Postprandial Disorders Syndrome. The treatment with melatonin seems to be suitable in combined therapy of functional dyspepsia.
功能性消化不良的发病机制非常复杂,其病因仍不明确。一种推测的病理生理机制是褪黑素缺乏。褪黑素缺乏会导致氧化反应形式(如一氧化氮代谢产物)的浓度增加,以及抗氧化酶活性降低。最后一个因素似乎对正常消化道功能非常重要。我们研究的目的是回答功能性消化不良患者与健康受试者胃液中一氧化氮代谢产物浓度是否存在差异,以及褪黑素治疗是否对正常消化道功能起作用。
该研究纳入了60名年龄在18至48岁之间、被诊断为功能性消化不良(根据罗马III标准)的受试者。研究组分为两个亚组:第一组——30名患有上腹部疼痛综合征(EPS)的受试者,第二组——30名患有餐后不适综合征(PDS)的受试者。对照组由25名健康受试者(无任何消化道疾病的临床或形态学症状)组成。对每位患者进行胃镜检查。在胃镜检查期间收集5毫升胃液。将胃液离心15分钟(4500转)。未稀释的上清液在-70摄氏度下冷冻。使用酶联免疫吸附测定(ELISA)测试(540纳米波长),通过酶标仪(Multiscan,Labsystems)基于分光光度法测定胃液中一氧化氮代谢产物的浓度。在功能性消化不良患者中,在褪黑素治疗6周前后各进行两次检测。褪黑素以每日5毫克的剂量,在晚上服用。
健康受试者胃液中一氧化氮代谢产物的浓度为6.81±2.23微摩尔。功能性消化不良患者的浓度显著更高;上腹部疼痛综合征患者为10.99±2.46微摩尔(p<0.05),餐后不适综合征患者为9.28±2.18微摩尔(p<0.05)。褪黑素治疗后,两组患者胃液中一氧化氮代谢产物的浓度均降低,上腹部疼痛综合征患者为8.21±1.83微摩尔,餐后不适综合征患者为6.93±1.61微摩尔。
功能性消化不良患者胃液中一氧化氮代谢产物的浓度显著高于对照组。褪黑素治疗后,两组患者胃液中一氧化氮代谢产物的浓度均降低——上腹部疼痛综合征患者和餐后不适综合征患者均如此。褪黑素治疗似乎适用于功能性消化不良的联合治疗。