Kiziltaş S, Imeryüz N, Gürcan T, Siva A, Saip S, Dumankar A, Kalayci C, Ulusoy N B
Department of Medicine, University of Marmara, Faculty of Medicine, Istanbul, Turkey.
Am J Gastroenterol. 1998 Dec;93(12):2420-5. doi: 10.1111/j.1572-0241.1998.00697.x.
The aim of the present study was to investigate whether corticosteroid therapy alters gastroduodenal mucosal permeability and whether permeability alteration is associated with macroscopic mucosal damage.
Eight patients taking oral corticosteroid therapy (total prednisone-equivalent dose, 1.5+/-0.1 g; duration, approximately 30 days), nine patients with multiple sclerosis taking high-dose intravenous methyl-prednisolone therapy (total dose, 11.7+/-0.5 g; duration, approximately 9 days), and 20 age- and gender-matched controls were studied. Gastroduodenal permeability was determined using sucrose as a site-specific permeability probe. Five-hour urine was collected after ingesting 100 g of sucrose and its urinary excretion rate was measured using high-pressure liquid chromatography. Gastroduodenal endoscopy was performed before steroid therapy to exclude subjects with evidence of macroscopic mucosal lesions. The sucrose test and endoscopy were repeated after completion of corticosteroid therapy.
The urinary sucrose excretion rates were similar in the control group and in patient groups before corticosteroid therapy. The median excretion rate of sucrose increased four (one to 28)- and eight (two to 35)-fold, respectively, as compared with pretreatment values in patients taking oral steroid and high-dose intravenous methyl-prednisolone therapy (p < 0.01). Considering all patients together, subjects who received a mean prednisone-equivalent dose of 8.4+/-1.5 g exhibited mucosal lesions, whereas patients who received 3.3+/-1.8 g did not (p = 0.06). The post-therapy increments in sucrose excretion rates were associated with neither the presence of macroscopic lesions nor with the total steroid dose received.
Corticosteroid therapy augments gastroduodenal permeability and high doses are associated with macroscopic mucosal lesions. Steroid-induced permeability increase does not appear to be associated with the presence of macroscopic mucosal lesions.
本研究旨在调查皮质类固醇疗法是否会改变胃十二指肠黏膜通透性，以及通透性改变是否与宏观黏膜损伤相关。
对8名接受口服皮质类固醇治疗的患者（泼尼松等效总剂量，1.5±0.1 g；疗程，约30天）、9名接受大剂量静脉注射甲泼尼龙治疗的多发性硬化症患者（总剂量，11.7±0.5 g；疗程，约9天）以及20名年龄和性别匹配的对照组进行研究。使用蔗糖作为部位特异性通透性探针测定胃十二指肠通透性。摄入100 g蔗糖后收集5小时尿液，并使用高压液相色谱法测量其尿排泄率。在类固醇治疗前进行胃十二指肠内镜检查，以排除有宏观黏膜病变证据的受试者。皮质类固醇治疗结束后重复进行蔗糖试验和内镜检查。
在皮质类固醇治疗前，对照组和患者组的尿蔗糖排泄率相似。与接受口服类固醇和大剂量静脉注射甲泼尼龙治疗的患者的治疗前值相比，蔗糖的排泄率中位数分别增加了4倍（1至28倍）和8倍（2至35倍）（p<0.01）。将所有患者综合考虑，接受平均泼尼松等效剂量为8.4±1.5 g的受试者出现黏膜病变，而接受3.3±1.8 g的患者未出现（p = 0.06）。治疗后蔗糖排泄率的增加与宏观病变的存在或接受的总类固醇剂量均无关。
皮质类固醇疗法会增加胃十二指肠通透性，高剂量与宏观黏膜病变相关。类固醇诱导的通透性增加似乎与宏观黏膜病变的存在无关。
