Guandalini S, Fasano A, Migliavacca M, Verga M C, Mastrantonio Gianfrilli P, Ferrara A, Alessio M, Malamisura B, Galati P, Pantosti A
Department of Pediatrics, 2nd School of Medicine, University of Naples, Italy.
Gut. 1988 May;29(5):598-602. doi: 10.1136/gut.29.5.598.
To elucidate the pathophysiological changes leading to postantibiotic diarrhoea caused by Clostridium difficile and its cytotoxin, oral ampicillin was given to rabbits, and jejunal, ileal, and caecal segments of those that developed diarrhoea were investigated in vitro. The rabbits that, in response to treatment, harboured Clostridium difficile in their colonic lumen were studied, and the results expressed according to the presence or absence of Clostridium difficile and/or its cytotoxin. Thus, we refer to either CD+ or CD- segments. The influx of glucose, phenylalanine, glycylphenylalanine, and lysine across the brush border of jejunum and ileum of CD+ segments was severely impaired, while only slightly blunted in CD-. No significant change was detected in the influx of glutamic acid in the jejunum of all treated animals and in the CD- ilea. Morphologic damage in ileum and caecum of CD+ was also more evident than in CD-. Transepithelial ion transport across short circuited ileal mucosa (CD+ and CD-) revealed secretory changes in Cl net transport that were more marked in CD-. We conclude that: (1) Clostridium difficile may also colonise the upper intestinal tract, where it induces morphological and functional damage, severely impairing nutrient absorption; and (2) the ileum contributes to the diarrhoea caused by CD even when the micro-organism is confined to the more distal gut by showing moderate impairment of nutrient absorption and marked electrolyte secretion.
为阐明艰难梭菌及其细胞毒素导致抗生素相关性腹泻的病理生理变化，给家兔口服氨苄西林，并对出现腹泻的家兔的空肠、回肠和盲肠段进行体外研究。对治疗后结肠腔中携带艰难梭菌的家兔进行研究，并根据是否存在艰难梭菌和/或其细胞毒素来表达结果。因此，我们将其分为CD+或CD-段。CD+段空肠和回肠刷状缘对葡萄糖、苯丙氨酸、甘氨酰苯丙氨酸和赖氨酸的摄取严重受损，而CD-段仅略有减弱。所有治疗动物空肠以及CD-回肠中谷氨酸的摄取均未检测到显著变化。CD+段回肠和盲肠的形态学损伤也比CD-段更明显。跨短路回肠黏膜（CD+和CD-）的跨上皮离子转运显示，Cl净转运的分泌变化在CD-段更为明显。我们得出以下结论：（1）艰难梭菌也可能定殖于上消化道，在那里它会引起形态和功能损伤，严重损害营养物质吸收；（2）即使微生物局限于更远端的肠道，回肠也会因营养物质吸收中度受损和明显的电解质分泌而导致由艰难梭菌引起的腹泻。
