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Cimetidine and neonatal small bowel adaptation: an experimental study
Insights
Histamine2-blockers like cimetidine improve weight gain in pediatric short gut patients. However, the exact mechanisms, including effects on lipid absorption and gut immunity, require further investigation.
Area of Science:
- Gastroenterology
- Pediatric Surgery
- Pharmacology
Background:
- Histamine2-blockers are increasingly used to enhance small bowel adaptation in pediatric short gut patients.
- Potential mechanisms include reversing lipid malabsorption and promoting intestinal cell growth.
Purpose of the Study:
- To investigate the effects of cimetidine on weight gain, lipid absorption, and intestinal morphology in a rat model of short bowel syndrome.
- To explore the role of immune system changes in cimetidine's efficacy.
Main Methods:
- Rats underwent 85% small bowel resection and were treated with cimetidine, cholestyramine, or a combination.
- Ileal and jejunal sections were analyzed for villous and crypt morphology and immune cell activity.
Main Results:
- Cimetidine administration led to improved weight gain compared to controls.
- Cimetidine alone reduced fecal fat loss, but this effect was lost when combined with cholestyramine.
- Increased lymphocytic activity was observed in the ileum of cimetidine-treated rats.
Conclusions:
- Cimetidine enhances weight gain in short bowel patients, but its effects on lipid absorption and gut morphology do not fully explain its benefits.
- The immunological changes observed suggest that the gut immune system plays a role in cimetidine's action, warranting further research.
Abstract:
Histamine2-blockers are being used more extensively in the pediatric short gut patient as an agent to accelerate small bowel adaptation. Reversal of lipid malabsorption and a direct trophic effect on the intestinal crypt cells have been postulated as the mechanism for the salutary influence of cimetidine. Weanling Sprague-Dawley rats underwent 85% small bowel resection. Controls had repair of a simple ileal transection. Rats received either a fat-defined rat chow only, or chow with high- or low-dose cimetidine, 2% cholestyramine, or cholestyramine/low-dose cimetidine. All animals were killed 2 weeks postresection, and ileal and jejunal sections were examined for changes in villous and crypt morphology. The animals receiving cimetidine showed earlier and more consistent weight gain than resected animals who received no adjunctive treatment. High- and low-dose regimens were equally efficacious. Cimetidine administered alone decreased fecal fat losses, but not when given with cholestyramine. The cimetidine/cholestyramine group showed increased weight gain when referenced to the resection controls despite continuing lipid malabsorption. Villous and crypt lengthening did not correlate with clinical evidence of adaptation. An augmented lymphocytic activity (plasma cell hyperplasia, enlargement Peyer's patches) was present in the hyperplastic ileal segments of the cimetidine-treated rats. Overall immunoreactivity was similar in all study groups. No significant differences in villous morphology or immunologic activity were seen in jejunal segments. The effects of H2-blockers on lipid absorption and intestinal hyperplasia are inadequate to explain the benefits of cimetidine in the short gut patient. Examination of the immunology of the short bowel complex merits further attention in elucidating cimetidine's action in this setting.