Digestive Diseases and Sciences

, Volume 26, Issue 2, pp 181–186

Chronic protracted diarrhea and jejunal atrophy in an infant

Cimetidine-associated stimulation of jejunal mucosal growth

Authors

  • Stanley E. Fisher
    • Departments of PediatricsUniversity of Pittsburgh School of Medicine
    • University of Pennsylvania School of Medicine
    • Pediatric GastroenterologyChildren's Hospitals of Pittsburgh
    • Children's Hospitals of Philadelphia
  • John T. Boyle
    • Departments of PediatricsUniversity of Pittsburgh School of Medicine
    • University of Pennsylvania School of Medicine
    • Pediatric GastroenterologyChildren's Hospitals of Pittsburgh
    • Children's Hospitals of Philadelphia
  • Philip Holtzapple
    • Departments of PediatricsUniversity of Pittsburgh School of Medicine
    • University of Pennsylvania School of Medicine
    • Pediatric GastroenterologyChildren's Hospitals of Pittsburgh
    • Children's Hospitals of Philadelphia
Case Report

DOI: 10.1007/BF01312239

Cite this article as:
Fisher, S.E., Boyle, J.T. & Holtzapple, P. Digest Dis Sci (1981) 26: 181. doi:10.1007/BF01312239

Summary

An infant with 21 months of chronic protracted diarrhea, associated with intestinal mucosal atrophy, decreased crypt mitotic activity, and anti-intestinal antibodies is reported. During a 4-month period, cimetidine was used in an attempt to stimulate mucosal growth. Thirty-minute postprandial serum gastrin levels rose significantly during cimetidine therapy (663±115 pg/ml, mean±sem). Coincident with the cimetidine therapy, the jejunal mucosa showed progressive histologic improvement and the index of crypt mitotic activity (MI) steadily rose: pretreatment MI=1.3 (mitoses/100 crypt cells); mid-study, 3.3; end of study, 4.5. There was a direct correlation between 30-min pp serum gastrin and MI (r=0.989,P<0.005). The patient died in renal failure one month after cessation of cimetidine. At autopsy, the small bowel had returned to an atrophic state. It is proposed that cimetidine may have influenced jejunal mucosal growth, possibly through meal-stimulated hypergastrinemia.

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Copyright information

© Digestive Disease Systems, Inc. 1981