Evidence of impaired acidification in vitro by human gall bladder mucosa in patients with gallstone disease

Iftikhar Hussain*, John N. Plevris, Peter C. Hayes, Ian A.D. Bouchier

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Objective: To study the capacity of the human gall bladder with and without gallstones to secrete H+ ions. Design: Human gall bladders were studied in vitro which permitted the measurement of the electrical potential difference and secretion of H+ ions. Results: Thirty-three gall bladders were studied (five normal, 20 with cholesterol and eight with pigment gallstones). The normal gall bladder group secreted 14.53 ± 1.04nmol (mean ± SEM), the mildly inflamed group 8.27 ± 1.71 nmol and the moderately inflamed group 4.03 ± 0.94 H+ over 60min in the mucosal bathing fluid. H+ secretion was significantly different when the mildly and moderately inflamed groups were compared with the normal group (P< 0.002 and P< 0.009, respectively). When the mildly (−6.14±0.36 nmol) and moderately (<2.54 ± 0.87 nmol) inflamed groups were compared with the normal group (<8.14 ± 0.93 nmol) over 60 min, there was a significant change in H+ secretion (P< 0.02 and P< 0.04, respectively) in the serosal bathing fluid. The potential difference was 9.68 ± 0.45 mV in the normal group, 8.25 ± 0.53 mV in the mildly inflamed group and 7.18 ± 0.67 mV in the moderately inflamed group. There was no association between H+ secretion and age, sex, alcohol and cigarette consumption, or contraceptive use. Conclusions: H+ secretion is abnormal in the gall bladders of patients with gallstone disease. Impairment correlates with the severity of cholecystitis, probably contributing to the formation of gallstones.

Original languageEnglish
Pages (from-to)935-940
Number of pages6
JournalEuropean Journal of Gastroenterology and Hepatology
Volume5
Issue number11
DOIs
Publication statusPublished - Nov 1993
Externally publishedYes

Keywords / Materials (for Non-textual outputs)

  • Acidification
  • Gallstone disease
  • Human gall bladder

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