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Gallbladder function is altered in sickle hemoglobinopathy.

G T Everson1, A Nemeth, S Kourourian

  • 1Division of Gastroenterology, Colorado Sickle Cell Treatment and Research Center, Denver.

Gastroenterology
|May 1, 1989
PubMed
Summary
This summary is machine-generated.

Patients with sickle hemoglobinopathy (SH) have enlarged gallbladders leading to bile retention and potential pigment gallstone formation, even with similar hemolysis rates. This suggests gallbladder dysfunction contributes to gallstone development in SH.

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Last Updated: Jan 8, 2026

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Area of Science:

  • Gastroenterology
  • Hematology
  • Pediatrics

Background:

  • Sickle hemoglobinopathy (SH) patients exhibit high hemolysis rates, yet only 50% develop pigment gallstones by age 20.
  • This suggests factors beyond hemolysis influence gallstone pathogenesis in SH.

Purpose of the Study:

  • To investigate gallbladder function and bile acid metabolism in adolescents and young adults with SH.
  • To identify potential contributing factors to pigment gallstone formation in SH.

Main Methods:

  • Real-time ultrasonography assessed gallbladder volume and emptying.
  • Isotope dilution-mass spectrometry measured bile acid metabolism.
  • Comparison between SH subjects and healthy controls, and between SH subjects with and without gallstones.

Main Results:

  • SH subjects displayed larger fasting and residual gallbladder volumes compared to controls.
  • Gallbladder emptying rates and percentages were similar between SH subjects and controls.
  • SH subjects with gallstones tended to have smaller bile acid pools than those without gallstones.

Conclusions:

  • Adolescents and young adults with SH have enlarged gallbladders with increased postprandial bile retention.
  • Bile retention and stasis within the gallbladder may be key contributors to pigment gallstone formation in SH.
  • Gallbladder dysfunction, not just hemolysis, plays a role in gallstone development in SH.