TY - JOUR
T1 - Cholecystokinin receptor positivity in children with chronic acalculous gallbladder dysfunction
T2 - a pilot study to investigate the etiology of chronic acalculous gallbladder dysfunction
AU - Karplus, G.
AU - Ruiz, R.
AU - Thomas, Dafydd G.
AU - Ehrlich, P. F.
PY - 2008/5
Y1 - 2008/5
N2 - Background: The etiology of chronic acalculous gallbladder dysfunction (CAGD) is unknown. However, cholecystectomy is being performed as treatment, based on gallbladder (GB) ejection fraction studies. The aim of this study was to examine the pathology and immunohistology of GBs from children with CAGD. Methods: Children with a diagnosis of CAGD were identified. Control patients had their GB removed for nonbiliary indications. Immunoperoxidase staining was performed using rabbit antihuman cholecystokinin receptor (CCK-R) antibody. The pathologist was blinded to the study and controls. Results: Fifteen children were evaluated: 6 children with CAGD and 9 controls. All children with CAGD had abnormal cholecystokinin-stimulated nuclear imaging. Ejection fractions ranged from 8% to 30%. All patients reported resolution of symptoms on follow-up at 6 months. Histopathology of the GB was normal for both the controls and children with CAGD. Both control and CAGD GBs demonstrated positive staining for CCK-R in the vascular endothelium and smooth muscle. Mucosal epithelial staining was only observed in 5 of 6 of GBs of children with CAGD. In the sixth GB, the epithelium was too necrotic to assess. Conclusions: In this pilot study, expression of CCK-Rs in the epithelial cells is noted in children with CAGD compared with controls. The significance of this finding requires further investigation.
AB - Background: The etiology of chronic acalculous gallbladder dysfunction (CAGD) is unknown. However, cholecystectomy is being performed as treatment, based on gallbladder (GB) ejection fraction studies. The aim of this study was to examine the pathology and immunohistology of GBs from children with CAGD. Methods: Children with a diagnosis of CAGD were identified. Control patients had their GB removed for nonbiliary indications. Immunoperoxidase staining was performed using rabbit antihuman cholecystokinin receptor (CCK-R) antibody. The pathologist was blinded to the study and controls. Results: Fifteen children were evaluated: 6 children with CAGD and 9 controls. All children with CAGD had abnormal cholecystokinin-stimulated nuclear imaging. Ejection fractions ranged from 8% to 30%. All patients reported resolution of symptoms on follow-up at 6 months. Histopathology of the GB was normal for both the controls and children with CAGD. Both control and CAGD GBs demonstrated positive staining for CCK-R in the vascular endothelium and smooth muscle. Mucosal epithelial staining was only observed in 5 of 6 of GBs of children with CAGD. In the sixth GB, the epithelium was too necrotic to assess. Conclusions: In this pilot study, expression of CCK-Rs in the epithelial cells is noted in children with CAGD compared with controls. The significance of this finding requires further investigation.
KW - Biliary dyskinesia
KW - Cholecystokinin
KW - Gallbladder dysfunction
UR - https://www.scopus.com/pages/publications/43249090586
U2 - 10.1016/j.jpedsurg.2007.12.023
DO - 10.1016/j.jpedsurg.2007.12.023
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C2 - 18485951
AN - SCOPUS:43249090586
SN - 0022-3468
VL - 43
SP - 850
EP - 853
JO - Journal of Pediatric Surgery
JF - Journal of Pediatric Surgery
IS - 5
ER -