Gallbladder emptying determines early gallstone clearance after shock-wave lithotripsy

Pauletzki, Jürgen; Sailer, Christian F.; Klüppelberg, U; Ritter, Christoph von; Neubrand, Michael; Holl, Joseph; Sauerbruch, Tilman; Sackmann, Michael; Paumgartner, Gustav

doi:10.1016/0016-5085(94)90555-x

Cited by 33 publications

(19 citation statements)

References 28 publications

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“…12,13 Ursodeoxycholic acid (UDCA) has been widely used for the dissolution of both cholesterol gallstones 14 and gallstone fragments after extracorporeal shock-wave lith-otripsy. 15,16 Furthermore, recent reports have indicated a variety of characteristics of UDCA in immunomodulation 17 and anti-apoptosis. 18 Despite its long history as a safe drug for patients with various hepatobiliary disorders, such as primary biliary cirrhosis 19,20 and chronic viral hepatitis, 21 the mechanism of action of UDCA has not been fully understood.…”

mentioning

confidence: 99%

Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells

et al. 2005

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mentioning

confidence: 99%

Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells

et al. 2005

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“…Also, fasting gallbladder volume is frequently increased in cholesterol stone patients [38•, 103,106], pointing to defective interdigestive gallbladder emptying poorly integrated with the intestinal migrating motor complex [47]. In contrast, effective gallbladder emptying facilitates gallstone clearance [108] and prevents recurrence [109] after medical therapy for cholesterol stones. We [38•] and others [110] found defective contractility in isolated smooth muscle gallbladder strips from cholesterol stone patients.…”

Section: From Smooth Muscle Cell Dysfunction In Vitro To Motility Defmentioning

confidence: 98%

Smooth muscle function and dysfunction in gallbladder disease

Portincasa

Ciaula

vanBerge-Henegouwen³

2004

Curr Gastroenterol Rep

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The gallbladder epithelium and smooth muscle layer are exposed to concentrated biliary solutes, including cholesterol and potentially toxic hydrophobic bile salts, which are able to influence muscle contraction. Physiologically, gallbladder tone is regulated by spontaneous muscle activity, hormones, and neurotransmitters released into the muscle from intrinsic neurons and extrinsic sympathetic nerves. Methods to explore gallbladder smooth muscle function in vitro include cholecystokinin (CCK) receptor-binding studies and contractility studies. In human and animal models, studies have focused on cellular and molecular events in health and disease, and in vitro findings mirror in vivo events. The interplay between contraction and relaxation of the gallbladder muscularis leads in vivo to appropriate gallbladder emptying and refilling during fasting and postprandially. Defective smooth muscle contractility and/or relaxation are found in cholesterol stone-containing gallbladders, featuring a type of gallbladder leiomyopathy; defects of CCKA receptors and signal transduction may coexist with abnormal responses to oxidative stress and inflammatory mediators. Abnormal smooth musculature contractility, impaired gallbladder motility, and increased stasis are key factors in the pathogenesis of cholesterol gallstones.

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“…Gallbladder motility is often impaired in high risk states for gallstone formation as mentioned in Table 1. Prospective studies indicate that impaired gallbladder motility is also an independent risk factor for gallstone recurrence after extracorporeal shock wave lithotripsy [16,17] …”

Section: Postprandial Gallbladder Motilitymentioning

confidence: 99%

Drugs Affecting Biliary Lipid Secretion and Gallbladder Motility: Their Potential Role in Gallstone Treatment and Prevention

vanBerge-Henegouwen¹,

Venneman²,

Erpecum³

et al. 2005

curr drug targets immune endocr metabol disord

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Gallstone disease in the Western world has an estimated prevalence of 10-15% and more than 75% are cholesterol-enriched gallstones. Defective gallbladder motility has been identified as an important pathogenic factor for cholesterol gallstone disease. Various agents may enhance or impair postprandial gallbladder motility, and their effects on interdigestive gallbladder and intestinal motility should also be taken into account. Patients in high-risk situations for gallstone disease, and those chronically treated with drugs inhibiting gallbladder motility (e.g. somatostatin analogues) may benefit from improving gallbladder motility with prokinetic agents. Whether such a strategy can really prevent gallstone formation is still unknown, long-term studies are lacking so far. The efficacy of bile acid therapy with UDCA for gallstone dissolution or for prevention in high risk patients is limited and hampered by high recurrence rates. The efficacy of UDCA in prevention of colics or gallstone related complications in symptomatic patients with gallbladder stones with contraindications for operation or on the waiting list should be explored further, since several retrospective studies showed favourable outcomes with this strategy.

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Gallbladder emptying determines early gallstone clearance after shock-wave lithotripsy

Cited by 33 publications

References 28 publications

Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells

Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells

Smooth muscle function and dysfunction in gallbladder disease

Drugs Affecting Biliary Lipid Secretion and Gallbladder Motility: Their Potential Role in Gallstone Treatment and Prevention

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