Occult microlithiasis in ‘idiopathic’ acute pancreatitis: Prevention of relapses by cholecystectomy or ursodeoxycholic acid therapy

Ros, Emilio; Navarro, Salvador; Bru, C.; García-Pugés, A; Valderrama, Rodrigo

doi:10.1016/0016-5085(91)90410-m

Cited by 326 publications

(72 citation statements)

References 27 publications

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“…Of these events, precipitation of cholesterol crystals from supersaturated bile is thought to be a prerequisite for gallstone formation: cholesterol crystals in bile are found in 70% of patients with "idiopathic" acute pancreatitis (Admirand and Small, 1968;Ros et al, 1991). In mice, cholesterol gallstones can be induced by feeding them a lithogenic diet containing cholesterol and cholic acid: the susceptible C57L strain is always used to establish gallstone animal models (Tepperman et al, 1964;van Erpecum et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Thyroid dysfunction, either hyper or hypothyroidism, promotes gallstone formation by different mechanisms

Wang

Xing

Zhao

et al. 2016

J. Zhejiang Univ. Sci. B

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Abstract:We have investigated comprehensively the effects of thyroid function on gallstone formation in a mouse model. Gonadectomized gallstone-susceptible male C57BL/6 mice were randomly distributed into three groups each of which received an intervention to induce hyperthyroidism, hypothyroidism, or euthyroidism. After 5 weeks of feeding a lithogenic diet of 15% (w/w) butter fat, 1% (w/w) cholesterol, and 0.5% (w/w) cholic acid, mice were killed for further experiments. The incidence of cholesterol monohydrate crystal formation was 100% in mice with hyperthyroidism, 83% in hypothyroidism, and 33% in euthyroidism, the differences being statistically significant. Among the hepatic lithogenic genes, Trβ was found to be up-regulated and Rxr down-regulated in the mice with hypothyroidism. In contrast, Lxrα, Rxr, and Cyp7α1 were up-regulated and Fxr down-regulated in the mice with hyperthyroidism. In conclusion, thyroid dysfunction, either hyperthyroidism or hypothyroidism, promotes the formation of cholesterol gallstones in C57BL/6 mice. Gene expression differences suggest that thyroid hormone disturbance leads to gallstone formation in different ways. Hyperthyroidism induces cholesterol gallstone formation by regulating expression of the hepatic nuclear receptor genes such as Lxrα and Rxr, which are significant in cholesterol metabolism pathways. However, hypothyroidism induces cholesterol gallstone formation by promoting cholesterol biosynthesis.

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Section: Introductionmentioning

confidence: 99%

Thyroid dysfunction, either hyper or hypothyroidism, promotes gallstone formation by different mechanisms

Wang

Xing

Zhao

et al. 2016

J. Zhejiang Univ. Sci. B

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“…Cholecystectomy is the strategy of choice in patients with a gallbladder in situ and without contraindications for abdominal surgery. Cholecystectomy decreases recurrence rates by decreasing the residence time of bile in the biliary tree, thus allowing less time for nucleation of cholesterol crystals from supersaturated bile [13]. After cholecystectomy, bile in the biliary tree is 4-5 fold less concentrated compared to gallbladder bile before surgery.…”

Section: Manipulation Of Biliary Lipids and Water: Secondary Preventimentioning

confidence: 96%

“…Also in patients with very fast crystallization due to a missense mutations in the MDR3 gene, UDCA decreases recurrence of biliary symptoms during long-term follow-up [42]. Maintenance therapy with UDCA has proven to be an effective treatment strategy for the secondary prevention of acute biliary pancreatitis [13,14].…”

Section: Manipulation Of Biliary Lipids and Water: Secondary Preventimentioning

confidence: 99%

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Pharmacological Manipulation of Biliary Water and Lipids: Potential Consequences for Prevention of Acute Biliary Pancreatitis

Venneman¹,

vanBerge-Henegouwen²,

Erpecum³

2005

curr drug targets immune endocr metabol disord

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Acute biliary pancreatitis, caused by macroscopic cholesterol gallstones or microlithiasis, is often a severe disease with considerable morbidity and mortality. Formation of cholesterol gallstones and microlithiasis is caused by cholesterol crystallization from cholesterol supersaturated gallbladder bile. Particularly patients with fast and extensive crystallization, due to highly concentrated bile, low biliary phospholipid contents and gallbladder mucin hypersecretion seem at risk for pancreatitis. Patients who suffered from acute biliary pancreatitis should undergo cholecystectomy as secondary prevention strategy. For patients at high surgical risk, endoscopic sphincterotomy may be an appropriate alternative. Pharmacological manipulation of biliary lipids by the hydrophilic bile salt ursodeoxycholic acid is reserved for patients with recurrent pancreatitis despite previous cholecystectomy or sphincterotomy, or with contraindications to surgical and endoscopic treatment. Maintenance therapy with ursodeoxycholic acid is however a very effective secondary prevention strategy. Potentially, secondary prevention of acute biliary pancreatitis could also be achieved through decreasing biliary mucin contents by UDCA, NSAIDs or N-acetylcystein, or through achieving bile dilution (currently not feasible).

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“…14 Biliary sludge accounted for approximately 67% of acute idiopathic pancreatitis. 15 Tissue specimens obtained during cholecystectomy from patients with acute pancreatitis contain precipitates of various descriptions in approximately 60% of the cases. [16][17][18] Abnormalities hepatic bile secretion and changes in the contractile function and mucosal properties of gall bladder contribute to formation of gall bladder sludge.…”

Section: Introductionmentioning

confidence: 99%

A clinical study of acute pancreatitis

Narender

Pappu

2016

Int Surg J

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Occult microlithiasis in ‘idiopathic’ acute pancreatitis: Prevention of relapses by cholecystectomy or ursodeoxycholic acid therapy

Cited by 326 publications

References 27 publications

Thyroid dysfunction, either hyper or hypothyroidism, promotes gallstone formation by different mechanisms

Thyroid dysfunction, either hyper or hypothyroidism, promotes gallstone formation by different mechanisms

Pharmacological Manipulation of Biliary Water and Lipids: Potential Consequences for Prevention of Acute Biliary Pancreatitis

A clinical study of acute pancreatitis

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