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Interruption of Bile Salt Circulation

Ileal disease or surgery can interrupt bile salt circulation and cause cholelithiasis or gallstone formation. When bile salt absorption is reduced in the terminal ileum, it depletes the hepatic bile salt pool and decreases bile salt content in bile. With a limited ability to replenish bile salts, the liver continues to secrete cholesterol at a fixed rate, resulting in bile that is supersaturated with cholesterol and more likely to form stones. Ileal dysfunction is also associated with urolithiasis or kidney stone formation possibly due to increased colonic permeability to oxalate from unabsorbed bile salts, leading to secondary hyperoxaluria.

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24 views

Interruption of Bile Salt Circulation

Ileal disease or surgery can interrupt bile salt circulation and cause cholelithiasis or gallstone formation. When bile salt absorption is reduced in the terminal ileum, it depletes the hepatic bile salt pool and decreases bile salt content in bile. With a limited ability to replenish bile salts, the liver continues to secrete cholesterol at a fixed rate, resulting in bile that is supersaturated with cholesterol and more likely to form stones. Ileal dysfunction is also associated with urolithiasis or kidney stone formation possibly due to increased colonic permeability to oxalate from unabsorbed bile salts, leading to secondary hyperoxaluria.

Uploaded by

drnazz
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© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Interruption of Bile Salt Circulation Cholelithiasis. There is a known association between ileal disease and cholelithiasis [4-6].

Ileal dysfunction secondary to inflammatory disease or surgery may cause a failure of adequate bile salt absorption from the terminal ileum. This depletes the hepatic bile salt pool and decreases the bile salt content within excreted bile . Liver has a limited capacity to convert cholesterol to bile salts in order to replenish the bile salt pool. Conversely, cholesterol continues to be secreted at a fixed rate by the hepatocyte into bile. The end result is the excretion of bile that is supersaturated with cholesterol [6]. This increase in bile lithogenicity causes cholesterol gallstone formation (fig. 4). Urolithiasis. There is also a definite association between ileal dysfunction and urolithiasis [7, 8]. The pathophysiology of acquired hyperoxaluria that leads to oxalate renal lithiasis remains controversial. Hofmann et al. [9] initially proposed that bacteria deconjugated the increased amounts of glycine -conjugated bile salts passing into the colon. They theorized that this increased load of glycine in the colon was further converted to glyoxalate by bacterial action, absorbed by the colon, transported to the liver, and converted to oxalate with subsequent hyperoxaluria. Earnest et al. [1 0] believed that excessive malabsorbed fatty acids may decrease the amount of intraluminal calcium available for binding with

dietary oxalate and thereby facilitate abnormal oxalate absorption leading to hyperoxaluria and nephrolithiasis in patients with extensive ileal resection or disease. Dobbins and Binder [11] noted that hyperoxaluria may occur in patients who have ileal dysfunction without steatorrhea (case 2). They concluded that unabsorbed bile salts increase the permeability of the colon to ingested oxalate and lead to secondary hyperoxaluria.

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