Relief of the Pruritus of Jaundice with a Bile-Acid Sequestering Resin

Carey, J. D.; Williams, Gale C.

doi:10.1001/jama.1961.03040180034008

Cited by 126 publications

(26 citation statements)

References 4 publications

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“…Carey and Williams (13) noted an 8-fold increase in fecal deoxycholic acid excretion in a normal human fed 10 g of cholestyramine daily. However, since they studied only one of the several bile acids excreted in man, an over-all estimation of the effect of the resin on cholesterol catabolism could not be made from their study.…”

Section: Discussionmentioning

confidence: 99%

“…However, since they studied only one of the several bile acids excreted in man, an over-all estimation of the effect of the resin on cholesterol catabolism could not be made from their study. This resin has been used to relieve the pruritis associated with jaundice and incomplete biliary obstruction in man (13,38,39), and a lowering of blood bile acid concentrations with relief of pruritis has been demonstrated in such patients (13). Tennent, Siegel, Zanetti, Kuron, Ott, and Wolf (1) reported an increase in both the bile acid (2.6-fold) and the sterol (1.8-fold) output in a dog given very large doses of cholestyramine (25 g/day).…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported to produce increased fecal excretion of both bile acids and neutral sterols in the dog (1) and the pig (10), and of bile acids alone in the rat (11,12). Carey and Williams (13) found a Received for publication 1 August 1967 and in revised form 5 March 1968. marked increase in fecal deoxycholic acid excretion in a normal man during the first 4 days of cholestyramine ingestion (at a dose of 10 g/day), but their study was not designed to measure total bile acid excretion, which is considerably greater than the amount of the one bile acid studied in their subject (14). Hashim and Van Itallie (9) reported a marked increase in fecal bile acid excretion with no significant change in neutral sterol output in two female hypercholesterolemic patients and in one normal man given 13.3 g of the resin daily.…”

Section: Introductionmentioning

confidence: 99%

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Effect of cholestyramine on the fecal excretion of intravenously administered cholesterol-4-14C and its degradation products in a hypercholesterolemic patient

Moore¹,

Crane²,

Frantz³

1968

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of cholestyramine on the fecal excretion of intravenously administered cholesterol-4-14C and its degradation products in a hypercholesterolemic patient

Moore¹,

Crane²,

Frantz³

1968

J. Clin. Invest.

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“…Beneficial effects for cholestyramine have been reported in several small uncontrolled case series [77,78,79,80,81,82,83,84]. Cholestyramine is recommended as a 4-gram sachet 1 h before and after breakfast and may be extended to 16 g/day.…”

Section: Managementmentioning

confidence: 99%

Advances in Pathogenesis and Management of Pruritus in Cholestasis

Kremer

Bolier

Dijk

et al. 2014

Dig Dis

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Chronic pruritus is a burdensome feature of numerous hepatobiliary disorders such as primary biliary cirrhosis, primary sclerosing cholangitis, cholangiocarcinoma, inherited forms of cholestasis and intrahepatic cholestasis of pregnancy. Bile salts, μ-opioids, serotonin, histamine and steroids have been controversially discussed in the pathogenesis of cholestatic pruritus. However, for these substances neither a correlation with itch severity nor a causative link has ever been established. Recent findings indicate that the potent neuronal activator lysophosphatidic acid and autotaxin, the enzyme forming lysophosphatidic acid, may play a key element in the pathogenesis of cholestatic pruritus. Serum activity of autotaxin correlated with itch intensity and response to antipruritic treatment in patients with cholestatic pruritus, but not other forms of pruritus. Autotaxin activity thereby represents the first biomarker for pruritus and had a positive predictive value of 70% in differentiating cholestatic pruritus from other forms of pruritus. Treatment options for patients with cholestatic pruritus include the anion exchange resin colestyramine, the PXR agonist rifampicin, the μ-opioid antagonist naltrexone, and the serotonin reuptake inhibitor sertraline. These drugs are recommended by evidence-based guidelines as a stepwise therapeutic approach. Patients unresponsive to these drugs should be referred to specialized centers to receive experimental approaches such as UVB phototherapy, albumin dialysis, plasmapheresis or nasobiliary drainage. This review discusses pruritogen candidates in cholestasis, gives novel insights into the neuronal signaling pathway of pruritus and summarizes evidence-based treatment options for patients suffering from pruritus in cholestasis.

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“…For PSC patients without biliary obstruction and PBC patients, the first-line drug treatment is cholestyramine ( table 1 ). This anion exchange resin has been reported to alleviate pruritus in several small uncontrolled case series [108][109][110][111][112][113][114][115] . Cholestyramine is recommended as a 4 g sachet 1 h before and after breakfast and may be extended to 16 g/day.…”

Section: Management Of Cholestatic Pruritusmentioning

confidence: 99%

Pathogenesis and Management of Pruritus in PBC and PSC

Kremer¹,

Namer

Bolier

et al. 2015

Dig Dis

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Pruritus is a preeminent symptom in patients with chronic cholestatic liver disorders such as primary biliary cirrhosis and primary sclerosing cholangitis. More than two-thirds of these patients experience itching during the course of their disease. This symptom is also frequently observed in patients with other causes of cholestasis such as cholangiocarcinoma, inherited forms of cholestasis and intrahepatic cholestasis of pregnancy, but may accompany almost any other liver disease. The pathogenesis of pruritus of cholestasis remains largely elusive. Increased concentrations of bile salts, histamine, serotonin, progesterone metabolites and endogenous opioids have been controversially discussed as potential pruritogens. However, for these molecules, neither a correlation with itch intensity nor a causative link could be established. The G protein-coupled receptor for bile salts, TGR5, has been shown to be expressed in dorsal root ganglia and give rise to itch in rodents, albeit upon stimuli with suprapathological concentrations of bile salts. The potent neuronal activator lysophosphatidic acid (LPA) and its forming enzyme, autotaxin (ATX), could be identified in the serum of patients with cholestatic pruritus. ATX activity correlated with itch severity and effectiveness of several anti-pruritic therapeutic interventions in cholestatic patients. Thus, the ATX-LPA-axis may represent a key element in the pathogenesis of this agonizing symptom. Treatment options for pruritus of cholestasis remain limited to a few evidence-based and several experimental medical and interventional therapies. The current guideline-based recommendations include the anion exchange resins colestyramine, the pregnane X receptor-agonist and enzyme inducer rifampicin, the μ-opioid antagonist naltrexone, and the selective serotonin reuptake inhibitors sertraline. Still, a considerable part of patients is unresponsive to these drugs and requires experimental approaches including phototherapy, plasmapheresis, albumin dialysis or nasobiliary drainage. This review outlines the current knowledge on pathogenesis of cholestatic pruritus and summarizes evidence-based and experimental therapeutic interventions for cholestatic patients with itch.

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Relief of the Pruritus of Jaundice with a Bile-Acid Sequestering Resin

Abstract: The purpose of this study was to determine

Cited by 126 publications

References 4 publications

Effect of cholestyramine on the fecal excretion of intravenously administered cholesterol-4-14C and its degradation products in a hypercholesterolemic patient

Effect of cholestyramine on the fecal excretion of intravenously administered cholesterol-4-14C and its degradation products in a hypercholesterolemic patient

Advances in Pathogenesis and Management of Pruritus in Cholestasis

Pathogenesis and Management of Pruritus in PBC and PSC

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