scholarly journals Serum Bile Acids in Cholestatic Liver Disease: Their Measurement and Significance

Author(s):  
G. M. Murphy

A relatively rapid and specific method for the estimation of serum individual bile acids, conjugated and free, in small volumes (1 ml) of sera from patients with liver disease has been developed. This method has been applied to a study of 25 patients with liver disease. Cholestatic liver disease has been found to be associated with an increase in serum monohydroxy bile acids which appear to be of an unsaturated nature. No association was found between the concentration of any particular bile acid and the presence or absence of pruritus.

1965 ◽  
Vol 11 (5) ◽  
pp. 547-553 ◽  
Author(s):  
Samuel J Levin ◽  
Morton K Schwartz

Abstract By means of a sensitive fluorometric technic, serum bile acids were determined in patients with various liver diseases. Correlations were shown between the bile acid values and those of transaminase and alkaline phosphatase in cases of liver metastases, and bile acid and transaminase values in cases of viral hepatitis. For most clinical purposes, however, the determination does not yield information which cannot be obtained more readily using currently accepted methods.


2020 ◽  
Vol 13 (6) ◽  
pp. e234185
Author(s):  
Christoph Slavetinsky ◽  
Ekkehard Sturm

Untreated progressive familial intrahepatic cholestasis (PFIC) type 2, or bile salt exporter protein deficiency, frequently leads to severe pruritus, impaired growth and progressive liver fibrosis with risk of organ failure. We describe a 15-month-old male patient with severe pruritus diagnosed with PFIC type 2 enrolled in an open-label phase 2 study who received 4 weeks of treatment with odevixibat, an ileal bile acid transporter inhibitor under development for cholestatic liver disease treatment. The patient experienced reductions in serum bile acids and improvement in itching and sleep scores, and odevixibat was well tolerated. After the odevixibat study, symptoms returned and the patient underwent partial external biliary diversion (PEBD). Odevixibat treatment and PEBD produced similar normalisation of serum bile acid levels and improvements in pruritus and sleep disruptions. Thus, odevixibat appeared to be as effective as invasive PEBD in treating serum bile acids and cholestatic pruritus in this patient.


2015 ◽  
Vol 33 (3) ◽  
pp. 440-446 ◽  
Author(s):  
Rohit Kohli ◽  
Andriy Myronovych ◽  
Brandon K. Tan ◽  
Rosa-Maria Salazar-Gonzalez ◽  
Lili Miles ◽  
...  

Bariatric surgery is the most effective and durable treatment option for obesity today. More importantly, beyond weight loss, bariatric procedures have many advantageous metabolic effects including reversal of obesity-related liver disease - nonalcoholic steatohepatitis (NASH). NASH is an important comorbidity of obesity given that it is a precursor to the development of liver cirrhosis that may necessitate liver transplantation in the long run. Simultaneously, we and others have observed increased serum bile acids in humans and animals that undergo bariatric surgery. Specifically, our preclinical studies have included experimental procedures such as ‘ileal transposition' or bile diversion and established procedures such as Roux-en-Y gastric bypass and the adjustable gastric band. Importantly, these effects are not simply the result of weight loss since our data show that the resolution of NASH and increase in serum bile acids are not seen in rodents that lose an equivalent amount of weight via food restriction. In particular, we have studied the role of altered bile acid signaling, in the potent impact of a bariatric procedure termed ‘vertical sleeve gastrectomy' (VSG). In this review we focus on the mechanisms of NASH resolution and weight loss after VSG surgery. We highlight the fact that bariatric surgeries can be used as ‘laboratories' to dissect the mechanisms by which these procedures work to improve obesity and fatty liver disease. We describe key bile acid signaling elements that may provide potential therapeutic targets for ‘bariatric-mimetic technologies' that could produce benefits similar to bariatric surgery - but without the surgery!


Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1496
Author(s):  
Noemí Cabré ◽  
Yi Duan ◽  
Cristina Llorente ◽  
Mary Conrad ◽  
Patrick Stern ◽  
...  

Alcohol-related liver disease is associated with intestinal dysbiosis. Functional changes in the microbiota affect bile acid metabolism and result in elevated serum bile acids in patients with alcohol-related liver disease. The aim of this study was to identify the potential role of the bile acid sequestrant colesevelam in a humanized mouse model of ethanol-induced liver disease. We colonized germ-free (GF) C57BL/6 mice with feces from patients with alcoholic hepatitis and subjected humanized mice to the chronic–binge ethanol feeding model. Ethanol-fed gnotobiotic mice treated with colesevelam showed reduced hepatic levels of triglycerides and cholesterol, but liver injury and inflammation were not decreased as compared with non-treated mice. Colesevelam reduced hepatic cytochrome P450, family 7, subfamily a, polypeptide 1 (Cyp7a1) protein expression, although serum bile acids were not lowered. In conclusion, our findings indicate that colesevelam treatment mitigates ethanol-induced liver steatosis in mice.


2002 ◽  
Vol 283 (6) ◽  
pp. F1281-F1289 ◽  
Author(s):  
Edmund Purucker ◽  
Hanns-Ulrich Marschall ◽  
Andreas Geier ◽  
Carsten Gartung ◽  
Siegfried Matern

Hepatic synthesis and plasma levels of glutathione are markedly decreased in chronic liver disease. Because glutathione turnover is highest in kidneys, we examined whether changes in kidney glutathione occur in chronic cholestasis and whether they are related to kidney dysfunction in liver disease. Kidney and plasma GSH and GSSG were measured 1) in bile duct-ligated (BDL) rats; 2) in healthy rats after bile acid loading to mimic cholestasis; and 3) after irreversible inhibition of glutathione synthetase with buthionine-sulfoximine (BSO), where glutathione consumption, urinary volume, and sodium excretion were also estimated. In addition, γ-glutamylcysteine synthetase (γ-GCS) mRNA, protein, and enzymatic specific activity were measured in kidney tissue after BDL. After BDL, kidney GSH and GSSG increased within hours by 67 and 66%, respectively. The increases were not related to plasma glutathione, which decreased below control values. Intravenous bile acid loading caused identical increases in GSH and GSSG as occurred after BDL, when glycine- or taurine-conjugated dihydroxy bile acids were administered. Glutathione consumption, as estimated after blocking of de novo synthesis with BSO, was significantly increased after BDL (127 vs. 44 nmol · g−1 · min−1). γ-GCS mRNA and enzymatic specific activity were significantly reduced 5 days after BDL, whereas protein concentrations did not change. The urinary sodium concentration was 70% lower in BDL than in control rats. Depletion of renal glutathione normalized sodium excretion by increasing urinary sodium concentration and urinary volume. The increase in kidney glutathione after BDL seems to be mediated by an increase in plasma bile acids and is critically related to sodium retention. The increase in GSH consumption despite reduced γ-GCS activity indicates a decreased GSH turnover tentatively due to reduced renal GSH efflux by competition with organic anions at membrane transport proteins.


2017 ◽  
pp. 135-144
Author(s):  
Hiroshi Nittono ◽  
Akihiko Kimura ◽  
Hajime Takei ◽  
Takao Kurosawa ◽  
Takashi Iida

Author(s):  
Nehal El Koofy ◽  
Noha Yassin ◽  
Sawsan Okasha ◽  
Hany William ◽  
Wafaa Elakel ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document