Clinical value of bile salt tests in anicteric liver disease.

Douglas, J. G.; Beckett, Geoffrey J.; Nimmo, Ian A.; Finlayson, N. D. C.; Percy‐Robb, I. W.

doi:10.1136/gut.22.2.141

Cited by 38 publications

(14 citation statements)

References 25 publications

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“…11-23 In our patient, the discordance between elevated transaminases and normal fasting and 2 hour postprandial cholylglycine levels was a potential indicator of the absence of significant liver disease, [24][25][26] There is a need to be aware of the possibility of occult primary muscle disease when evaluating children with mild to moderate persistently elevated transaminases, even in the absence of suggestive historical or physical findings. chronic active hepatitis or cirrhosis.…”

Section: Discussionmentioning

confidence: 76%

Persistent Elevation of Transaminases as the Presenting Finding in an Adolescent With an Unsuspected Muscle Glycogenosis

Treem

1987

Clin Pediatr (Phila)

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E LEVATIONS of the serum transaminases, alanine amino transferase (ALT) (SGPT) and aspartate aminotransferase (AST) (SGOT) in the pediatric and adolescent population are usually attributed to hepatic abnormalities. The persistence of these elevations over 3 months in spite of the lack of a previous identifiable &dquo;hepatitis-like&dquo; illness, hepatomegaly, or any abnormalities of alkaline phosphatase, gammaglutamyl transpeptidase, or bilirubin, is thought to be reason to initiate an investigation into causes of chronic hepatitis Recently, two reports have emphasized persistently elevated transaminases as the presentation of unsuspected childhood myopathies, including most prominently Duchenne's muscular dystrophy, and also Becker's muscular dystrophy, Kugelberg-Welander's syndrome, and scapuloperoneal muscular dystrophy. 2,3 In retrospect, many of these children gave historical clues and had identifiable muscle weakness during a careful physical examination. We report an adolescent with a completely silent muscle glycogenosis who was diagnosed after a chance finding of elevated transaminases and a negative diagnostic work up for chronic liver disease. Case HistoryA 15-year-old white male was found to have elevated transaminases as part of a routine physical examination for participation in school sports. He had been previously healthy, had no exercise intolerance, and was considered a well-coordinated, good athlete, who played football, basketball, and baseball. There was no history of fever, malaise, rash, myalgias or arthralgias, dark or red urine, jaundice, or exposure to hepatitis. There was no prior history of blood transfusions, or consumption of alcohol or other drugs. The patient was taking no medications. Two siblings ages 7 and 9 years were well and there was no family history of chronic liver or muscle disease. Physical examination showed no hepatomegaly or splenomegaly.Because of persistent elevations in transaminases (Table 1), further investigations were carried out over a 12 month period. These included a normal CBC, sedimentation rate, prothrombin time, partial thromboplastin time, total protein, albumin, globulin, iron, alpha-1-antitrypsin, and ceruloplasmin levels. Serologic examination was negative for antinuclear antibody, anti smooth muscle antibody, and markers of infection with Hepatitis A, Hepatitis B, Ebstein-Barr Virus, and Cytomegalovirus. An ophthalmologic examination did not show Kayser-Fleischer rings and a 24 hour urine copper quantitation was normal. An abdominal ultrasound showed a large spleen (12 cm in length) and a normal size homogenous liver.After 12 months of elevated transaminases, the patient was referred for consideration of a liver biopsy. In order to confirm the presence of occult liver disease, fasting and 2-hour postprandial serum cholylglycine levels were obtained (RIA-Abbott Laboratories, Abbott Park, IL), and were normal. Subsequently, a creatine kinase (CPK) was found to be 11,370 IU/L (Table 1). A repeat determination 1 week later again showed massive elevati...

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Section: Discussionmentioning

confidence: 76%

Persistent Elevation of Transaminases as the Presenting Finding in an Adolescent With an Unsuspected Muscle Glycogenosis

Treem

1987

Clin Pediatr (Phila)

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“…), which reflect acute disruption of cell membrane integrity (liver cell ‘leakage’) rather than functional activity of the liver, i.e., uptake, metabolism, storage and excretion, we investigated the effect of DDB on serum TBA level. The association of serum bile acid concentrations and liver disease has been demonstrated in numerous clinical studies (34–39). A significant increase in TBA level was detected after Con A injection, and DDB manifested a remarkable decrease at doses of 75 and 150 mg/kg.…”

Section: Discussionmentioning

confidence: 99%

Effect of diphenyl dimethyl bicarboxylate on concanavalin A‐induced liver injury in mice

Gao

Zhang

Liu

2005

Liver International

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Diphenyl dimethyl bicarboxylate (DDB) is a hepatoprotectant and used in the treatment of chronic viral hepatitis patients in China. The aim of the present paper was to investigate the effect of DDB on liver injury mediated by immune response in concanavalin A (Con A)-treated mice. A dose of Con A 30 mg/kg was injected via the tailvein to induce liver injury in mice. Serum alanine transaminase (ALT), aspartate aminotransferase (AST), total bile acid (TBA), total bilirubin (TBIL) and tumor necrosis factor alpha (TNF-alpha) level as well as liver TNF-alpha mRNA expression were determined. The following results were obtained: (1) Prior oral administration of DDB 150 mg/kg markedly reduced the elevated serum ALT, TBA and TBIL levels, and the liver lesions in Con A-treated mice; (2) DDB significantly inhibited the elevation of serum TNF-alpha and liver TNF-alpha mRNA expression 2 h after Con A injection; (3) DDB significantly inhibited hepatocyte nuclear DNA fragmentation 12 h after Con A injection; (4) DDB dose-dependently prevented the direct DNA damage induced by CuSO(4)-Phen-Vit C-H(2)O(2) system in vitro, and the ex vivo experiment also showed that the administration of DDB reduced the susceptibility of mouse liver nuclei DNA to CuSO(4)-Phen-Vit C-H(2)O(2) system. These results suggest that DDB could directly protect hepatocyte DNA from oxidative damage, and inhibit TNF-alpha mRNA expression in liver tissue, which resulted in prevention of liver damage induced by Con A in mice.

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“…Since liver is the organ for bile acid synthesis and metabolism and biliary excretion of bile acids is the limiting step for the enterohepatic circulation [35,36], impairment of liver function as a result of various liver disorders leads to dysregulation of bile acids. Indeed, the measurement of bile acids is considered a biomarker of liver function and serves as an indicator of hepatobiliary impairment or diseases [37][38][39][40][41]. On the other hand, excessive accumulation of bile acids in the liver causes liver damages by multiple mechanisms including disrupting the integrity of cell membranes through their detergent property [42][43][44], causing mitochondrial stress and promoting the generation of reactive oxygen species [45][46][47][48], and inducing endoplasmic reticulum stress [49][50][51] and inflammatory responses [52][53][54], resulting in cell death via apoptosis and/or necrosis [55][56][57][58].…”

Section: Introductionmentioning

confidence: 99%

Dysregulation of Bile Acids in Patients with NAFLD

Zhang¹,

Deng²

2019

Nonalcoholic Fatty Liver Disease - An Update

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Bile acids are synthesized in the liver and tightly regulated through the enterohepatic circulation. Recent studies reveal that bile acids serve as hormone-like signaling molecules to activate nuclear receptors, notably farnesoid X receptor (FXR), regulating metabolic homeostasis of bile acids, cholesterol, lipids, and glucose. A connection between bile acids and nonalcoholic fatty liver disease (NAFLD) has long been recognized. Although inconsistent or even contradictory results are reported, a large body of evidence from clinical as well as preclinical studies demonstrates that bile acid homeostasis is disrupted in patients with NAFLD. The bile acid dysregulation gets worsening as NAFLD progresses from early stage simple steatosis to late stage nonalcoholic steatohepatitis (NASH) and NASH with fibrosis. As the risk factors for NAFLD, obesity and insulin resistance, which are often associated with NAFLD, contribute to the dysregulation of bile acids in patients with NAFLD. Total serum and fecal bile acid concentrations are mostly elevated in patients with NAFLD as a result of increased bile acid synthesis, elevated hepatic bile acids, and upregulation of bile acid transporters. The two negative feedback regulatory pathways for bile acid synthesis, FXR/SHP (small heterodimer partner) and fibroblast growth factor-19 (FGF19)/FGF receptor-4 (FGFR4), are impaired in patients with NAFLD.

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Clinical value of bile salt tests in anicteric liver disease.

Cited by 38 publications

References 25 publications

Persistent Elevation of Transaminases as the Presenting Finding in an Adolescent With an Unsuspected Muscle Glycogenosis

Persistent Elevation of Transaminases as the Presenting Finding in an Adolescent With an Unsuspected Muscle Glycogenosis

Effect of diphenyl dimethyl bicarboxylate on concanavalin A‐induced liver injury in mice

Dysregulation of Bile Acids in Patients with NAFLD

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