Fundamental Examination for Liver Function Parameter LU15 by 99mTc-GSA.

Objectives: Cadmium is widely used, leading to extensive environmental and occupational exposure. Unlike other organs, for which the harmful and carcinogenic effects of cadmium have been established, the hepatotoxicity of cadmium remains unclear. Some studies detected correlations between cadmium exposure and hepatotoxicity, but others concluded that they were not associated. Thus, we investigated the relationship between cadmium and liver damage in the general population.Methods: In total, 11 838 adult participants from National Health and Nutrition Examination Survey 1999-2015 were included. Urinary cadmium levels and the following liver function parameters were measured: alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transferase (GGT), total bilirubin (TB), and alkaline phosphatase (ALP). Linear and logistic regression analyses were performed to assess the associations between urinary cadmium concentrations and each liver function parameter after adjusting for age, sex, race/ethnicity, annual family income, smoking status, alcohol consumption status, physical activity, and body mass index.Results: The covariate-adjusted results of the linear regression analyses showed significant positive relationships between log-transformed urinary cadmium levels and each log-transformed liver function parameter, where beta±standard error of ALT, AST, GGT, TB, and ALP were 0.049±0.008 (p<0.001), 0.030±0.006 (p<0.001), 0.093±0.011 (p<0.001), 0.034±0.009 (p<0.001), and 0.040±0.005 (p<0.001), respectively. Logistic regression also revealed statistically significant results. The odds ratios (95% confidence intervals) of elevated ALT, AST, GGT, TB, and ALP per unit increase in log-transformed urinary cadmium concentration were 1.360 (1.210 to 1.528), 1.307 (1.149 to 1.486), 1.520 (1.357 to 1.704), 1.201 (1.003 to 1.438), and 1.568 (1.277 to 1.926), respectively.Conclusions: Chronic exposure to cadmium showed positive associations with liver damage.

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Characterization of Liver Function Parameter Alterations After Transjugular Intrahepatic Portosystemic Shunt Creation and Association With Early Mortality

American Journal of Roentgenology ◽

10.2214/ajr.13.12232 ◽

2014 ◽

Vol 203 (6) ◽

pp. 1363-1370 ◽

Cited By ~ 5

Author(s):

Leigh C. Casadaban ◽

Ahmad Parvinian ◽

Patrick M. Couture ◽

Jeet Minocha ◽

M. Grace Knuttinen ◽

...

Keyword(s):

Liver Function ◽

Transjugular Intrahepatic Portosystemic Shunt ◽

Portosystemic Shunt ◽

Early Mortality ◽

Function Parameter ◽

Intrahepatic Portosystemic Shunt ◽

Liver Function Parameter

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Ursodeoxycholic acid in neonatal sepsis-associated cholestasis

Paediatrica Indonesiana ◽

10.14238/pi54.4.2014.206-12 ◽

2014 ◽

Vol 54 (4) ◽

pp. 206

Author(s):

Rita Mey Rina ◽

Hanifah Oswari ◽

Pustika Amalia

Keyword(s):

Liver Function ◽

Ursodeoxycholic Acid ◽

Total Bilirubin ◽

Controlled Trial ◽

Intervention Group ◽

Direct Bilirubin ◽

Function Parameter ◽

Control Group ◽

Gamma Glutamyl Transpeptidase ◽

Double Blind

Background Sepsis-associated cholestasis (SAC) is an intrahepatic cholestasis caused by inflammatory cytokines. Patients with this condition have poor prognoses. Antibiotics are the mainstay of therapy, however, other adjuvant therapies, such as ursodeoxycholic acid (UDCA), have not been well established.Objective To assess the effect ofUDCA for treatment ofneonatal sepsis-associated cholestasis.Methods We performed a randomized, double-blind, controlled trial in 3 7 neonates who were diagnosed with sepsis-associated cholestasis in the Neonatal Care Unit of Cipto Mangunkusumo Hospital. Subjects were divided into two groups, with 19 neonates randomly allocated to the intervention group (received UDCA at 30 tngikg/day divided into 3 doses for 7 days) and 18 neonates to the control group (received placebo) . After 7 days of treatment, we evaluated the subjects' liver function parameters and performed asurvival analysis.Results Liver function parameter improvements at day 7 were not significantly different between the UDCA group and the control group, including for mean decrease of total bilirubin (TB) levels [2.2 (SD 2.9) mg/dL vs 1.7 (SD 4.6) mg/dL; P=0.080), mean decrease of direct bilirubin (DB) levels [1.1 (SD 2.3) mg/dL vs 0.6 (SD 3.6) mg/dL; P=0.080), median indirect bilirubin (lB) levels [0.4 (range 0.1- 5.6) mg/dL vs 0.9 (range 0.1-4.1) mg/dL; P=0.358) , mean decrease of alanine aminotransferase (ALT) levels [0.5 (-80.0 -21.0) U/L vs -2.0 (ranged -167 .0 - 85.0) U/L; P= 0.730), median aspartate aminotransferase (AST) levels [ 43 .0 (range 14.0-297 .0) U/L vs 150.0 (range 24.0-840.0) U/L; P=0.081), and median gamma-glutamyl transpeptidase (GGf) levels [125.0 (48.0-481.0) U/L vs 235.0 (56.0-456.0) U/L; P=0.108)). Five neonates in control group died compared to two in the UDCA group (P=0.232). In addition, UDCA did not significantly lengthen the survival time (hazard ratio/HR 3.62; 95%CI 0.69 to 18.77) .Conclusion Ursodeoxycholic acid tends to improve total bilirubin, direct bilirubin, and AST levels in sepsis associated cholestasis .

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Acetaminophen: Macula densa hypersecretory activity by induced hepatotoxicity

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010012895x ◽

1987 ◽

Vol 45 ◽

pp. 934-935

Author(s):

S.S. Poolsawat ◽

C.A. Huerta ◽

S.TY. Lae ◽

G.A. Miranda

Keyword(s):

Cell Proliferation ◽

Liver Function ◽

Chronic Inflammation ◽

Foam Cell ◽

Term Effect ◽

Short Term ◽

Drug Induced ◽

Experimental Induction ◽

Tissue Alterations ◽

Toxic Responses

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.

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