Prescribing for patients with liver damage

1970 ◽  
Vol 8 (24) ◽  
pp. 93-94
Keyword(s):  
Liver Disease ◽  
Liver Damage ◽  
Enzyme Induction ◽  
Liver Enzymes ◽  
Liver Microsomes ◽  
Microsomal Enzymes ◽  
Impaired Liver ◽  
Conjugated Bilirubin

Many drugs are metabolised in the liver, and the duration and intensity of action of such drugs are increased in some patients with liver disease. However, many patients react normally to drugs, for although some mechanisms, such as the secretion of conjugated bilirubin into the bile, may be impaired, liver enzymes may continue to metabolise drugs normally. The function of liver microsomes is probably preserved because many drugs stimulate the synthesis of microsomal enzymes (enzyme induction), even in the failing liver,1 and thereby increase the metabolism of a variety of drugs. About 200 compounds have so far been shown to induce these enzymes.

scholarly journals StudIES oN the Toxic Interaction between Monensin and Tiamulin in Rats: EFFECTS ON P450 ACTIVITIES

2000 ◽  
Vol 48 (3) ◽  
pp. 361-368 ◽  
Author(s):  
G. Szűcs ◽  
P. Laczay ◽  
Judit Bajnógel ◽  
Zsuzsa Móra
Keyword(s):  
Enzyme Induction ◽  
Enzyme Activities ◽  
Liver Enzymes ◽  
Simultaneous Administration ◽  
Microsomal Enzymes ◽  
Microsomal Liver ◽  
Combined Administration ◽  
Related Enzyme ◽  
Dose Dependent ◽  
Slight Inhibition

Studies were carried out to investigate the effects of monensin and tiamulin, and the simultaneous administration of both compounds on microsomal enzymes in rats. In Phase I of the experiments the effects of monensin and tiamulin were studied separately (monensin 10, 30, and 50 mg/kg or tiamulin 40, 120, and 200 mg/kg body weight, respectively), while in Phase II the two compounds were administered simultaneously (monensin 10 mg/kg and tiamulin 40 mg/kg b.w., respectively). When monensin was administered by itself, it exerted no significant effect on microsomal liver enzymes. In a few cases, slight inhibition of certain enzyme activities was seen. Tiamulin provoked a dose-dependent hepatic enzyme induction. The combined administration of monensin and tiamulin at low doses (10 and 40 mg/kg, respectively) resulted in marked elevation of P450-related enzyme activities. The enzyme induction was more pronounced in females than in males. The results suggest that the simultaneous administration of tiamulin may influence the biotransformation of monensin, possibly increasing the amount of reactive metabolite(s) of the ionophore antibiotic.

scholarly journals Direct or Collateral Liver Damage in SARS-CoV-2–Infected Patients

2020 ◽  
Vol 40 (03) ◽  
pp. 321-330
Author(s):  
Maria J. Lizardo-Thiebaud ◽  
Eduardo Cervantes-Alvarez ◽  
Nathaly Limon-de la Rosa ◽  
Farid Tejeda-Dominguez ◽  
Mildred Palacios-Jimenez ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Liver Damage ◽  
Cytopathic Effect ◽  
Liver Enzymes ◽  
Collateral Damage ◽  
Viral Response ◽  
Immune Mediated ◽  
Vascular Congestion ◽  
Elevated Liver Enzymes

AbstractLiver injury can result from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection with more than one-third of COVID-19 patients exhibiting elevated liver enzymes. Microvesicular steatosis, inflammation, vascular congestion, and thrombosis in the liver have been described in autopsy samples from COVID-19 patients. Several factors, including direct cytopathic effect of the virus, immune-mediated collateral damage, or an exacerbation of preexisting liver disease may contribute to liver pathology in COVID-19. Due to its immunological functions, the liver is an organ likely to participate in the viral response against SARS-CoV-2 and this may predispose it to injury. A better understanding of the mechanism contributing to liver injury is needed to develop and implement early measures to prevent serious liver damage in patients suffering from COVID-19. This review summarizes current reports of SARS-CoV-2 with an emphasis on how direct infection and subsequent severe inflammatory response may contribute to liver injury in patients with and without preexisting liver disease.

Urokinase Antigen in Plasma of Patients with Liver Cirrhosis and Hepatoma

1985 ◽  
Vol 54 (03) ◽  
pp. 617-618 ◽  
Author(s):  
J C Kirchheimer ◽  
K Huber ◽  
P Polterauer ◽  
B R Binder
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Liver Function ◽  
Matched Control ◽  
Malignant Growth ◽  
Control Groups ◽  
Impaired Liver Function ◽  
Impaired Liver ◽  
Specific Medication ◽  
History Of

SummaryPlasma urokinase antigen levels were studied in 78 patients suffering from liver diseases. Blood was drawn before any specific medication was initiated. Impairment of liver function was comparable in all patients. In both groups of cirrhotic liver disease (alcoholic and non-alcoholic), normal levels of plasma urokinase antigen were found as compared to age-matched control groups. In both groups of patients with hepatomas (with or without a history of liver cirrhosis), however, significantly increased plasma urokinase antigen levels could be determined. These data indicate that an increase in plasma urokinase antigen might rather relate to malignant growth in liver disease than to impaired liver function.

Mechanisms of liver damage in COVID-19

2020 ◽  
Vol 1 (19) ◽  
pp. 39-46
Author(s):  
T. V. Pinchuk ◽  
N. V. Orlova ◽  
T. G. Suranova ◽  
T. I. Bonkalo
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Transplantation ◽  
Risk Factor ◽  
Liver Disease ◽  
Liver Function ◽  
Liver Damage ◽  
The World ◽  
Coronavirus Infection ◽  
The Impact ◽  
Analyze Data

At the end of 2019, a new coronavirus (SARS-CoV-2) was discovered in China, causing the coronavirus infection COVID-19. The ongoing COVID-19 pandemic poses a major challenge to health systems around the world. There is still little information on how infection affects liver function and the significance of pre-existing liver disease as a risk factor for infection and severe COVID-19. In addition, some drugs used to treat the new coronavirus infection are hepatotoxic. In this article, we analyze data on the impact of COVID-19 on liver function, as well as on the course and outcome of COVID-19 in patients with liver disease, including hepatocellular carcinoma, or those on immunosuppressive therapy after liver transplantation.

NR1H4 rs35724 G>C Variant Modulates Liver Damage in Nonalcoholic Fatty Liver Disease

2020 ◽  
Author(s):  
Stefania Grimaudo ◽  
Paola Dongiovanni ◽  
Jussi Pihlajamäki ◽  
Mohammed Eslam ◽  
Hannele Yki-Järvinen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Liver Damage ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver

NR1H4 rs35724 G>C Variant Modulates Liver Damage in Nonalcoholic Fatty Liver Disease

2021 ◽  
Author(s):  
Stefania Grimaudo ◽  
Paola Dongiovanni ◽  
Jussi Pihlajamäki ◽  
Mohammed Eslam ◽  
Hannele Yki‐Järvinen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Liver Damage ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver

scholarly journals Markers of Intestinal Permeability Are Rapidly Improved by Alcohol Withdrawal in Patients with Alcohol-Related Liver Disease

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1659
Author(s):  
Finn Jung ◽  
Katharina Burger ◽  
Raphaela Staltner ◽  
Annette Brandt ◽  
Sebastian Mueller ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Damage ◽  
Alcohol Withdrawal ◽  
Barrier Function ◽  
Binding Protein ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Fatty Acid Binding ◽  
Liver Health ◽  
Related Liver Disease

Changes in intestinal microbiome and barrier function are critical in the development of alcohol-related liver disease (ALD). Here, we determined the effects of a one-week alcohol withdrawal on parameters of intestinal barrier function in heavy drinkers with ALD in comparison to healthy non-drinkers (controls). In serum samples of 17 controls (m = 10/f = 7) and 37 age-matched ALD patients (m = 26/f = 11) undergoing a one-week alcohol withdrawal, markers of liver health and intestinal barrier function were assessed. Liver damage, e.g., fibrosis and hepatic steatosis, were assessed using FibroScan. Before alcohol withdrawal, markers of liver damage, lipopolysaccharide binding protein (LBP) and overall TLR4/TLR2 ligands in serum were significantly higher in ALD patients than in controls, whereas intestinal fatty acid binding protein (I-FABP) and zonulin protein concentrations in serum were lower. All parameters, with the exception of LBP, were significantly improved after alcohol withdrawal; however, not to the level of controls. Our data suggest that one-week of abstinence improves markers of intestinal barrier function and liver health in ALD patients.

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