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Drug-Induced Vanishing Bile Duct Syndromes
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
Tania A. Roskams, Valeer J. Desmet
A number of drugs have the potential to induce a peculiar form of liver toxicity, in which bile duct damage is a prominent feature. This bile duct damage may be acute and self limited, or prolonged, with ductopenia, occasionally leading to biliary cirrhosis. An immune mechanism has been proposed. Recent studies provided strong arguments in favor of a genetic predisposition. Treatment options are poor: ursodeoxycholic acid has been reported to speed recovery in some instances.68 Liver transplantation has to be considered in patients who develop secondary biliary cirrhosis.69,70
Hepatobiliary Surgery
Published in Gozie Offiah, Arnold Hill, RCSI Handbook of Clinical Surgery for Finals, 2019
➢ Chronic CholecystitisThe most common form of symptomatic gallbladder disease.Clinical examination may be unremarkable.During an attack, patients may report RUQ tenderness.Adequate analgesia and routine elective cholecystectomy is sufficient in most patients.Medical management is rarely advisedUrsodeoxycholic acid reduces cholesterol in bile by inhibiting cholesterol secretion and is occasionally used to reduce gallstone size.
Non-viral liver disease
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
John ML Christie, Roger WG Chapman
The medical treatment of primary sclerosing cholangitis has included trials of corticosteroids, immunosuppressive drugs and antibiotics, either alone or in combination. Ursodeoxycholic acid is a non-hepatotoxic hydrophillic bile acid that has been used widely for the treatment of cholestasis.22 It reduces levels of cholestatic liver enzymes but controlled trials in conventional doses have shown no effect on symptoms, histology or survival. Larger doses may be needed to produce a more beneficial effect.23 Several immunosuppressive agents have been tried, including prednisone, colchicine,24 azathioprine,25 methotrexate26 and cyclosporin;27 overall, the results have been disappointing.
Intrahepatic cholestasis of pregnancy: from an obstetrician point of view
Published in Journal of Obstetrics and Gynaecology, 2022
Mohsen M. A. Abdelhafez, Karim A. M. Ahmed, Win Win Than, Dg Marshitah Pg Baharuddin, Fairrul Kadir, Saffree Jeffree, Mohammad Firdaus Hayati, Mohd Nazri Bin Mohd Daud, Aya M. Eldiastey, Kai Xin Tay
Intrahepatic cholestasis of pregnancy (ICP) is the commonest among pregnancy specific dermatoses, with an estimated incidence of 0.2–2% of the pregnant women. The exact aetiology of the disease is not clearly understood, with probable genetic, cultural, and hormonal backgrounds. The diagnosis of the disease depends mainly on the characteristic presentation of intense pruritus of palms and soles, which will propagate to involve the whole body, with elevated serum bile acid levels and deranged liver function tests. The perinatal adverse effects associated with the disease may include, preterm birth, meconium-stained liquor, intrauterine foetal death, respiratory distress syndrome and neonatal depression. Ursodeoxycholic acid (UDCA) is the first line therapy, even so, it is not licenced for use during pregnancy, it has been shown to improve the pruritus and reduce the serum bile acid levels but no evidence to improve perinatal outcomes. Early elective delivery at 37weeks of gestation is recommended to avoid sudden foetal demise. Postnatally, women should be counselled on the high risk of recurrence (up to 90%) hence, the use of an appropriate method of contraception.
miR-26a-5p protects against drug-induced liver injury via targeting bid
Published in Toxicology Mechanisms and Methods, 2022
Qian Zhang, Yan Liu, Yujie Yuan, Feifei Yao, Hongmei Zhang, Caiyan Zhao, Yanli Luo
Drug-induced liver injury (DILI) is usually caused by the direct toxicity of drug or its metabolites to the liver during drug treatment, or induced by allergic reactions to drugs in people with special constitution (Katarey and Verma 2016; A 2019). Researchers have demonstrated that DILI accounts for about 10%–15% of all adverse drug events and is the main cause of acute liver failure (Katarey and Verma 2016). Due to the rapid replacement rate of drug and insufficient understanding of the hepatotoxicity of drugs, the incidence of DILI has increased (Katarey and Verma 2016; A 2019). DILI has become the most common cause of liver disease other than viral hepatitis and fatty liver disease. Currently, there are no approved drugs for the treatment of DILI; the basic approach is to stop the use of drugs that damage the liver so that pharmaceutical ingredients can be excreted and removed from the body (Stine and Lewis 2016). Therapeutic drugs such as N-acetylcysteine, glycyrrhizic acid, and ursodeoxycholic acid are available but often cause gastrointestinal discomfort, allergic skin diseases, and other adverse reactions (Chughlay et al. 2016; Bordbar et al. 2018; Tian et al. 2019). Therefore, there is an urgent need for new targets or methods for treating DILI.
Pharmacological effects of nanoencapsulation of human-based dosing of probucol on ratio of secondary to primary bile acids in gut, during induction and progression of type 1 diabetes
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Armin Mooranian, Nassim Zamani, Ryu Takechi, Hesham Al-Sallami, Momir Mikov, Svetlana Goločorbin-Kon, Bozica Kovacevic, Frank Arfuso, Hani Al-Salami
Rau et al. investigated the effects of inflammation on bile acid profile. The authors examined changes in bile acid metabolism and enterohepatic regulation processes associated with inflammatory bowel disorders. They found that there was strong association between bile acid levels in gut and liver, and inflammation, through effects on gene expression and signalling pathways including farnesoid X receptors [29]. This suggests that bile acid based feedback mechanisms take place at the genetic and molecular levels and are not confined only to the gut. Stiehl et al. investigated the effects of chenodeoxycholic acid and ursodeoxycholic acid treatments on the bile acid profile in gallstone patients. The authors explored the effects of chronic daily intake of chenodeoxycholic acid and ursodeoxycholic acids on bile acid metabolism and ratio. The authors found that treatment chenodeoxycholic acid and ursodeoxycholic acid resulted in significant changes in bile acid profile, metabolism and ratios via alteration of liver bile acid synthesis and conjugation [30]. This was not consistent with a previous study in our laboratory which showed that acute treatment of diabetic rats with a conjugated bile acid did not significantly change the concentrations of the bile acid in plasma or tissues [3].