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Recent Advances in Artificial Cells With Emphasis on Biotechnological and Medical Approaches Based on Microencapsulation
Published in Max Donbrow, Microcapsules and Nanoparticles in Medicine and Pharmacy, 2020
No complete artificial liver is yet available to replace all the functions of the liver. Hemoperfusion can remove toxic products in deeply comatose liver failure patients and result in temporary recovery of consciousness21,22 (Table 3). In acute liver failure the liver has the potential to recover its full function. Thus, hemoperfusion can increase the survival rates of patients with certain types of acute liver failure.22 On the other hand, livers in end-stage chronic liver failure cannot recover. This condition requires continuous support of all the many liver functions. Detoxification by hemoperfusion only supports one of the many functions, so that for end-stage chronic liver failure, additional systems are required.22
Drug Discovery, Development, and Distribution
Published in Richard J. Sundberg, The Chemical Century, 2017
One of the most frequent causes of drug withdrawal or warnings is toxicity associated with liver metabolism, which can result in the generation of toxic metabolites. Around 7–15% of cases of acute liver failure are attributed to adverse drug reactions. Some drugs carry labels that recommend periodic tests of liver function, although these recommendations are not always followed. There can be wide variations in patient sensitivity to some drugs, based on genetic factors.8 We will consider several specific cases of withdrawal of approved drugs, such as rofecoxib (Section 13.4.2), troglitazone (Section 16.4) and the appetite suppressant fenfluramine (Section 17.6.2).
The roadmap towards cure of chronic hepatitis B virus infection
Published in Journal of the Royal Society of New Zealand, 2022
Although nucleos(t)ide polymerase inhibitors can maintain viral suppression and reduce complications, the need for life-long therapy has several disadvantages. Only a minority of people with chronic HBV Infection are suitable for current treatment – those with significant viraemia and either elevated ALT or significant fibrosis (so-called chronic hepatitis B). For those who commence therapy, there are no widely accepted stopping criteria and treatment is usually lifelong. Despite the availability of generic ETV, TDF and TAF, the cost associated with life-long treatment limits access in low-income countries. Non-adherence will usually result in virologic breakthrough which can lead to severe hepatitis flares and occasionally acute liver failure, emergency transplantation or death. In low income countries, sequential therapy with older therapies (lamivudine, adefovir and telbivudine) may lead to high rates of treatment failure from the emergence of multi-resistant HBV.
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
Given their critical role in maintaining homeostasis, it is not surprising that gap junctions are frequently involved in pathological conditions (Yamasaki et al. 1999). A wide spectrum of alterations were found in connexin expression and gap junction functionality in liver diseases, including cholestasis (Fallon et al. 1995), nonalcoholic steatohepatitis (Luther et al. 2018), fibrosis (Fischer et al. 2005), cirrhosis (Yang et al. 2019) and liver cancer (Xiang et al. 2019). The nature of the GJIC and/or connexin modifications depends upon the type of cell and disease involved (Hernandez-Guerra, Hadjihambi, and Jalan 2019; Maes et al. 2015a). In acute liver failure (Maes et al. 2016) and hepatitis (Balasubramaniyan et al. 2013), Cx32 and Cx26 production is typically downregulated, while Cx43 expression is upregulated. Generally, Cx43 appears elevated at the expense of Cx32 production in liver disease, owing to both increased production by non-parenchymal cells as well as through de novo expression by hepatocytes (Cooreman et al. 2019).
Pick your poison: do cyanotoxins or disinfection by-products pose the greater risk?
Published in Inland Waters, 2019
Justin D. Brookes, Adam Tomlinson
A tragic cyanobacterial intoxication event occurred in Brazil when 50 dialysis patients died after intravenously receiving water contaminated with microcystins. A further 51 patients had acute liver failure (Jochimsen et al. 1998). While no other fatalities of acute toxicity from cyanobacterial toxins have been reported, there is evidence of liver damage in populations exposed to cyanotoxins through drinking water. Models to determine cancer risk from DBP ingestion, dermal absorption, and inhalation predict that 10 of the 7 million residents of Hong Kong contract cancer annually (Lee et al. 2004). It follows that a proportion of DBPs inducing this cancer arise from algae precursors. Scaled globally, acknowledging that DOC varies among waterbodies, algal-derived DBPs may present a significant burden given 4.9 billion people have access to treated drinking water.