scholarly journals Oral Azole Antifungal Medications and Risk of Acute Liver Injury, Overall and by Chronic Liver Disease Status

2016 ◽  
Vol 129 (3) ◽  
pp. 283-291.e5 ◽  
Author(s):  
Vincent Lo Re ◽  
Dena M. Carbonari ◽  
James D. Lewis ◽  
Kimberly A. Forde ◽  
David S. Goldberg ◽  
...  
2021 ◽  
Vol 60 (2) ◽  
Author(s):  
S Kerdsin ◽  
◽  
R Norasetkun ◽  
W Khamwang ◽  
A Phensombun ◽  
...  

Objectives To study factors related to acute liver injury and compare the severity and risk of those factors in patients with and without chronic liver disease. Methods This cross-sectional study of 323 patients admitted to Somdejphrajaotaksin Maharaj Hospital between 1 January and 30 September 2019, analyzing data collected on the clinical background, signs and symptoms, and laboratory results of those patients. Results Of the 323 patients in the study, 188 did not have chronic liver disease (58.2%) and 135 had chronic liver disease (41.8%). Risk factors for acute liver injury in the chronic liver disease group included bacterial infection (33.3%) and spontaneous bacterial peritonitis (4.4%), much significantly higher than the rates in the no chronic disease group. However, the risk factors excessive consumption of alcohol (30.3%) and dengue infection (11.2%) in the no chronic liver disease group were significantly higher than in the chronic disease group. Both groups had a high incidence of disease severity as well as a high incidence of complications and mortality, although the mortality rate was higher in the chronic liver disease group (15.0% vs. 6.9%). Conclusions The types and frequencies of risk factors for acute liver injury in patients with chronic liver disease and those with no chronic liver disease groups are different. The incidence of bacterial infection and spontaneous bacterial peritonitis is higher in patients with chronic liver disease. The incidence of excessive alcohol consumption and dengue infection is much higher in patients without chronic liver disease. Both groups have high levels of disease severity, complications and mortality. Sepsis is the major cause of mortality, especially in patients with chronic liver disease.


2013 ◽  
Vol 44 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Takeshi Nowatari ◽  
Soichiro Murata ◽  
Kiyoshi Fukunaga ◽  
Nobuhiro Ohkohchi

2021 ◽  
Vol 14 ◽  
pp. 175628482110234
Author(s):  
Mario Romero-Cristóbal ◽  
Ana Clemente-Sánchez ◽  
Patricia Piñeiro ◽  
Jamil Cedeño ◽  
Laura Rayón ◽  
...  

Background: Coronavirus disease (COVID-19) with acute respiratory distress syndrome is a life-threatening condition. A previous diagnosis of chronic liver disease is associated with poorer outcomes. Nevertheless, the impact of silent liver injury has not been investigated. We aimed to explore the association of pre-admission liver fibrosis indices with the prognosis of critically ill COVID-19 patients. Methods: The work presented was an observational study in 214 patients with COVID-19 consecutively admitted to the intensive care unit (ICU). Pre-admission liver fibrosis indices were calculated. In-hospital mortality and predictive factors were explored with Kaplan–Meier and Cox regression analysis. Results: The mean age was 59.58 (13.79) years; 16 patients (7.48%) had previously recognised chronic liver disease. Up to 78.84% of patients according to Forns, and 45.76% according to FIB-4, had more than minimal fibrosis. Fibrosis indices were higher in non-survivors [Forns: 6.04 (1.42) versus 4.99 (1.58), p < 0.001; FIB-4: 1.77 (1.17) versus 1.41 (0.91), p = 0.020)], but no differences were found in liver biochemistry parameters. Patients with any degree of fibrosis either by Forns or FIB-4 had a higher mortality, which increased according to the severity of fibrosis ( p < 0.05 for both indexes). Both Forns [HR 1.41 (1.11–1.81); p = 0.006] and FIB-4 [HR 1.31 (0.99–1.72); p = 0.051] were independently related to survival after adjusting for the Charlson comorbidity index, APACHE II, and ferritin. Conclusion: Unrecognised liver fibrosis, assessed by serological tests prior to admission, is independently associated with a higher risk of death in patients with severe COVID-19 admitted to the ICU.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jiahao Lin ◽  
Bingting Bao ◽  
Nigar Anjuman Khurram ◽  
Kasey Halsey ◽  
Ji Whae Choi ◽  
...  

AbstractTo explore the role of chronic liver disease (CLD) in COVID-19. A total of 1439 consecutively hospitalized patients with COVID-19 from one large medical center in the United States from March 16, 2020 to April 23, 2020 were retrospectively identified. Clinical characteristics and outcomes were compared between patients with and without CLD. Postmortem examination of liver in 8 critically ill COVID-19 patients was performed. There was no significant difference in the incidence of CLD between critical and non-critical groups (4.1% vs 2.9%, p = 0.259), or COVID-19 related liver injury between patients with and without CLD (65.7% vs 49.7%, p = 0.065). Postmortem examination of liver demonstrated mild liver injury associated central vein outflow obstruction and minimal to moderate portal lymphocytic infiltrate without evidence of CLD. Patients with CLD were not associated with a higher risk of liver injury or critical/fatal outcomes. CLD was not a significant comorbid condition for COVID-19.


2019 ◽  
Vol 7 ◽  
pp. 232470961983613 ◽  
Author(s):  
Christopher T. Fernandes ◽  
Umair Iqbal ◽  
Sean P. Tighe ◽  
Aijaz Ahmed

Drug-induced liver injury (DILI) is a common cause of hepatotoxicity associated with prescription-based and over-the-counter exposure to medications and herbal supplements. Use of unapproved and inadequately tested herbal supplements can cause DILI. Therefore, thorough history-taking on exposure to herbal supplements must be an integral part of clinical evaluation of DILI. Kratom is an herbal supplement or remedy that has been known for its analgesic effects and has also been used for self-treatment of opiate withdrawals. A 52-year-old man was seen for evaluation of yellow discoloration of the eyes and skin. He reported taking kratom for right shoulder strain for at least a couple of months. On workup, his total bilirubin was noted to be 23.2 mg/dL, which peaked at 28.9 mg/dL. He was noted to have mild elevation of aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase. Extensive laboratory tests were ordered and known causes of chronic liver disease ruled out. Magnetic resonance imaging of the abdomen was unremarkable without stigmata of portal hypertension or signs of chronic liver disease. He demonstrated no evidence of coagulopathy or hepatic encephalopathy during his illness. He underwent liver biopsy, which demonstrated histologic evidence of acute cholestatic hepatitis highly suspicious of DILI. He was advised to avoid kratom or other herbal supplements in future and prescribed ursodeoxycholic acid with significant improvement in his liver chemistries. Kratom is associated with significant liver enzymes derangements leading to DILI. Kratom is not approved for use in the United States and should be avoided.


2012 ◽  
Vol 303 (4) ◽  
pp. G498-G506 ◽  
Author(s):  
Jörn M. Schattenberg ◽  
Michael Nagel ◽  
Yong Ook Kim ◽  
Tobias Kohl ◽  
Marcus A. Wörns ◽  
...  

Chronic liver disease promotes hepatocellular injury involving apoptosis and triggers compensatory regeneration that leads to the activation of quiescent stellate cells in the liver. The deposition of extracellular matrix from activated myofibroblasts promotes hepatic fibrosis and the progression to cirrhosis with deleterious effects on liver physiology. The role of apoptosis signaling pathways in the development of fibrosis remains undefined. The aim of the current study was to determine the involvement of the caspase-8 homologue cellular FLICE-inhibitory protein (cFLIP) during the initiation and progression of fibrosis. Liver injury and fibrosis from carbon tetrachloride (CCl4) and thioacetamide (TAA) were examined in mice exhibiting a hepatocyte-specific deletion of cFLIP ( flip −/−). Acute liver injury from CCl4 and TAA were enhanced in flip −/− mice. This was accompanied by increased activation of caspase-3 and -9, pronounced phosphorylation of JNK, and decreased phosphorylation of Erk. Deletion of the cJun NH2-terminal kinase 2 (JNK2) in flip −/− mice protected from injury. Hepatic fibrosis was increased at baseline in 12-wk-old flip −/− mice, and progression of fibrosis from TAA was accelerated compared with the wild type. In conclusion, deletion of cFLIP in hepatocytes leads to increased fibrosis and accelerated fibrosis progression. This is accompanied by increased injury involving the activation of caspases and JNK2. Thus predisposition to liver injury involving increased hepatocellular apoptosis is a critical mediator of accelerated fibrogenesis, and prevention of liver injury will be a most important measure for patients with chronic liver disease.


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