scholarly journals A Rare Case of Rivaroxaban Causing Delayed Symptomatic Hepatocellular Injury and Hyperbilirubinemia

2017 ◽  
Vol 2017 ◽  
pp. 1-3 ◽  
Author(s):  
Keith Glenn ◽  
Patrick Chen ◽  
Mustafa Musleh ◽  
Rao Pallivi ◽  
Melissa Grilliot

Importance. As Rivaroxaban has increased in popularity, it has been accompanied with a growing body of evidence displaying its ability to cause drug induced liver injury (DILI). Observation. A 74-year-old Caucasian female developed Rivaroxaban DILI two weeks after finishing a 14-day course. The patient was symptomatic and jaundiced with elevated transaminases and hyperbilirubinemia with normal lab values two months priorly. Liver biopsies showed mixed inflammatory infiltrate of lymphocytes, neutrophils and eosinophils, rare necrotic hepatocytes, and canalicular and intrahepatocellular cholestasis, all of which are consistent with DILI. Conclusion and Relevance. We present this case to add to the growing evidence that Rivaroxaban can be associated with severe, symptomatic liver injury and to ensure physicians are aware of these possible side effects of novel anticoagulants with their increasing use.

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Madison Davis ◽  
Brendan D. Stamper

In vitro models for hepatotoxicity can be useful tools to predict in vivo responses. In this review, we discuss the use of the transforming growth factor-αtransgenic mouse hepatocyte (TAMH) cell line, which is an attractive model to study drug-induced liver injury due to its ability to retain a stable phenotype and express drug-metabolizing enzymes. Hepatotoxicity involves damage to the liver and is often associated with chemical exposure. Since the liver is a major site for drug metabolism, drug-induced liver injury is a serious health concern for certain agents. At the molecular level, various mechanisms may protect or harm the liver during drug-induced hepatocellular injury including signaling pathways and endogenous factors (e.g., Bcl-2, GSH, Nrf2, or MAPK). The interplay between these and other pathways in the hepatocyte can change upon drug or drug metabolite exposure leading to intracellular stress and eventually cell death and liver injury. This review focuses on mechanistic studies investigating drug-induced toxicity in the TAMH line and how alterations to hepatotoxic mechanisms in this model relate to the in vivo situation. The agents discussed herein include acetaminophen (APAP), tetrafluoroethylcysteine (TFEC), flutamide, PD0325901, lapatinib, and flupirtine.


2021 ◽  
Vol 12 ◽  
Author(s):  
Maermaer Tuohutaerbieke ◽  
Xinjie Li ◽  
Yue Yin ◽  
Wei Chen ◽  
Dongmei Wu ◽  
...  

Background: We investigated the prevalence, demographic and clinical features, and risk factors associated with drug-induced liver injury (DILI) during the treatment of brucellosis inpatients in a retrospective study.Methods: We collected the clinical data of 782 brucellosis inpatients admitted at the Shawan County People’s Hospital, Xinjiang, from 2015–2019. All cases were re-evaluated using the international consensus of DILI criteria and RUCAM rating scale. 71 patients were confirmed as DILI cases and compared with 523 other patients with normal liver function.Results: It was indicated that DILI occurred with a prevalence of about 9.08% among brucellosis inpatients receiving drug therapy. Hepatocellular injury was the most common type of DILI (61.97%, 95% confidence interval [CI] 50.34–72.37), followed by mixed (23.94%, 95% CI 15.52–35.04) and cholestatic types (14.08%, 95% CI 7.83–24.02). In addition, 13.64% of the hepatocellular DILI cases fulfilled Hy’s law criteria and only two cases (2.82%) progressed to severe DILI. Most patients adopted the combination of rifampicin, antipyretic analgesics, anti-infective agents, and traditional Chinese medicine for the treatment of brucellosis, with all the 71 patients taking rifampicin as the drug of choice. Multivariable logistic regression analyses indicated that obesity, regular alcohol intake, and decreased serum albumin were the independent risk factors of DILI in patients with brucellosis after adjusting for gender, age, and ethnicity.Conclusion: DILI occurred in a minority of inpatients diagnosed with brucellosis receiving rifampicin-based therapeutic regimen. In addition, obesity, alcohol abuse, and decreased serum albumin were valuable predictors of the risk of DILI in patients with brucellosis.


2021 ◽  
Vol 14 (4) ◽  
pp. e239488
Author(s):  
Melvin Qiyu Lee ◽  
Royale Chigozie ◽  
Irfan Khan ◽  
Gerard O'Mara

A 68-year-old patient presented with symptoms of a urinary tract infection. A deterioration in the patient’s liver function tests (LFTs) was noted 1 week following completion of a course of amoxicillin–clavunalate. This progressively worsened, reaching its peak by day 30. Our investigations excluded other possible causes for deranged LFTs and there was no improvement of same despite reduced dosing of potentially hepatotoxic medications.A trial of 30 mg/day prednisolone was commenced, resulting in an immediate and progressive improvement in LFTs to baseline over a period of 22 days and an improvement in constitutional symptoms such as tiredness and poor appetite. Drug-induced liver injury (DILI) is one of the common causes of acute hepatitis and a leading cause of acute liver failure in the US and Europe. Patterns of DILI can be generally divided into: (1) hepatocellular injury, (2) cholestatic injury and (3) mixed injury.


2016 ◽  
Vol 111 ◽  
pp. S959-S960
Author(s):  
Rooma Nankani ◽  
Amruta Panwala ◽  
Deepa Nankani ◽  
Ameet Kumar ◽  
Lisa Rossi

2019 ◽  
Vol 2019 ◽  
pp. 1-3 ◽  
Author(s):  
Douglas Tremblay ◽  
Juan Putra ◽  
Alexander Vogel ◽  
Adam Winters ◽  
Ronald Hoffman ◽  
...  

Ruxolitinib is increasingly being utilized for the treatment of myelofibrosis and polycythemia vera, but the potential for hepatic toxicity is poorly understood. We performed a retrospective review of hepatic damage occurring in patients with myeloproliferative neoplasms receiving ruxolitinib. Relevant histologic images of liver biopsies were reviewed by an experienced liver pathologist and reported to a multidisciplinary team including hepatology and hematology. A variety of liver pathology was observed including extramedullary hematopoiesis, obliterative portal venopathy, and drug-induced liver injury. In all cases reviewed, the liver biopsy had significant treatment implications. We conclude that hepatology referral and liver biopsy in patients receiving ruxolitinib therapy with biochemical evidence of liver injury reveals a variety of etiologies which have significant treatment impact. Clinicians should be aware of the potential causes of liver damage in this population and initiate prompt referral and liver biopsy.


2016 ◽  
Vol 111 ◽  
pp. S943
Author(s):  
Mohamed Barakat ◽  
Mostafa Alfishawy ◽  
Saphwat Eskaros ◽  
Ahmed Kawser

Author(s):  
Rajnish Raj ◽  
Nisha Bhagat

Drug Induced Liver Injury (DILI) is one of the leading causes of liver damage worldwide and raises concerns about its prescription in lieu of the limited drug options available for the depression. Venlafaxine (VEN) is an antidepressant with dual neurotransmitter receptor modulations i.e., serotonin and norepinephrine reuptake inhibitor (SNRI) and having an additional benefit in management of vasomotor symptoms especially in menopausal patients where hormone replacement therapy (HRT) is contraindicated. VEN induced hepatotoxicity have been reported to occur in less than 1% of patients. Until now, less than 11 cases of VEN-related liver injuries have been reported in literature. We hereby, report a rare case of VEN induced liver injury in a 40-year-old breast cancer survivor with co-morbid depression.


2020 ◽  
Vol 2020 ◽  
pp. 1-2
Author(s):  
Phillip P. Santoiemma ◽  
Haripriya Maddur ◽  
Christopher M. Moore

A 33-year-old Caucasian female with relapsing-remitting multiple sclerosis presented with abdominal pain, nausea, and vomiting and was found to have acute liver injury. After thorough investigation, she was diagnosed with drug-induced liver injury (DILI) thought secondary to redosing of Natalizumab therapy.


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