scholarly journals A Patient with Nafcillin-Associated Drug-Induced Liver Failure

2017 ◽  
Vol 11 (3) ◽  
pp. 564-568 ◽  
Author(s):  
Qin Rao ◽  
Isaiah Schuster ◽  
Talal Seoud ◽  
Kevin Zarrabi ◽  
Nirvani Goolsarran

Nafcillin-induced acute liver injury is a rare and potentially fatal complication that has been known since the 1960s but inadequately studied. At this time, the only proven treatment is early discontinuation of the drug. Because of the high prevalence of nafcillin class antibiotic use in the United States, it is important for clinicians to have a high clinical suspicion for this diagnosis. We present a case of liver failure attributable to nafcillin use in a 68-year-old male with a history methicillin-sensitive Staphylococcus and L3/L4 osteomyelitis. After starting long-term antibiotic therapy, he presented with painless jaundice which necessitated discontinuation of the drug. At the time of presentation, the patient’s lab work exhibited a bilirubin/direct bilirubin of 9.4/8.2 mg/dL, alkaline phosphatase of 311 IU/L, and aspartate transaminase/alanine transaminase of 109/127 IU/L. The patient was switched to i.v. vancomycin given the concern for drug-induced liver injury. Imaging did not show obstruction of the hepatobiliary or pancreaticobiliary trees. Serology was unremarkable for viral etiology, autoimmune processes, Wilson disease, and hemochromatosis. A liver biopsy showed findings consistent with drug-induced liver injury. The patient’s liver function tests peaked at day 7 of admission and trended towards normal levels with cessation of nafcillin therapy. The patient was discharged with a diagnosis of nafcillin-induced acute liver injury. Our case highlights the importance of early recognition of the diagnosis and careful monitoring of liver function when nafcillin is employed in the clinical setting.

PLoS ONE ◽  
2019 ◽  
Vol 14 (2) ◽  
pp. e0212394 ◽  
Author(s):  
Herbert L. Bonkovsky ◽  
Huiman X. Barnhart ◽  
David M. Foureau ◽  
Nury Steuerwald ◽  
William M. Lee ◽  
...  

Author(s):  
Anooja Thampi

 Acute liver failure is a clinical entity associated with a high mortality rate and majority of these patients may require liver transplantation. N-Acetylcysteine (NAC), an antioxidant agent that replenishes mitochondrial and cytosolic glutathione stores, is an antidote for acetaminophen poisoning. But their role in non–acetaminophen-related acute liver failure is still not proven. Here, we discuss about a 67 year old male patient diagnosed with hepatitis with acute liver injury who was admitted in Emergency Medicine. He was treated with N- Acetylcysteine infusion for an average of 48 hours and later it was found that his liver function tests improved. In this study, we could find that N-Acetylcysteine plays a major role in improving the liver function test of patients with non–acetaminophen-related acute liver failure.


2021 ◽  
Vol 14 (12) ◽  
pp. e246571
Author(s):  
Tayyab Shah ◽  
James A Joslyn ◽  
James Lai

A 65-year-old woman with type II diabetes mellitus complicated by non-healing ulcers with recurrent osteomyelitis was admitted for progression of cellulitis after treatment failure with an outpatient course of amoxicillin-clavulanate. She was found to have persistent osteomyelitis and started on ceftazidime for a culture documented Pseudomonas aeruginosa infection. After two parenteral doses, she had a rapid rise in liver function tests (LFTs) in a hepatocellular pattern. Due to rapid identification, all medications with potential hepatotoxicity, including ceftazidime, were discontinued and the LFTs promptly returned to baseline over 3 days. Of note, the patient did not experience any symptoms of liver injury. Other causes of acute liver injury were effectively ruled out, but the case was confounded by usage of other potential hepatotoxic medications. Still, the most likely culprit was ceftazidime, a rare cause of drug induced liver injury with very few reports in the literature.


2021 ◽  
Vol 14 (4) ◽  
pp. e240719
Author(s):  
Vikram Rao ◽  
Anna Munasinghe

Rivaroxaban is a commonly used anticoagulant agent for treatment and prevention of thromboembolism. There are case reports demonstrating an association between its use and drug-induced liver injury. However, this has not been reported in a patient who previously tolerated apixaban. An 88-year-old man presented to hospital with worsening lethargy, jaundice and vomiting. He had severely elevated liver transaminases, an abnormal coagulation profile and elevated bilirubin in keeping with acute liver injury. This is in the context of having had his anticoagulation medication switched from apixaban to rivaroxaban 2 weeks prior. The patient recovered well after cessation of rivaroxaban, suggesting that it was the likely offending agent. The mechanism of rivaroxaban-induced liver injury remains to be investigated. Drug-induced liver injury should be discussed and monitored for as a potential adverse reaction when commencing rivaroxaban, even if a patient has previously tolerated a drug of the same class.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Preethi Dileep Menon ◽  
Tamneet Singh ◽  
Hopethe Hubbard ◽  
Sarah Hackman ◽  
Francis E. Sharkey

Atorvastatin is a commonly used oral cholesterol-lowering agent. Side effects associated with statin therapy include arthralgia, myalgia, dyspepsia, weakness, and headache. Prospective and retrospective studies of drug-induced liver injury have identified statin-induced hepatotoxicity, with atorvastatin being the most commonly cited. Associated liver function test elevations have varied from hepatocellular to cholestatic/mixed pattern. We report a case of a 58-year-old woman that illustrates unusual histologic findings associated with a mixed pattern of statin-induced liver injury. While being treated with atorvastatin, the patient exhibited repeated bouts of abdominal pain over a year associated with biliary tree dilation, variably attributed to postcholecystectomy dilation and stenosis of the ampulla of Vater. Following sphincterotomy, the patient’s bilirubin normalized but the other liver function tests remained elevated. Liver biopsy revealed portal and lobular inflammation with cholangiolysis. The patient’s liver function tests normalized following cessation of atorvastatin therapy.


PLoS ONE ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. e0206389 ◽  
Author(s):  
Herbert L. Bonkovsky ◽  
Huiman X. Barnhart ◽  
David M. Foureau ◽  
Nury Steuerwald ◽  
William M. Lee ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Liangliang Yao ◽  
Muhammad Farrukh Nisar ◽  
Tingdong Yan ◽  
Chunpeng (Craig) Wan

Numerous prescribed drugs and herbal and dietary supplements have been reported to cause drug-induced acute liver injury, which is a frequent cause of acute liver failure (ALF). It is a tremendous challenge with ever-increasing drug application in the medication system for huge populations. Drug-induced acute liver injury can lead to diverse pathologies similar to acute and chronic hepatitis, acute liver failure, biliary obstruction, fatty liver disease, and so on. Recently, extensive work demonstrated that isoflavones play an essential and protecting role in drug-induced liver injury (DILI). The isoflavones mediated hepatoprotection by modulating specific genes linked with control of cellular redox homeostasis and inflammatory responses. Isoflavones upregulate oxidative stress-responsive nuclear factor erythroid 2-like 2 (Nrf2), downregulate inflammatory nuclear factor-κB (NF-κB) signaling pathways, and modulate a balance between cell survival and death. Moreover, isoflavones actively inhibit the expression of cytochromes P450 (CYPs) enzyme during drug metabolism. Moreover, isoflavones are also linked with farnesoid X receptor (FXR) activation and signal transducer and activator of transcription factor 3 (STAT3) phosphorylation in hepatoprotection DILI. In vivo and in vitro studies clearly stated that isoflavones bear strong antioxidant potential and promising agents for hepatotoxicity prevention and stressed their potential role as therapeutic supplements in DILI. The current review will elaborate on isoflavones’ preventive and therapeutic potential concisely and highlight various molecular targets to exert a protective effect on DILI.


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