Ceftazidime induced liver injury

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.

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.


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.


2020 ◽  
Vol 20 (2) ◽  
pp. 125-138 ◽  
Author(s):  
Bharat Bhushan ◽  
Udayan Apte

Acetaminophen (APAP) overdose is the major cause of acute liver failure (ALF) in the Western world. Extensive research is ongoing to identify the mechanisms of APAP-induced ALF. APAP-induced acute liver injury is also one of the most commonly studied drug-induced liver injury models in the field of hepatotoxicity. APAP toxicity is triphasic and includes three mechanistically interlinked but temporally distinct phases of initiation, progression, and recovery/regeneration. Despite how commonly it is studied, the methods to study APAP toxicity differ significantly, often leading to confusing and contradictory data. There are number of reviews on mechanisms of APAP toxicity, but a detailed mechanism-based comprehensive method and list of assays that covers all phases of APAP hepatotoxicity are missing. The goal of this review is to provide a standard protocol and guidelines to study APAP toxicity in mice including a test battery that can help investigators to comprehensively analyze APAP toxicity in the specific context of their hypothesis. Further, we will identify the major roadblocks and common technical problems that can significantly affect the results. This acetaminophen test battery (ATB) will be an excellent guide for scientists studying this most common and clinically relevant drug-induced liver injury and will also be helpful as a roadmap for hypothesis development to study novel mechanisms.


2017 ◽  
Vol 03 (01) ◽  
Author(s):  
Omkolsoum M Alhaddad ◽  
Maha M Elsabaawy ◽  
Mohammed S Essa ◽  
Ahmed Shaaban ◽  
Omar Elsaharaawy ◽  
...  

Author(s):  
Diogo Costa Santos ◽  
Graça Lérias ◽  
Isabel Madruga

Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Western world. In recent years, natural herbal and dietary supplements have become widely available to the general public and have increased in popularity. Reports of idiosyncratic liver injury caused by such supplements have also increased over the last decade. Horse chestnut is a herb used in dietary supplements primarily for complications of venous insufficiency. Clinically significant acute liver injury has been very rarely associated with its use. We present the case of a 70-year-old man with idiosyncratic horse chestnut-induced liver injury.


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

2020 ◽  
pp. 001857872096543 ◽  
Author(s):  
Jason Samuel Haney ◽  
Cassandra Tatum Carter ◽  
Jacklyn Downey ◽  
Romina Ilic

The authors describe a case of clinically apparent idiosyncratic hepatotoxicity in association with unfractionated heparin (UFH). A 52-year-old woman with increasingly symptomatic rheumatic mitral valvular disease and severe pulmonary hypertension underwent elective minimally-invasive bioprosthetic mitral valve replacement. The patient received 42 000 units of UFH intraoperatively 10 days after receiving 3100 units during a left heart catheterization. Standard prophylactic doses of unfractionated heparin were started on POD 2 for prevention of venous thromboembolism. On the evening of postoperative day (POD) 3, the patient was lethargic, encephalopathic, and hypoglycemic with an acute liver injury and hyperlactatemia. Similar events occurred on POD 7 after clinical improvement from the initial injury and an unintentional rechallenge with UFH. Heparins are usually not suspected of idiosyncratic hepatotoxicity due to their widespread utilization and reports of milder episodes of hepatotoxicity. This case highlights the need to consider UFH in the differential of drug-induced liver injury, including severe cases.


2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Yunseok Namn ◽  
Yecheskel Schneider ◽  
Isabelle H. Cui ◽  
Arun Jesudian

Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Unites States and accounts for 10% of acute hepatitis cases. We report the only known case of diphenhydramine-induced acute liver injury in the absence of concomitant medications. A 28-year-old man with history of 13/14-chromosomal translocation presented with fevers, vomiting, and jaundice. Aspartate-aminotransferase and alanine-aminotransferase levels peaked above 20,000 IU/L and 5,000 IU/L, respectively. He developed coagulopathy but without altered mental status. Patient reported taking up to 400 mg diphenhydramine nightly, without concomitant acetaminophen, for insomnia. He denied taking other medications, supplements, antibiotics, and herbals. A thorough workup of liver injury ruled out viral hepatitis (including A, B, C, and E), autoimmune, toxic, ischemic, and metabolic etiologies including Wilson’s disease. A liver biopsy was consistent with DILI without evidence of iron or copper deposition. Diphenhydramine was determined to be the likely culprit. This is the first reported case of diphenhydramine-induced liver injury without concomitant use of acetaminophen.


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