scholarly journals Meropenem-induced liver injury and beta-lactam cross-reactivity

2018 ◽  
Vol 11 (1) ◽  
pp. e227124 ◽  
Author(s):  
Timothy Tattersall ◽  
Hugh Wright ◽  
Andrew Redmond

A 63-year-old man admitted to hospital for the management of a frontal lobe abscess developed elevated liver enzymes within 48 hours of receiving meropenem. Liver enzymes reached a maximum at 5 days postadministration of meropenem, with alanine aminotransferase 1160 U/L, aspartate aminotransferase 787 U/L, alkaline phosphatase 297 U/L and gamma-glutamyltransferase 252 U/L. Meropenem was ceased and liver function normalised. Meropenem was administered for a second time later in the patient’s admission and again the patient developed rapidly increasing liver enzymes, with a mixed hepatocellular/cholestatic pattern. Other possible causes of liver injury were excluded following extensive investigations, and the patient’s liver enzymes continued to normalise following meropenem discontinuation. The patient was asymptomatic during the admission and was transferred to a rehabilitation facility. This case demonstrates that meropenem can cause severe liver injury and that early recognition of drug-induced liver injury is important.

2019 ◽  
Vol 12 (11) ◽  
pp. e231741 ◽  
Author(s):  
Chencheng Xie ◽  
Hafez Mohammad Ammar Abdullah ◽  
Mohamed Abdallah ◽  
Erin Quist ◽  
Mumtaz Niazi

Anastrozole is an aromatase inhibitor that has been used more frequently over the last decade especially for oestrogen receptor-positive breast cancer. It has a relatively safe side effect profile. However, occasionally it has been associated with serious adverse events. Here, we present the case of a 58-year-old woman who presented with significantly elevated liver enzymes 4 years after starting anastrozole. She was not taking any other medications and an extensive workup did not reveal any other cause for her liver injury. The patient’s liver enzymes normalised after discounting the anastrozole. She scored 4 on the updated Roussel Uclaf Causality Assessment Method grading system which was possible for drug-induced liver injury. A review of the literature revealed six prior cases of anastrozole-related liver injury. Anastrozole should be considered as a possible culprit in patients who develop an unexplained acute liver injury.


2017 ◽  
Vol 10 ◽  
pp. 117954761773137 ◽  
Author(s):  
Silje Bergland Ellingsen ◽  
Elisabet Nordmo ◽  
Knut Tore Lappegård

Severe hepatotoxicity is a rare but well-known adverse reaction to statins. However, despite the widespread use of statins, only a few cases describing statin reexposure or switch to another statin after liver injury have been published. The literature on hepatotoxicity with ezetimibe alone or in combination with statins is also scarce. We report a case where a patient with a history of elevated liver enzymes while using atorvastatin, but prior and subsequent good tolerance to simvastatin and pravastatin, developed drug-induced liver injury on reexposure to a combination of atorvastatin and ezetimibe. The hepatotoxicity in our patient was most likely caused by reexposure to atorvastatin, although we cannot exclude ezetimibe as a contributing factor. This case highlights the risk of hepatotoxicity recurrence on rechallenge with the same statin. The tolerance to other statins in this case also strengthens the suspicion that statin-induced liver injury may not be a class effect, although the current data are too scarce to draw any definite conclusions.


2020 ◽  
Vol 8 ◽  
pp. 2050313X2091782
Author(s):  
Ginny Varghese ◽  
Lama Madi ◽  
Muna Ghannam ◽  
Rafaat Saad

Amlodipine is a commonly prescribed antihypertensive drug, well tolerated and has rarely been attributed as a cause for elevated liver enzymes. Here, we present a 47-year-old male patient known to be hypertensive and admitted to our rehabilitation facility after an acute stroke. During his stay, amlodipine was started in addition to other antihypertensive medications to control his blood pressure. His liver transaminases after 4 days (notably alanine aminotransferase) were found to be markedly elevated. After reviewing the medications and investigating probable causes, amlodipine was suspended. After 5 days of suspending amlodipine, the transaminases started to trend downward. The Naranjo Adverse Drug Reaction Probability Scale and the Roussel Uclaf Causality Assessment Method were performed to assess causality in this suspected idiosyncratic drug-induced liver injury case. Both the scores denoted a probable amlodipine-induced liver injury. Previous case reports related to amlodipine-induced liver injury are mentioned and presented in the table below. In conclusion, amlodipine, though not well known to be hepatotoxic, can induce liver enzyme elevations in an idiosyncratic manner.


2020 ◽  
Vol 8 ◽  
pp. 232470962095132
Author(s):  
Simcha Weissman ◽  
Nishan G. Rajaratnam ◽  
Nabeel Qureshi ◽  
Faisal Inayat ◽  
Sameh Elias

Antithyroid drug-induced severe liver injury is an uncommon but serious complication. We hereby delineate the case of a 38-year-old female who presented to the emergency department for an impending thyroid storm. After initiation of a single dose of propylthiouracil, her liver enzymes went into the thousands. She was subsequently admitted to the intensive care unit. Propylthiouracil was discontinued and corticosteroids were initiated with the resolution of her elevated liver enzymes. On follow-up, her liver function was at its baseline and thyroid hormone levels were under control. We hope this report will encourage clinicians to cast a broad differential diagnosis in patients presenting with liver injury in the acute setting. Furthermore, it is imperative to raise awareness regarding the ever-increasing list of pharmacologic agents that can perpetuate drug-induced hepatotoxicity.


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 5 (4) ◽  
pp. 279-286
Author(s):  
Rodrigo Dorelo ◽  
Samantha T.A. Barcelos ◽  
Magela Barros ◽  
Valeria Elustondo ◽  
Ysela Y.P. Pérez ◽  
...  

Introduction and aim: Drug-induced liver injury (DILI) manifests as a spectrum of clinical presentations that carries morbidity and mortality. Patients with chronic liver disease (CLD), particularly hospitalized, are at high risk for developing DILI. We aimed to investigate the use of potentially hepatotoxic drugs (PHD) in patients with CLD in a tertiary university hospital. Materials and methods: Adult (≥ 18 years-old) with CLD admitted to the hospital from January 2016 to December 2018 were evaluated regarding PHD, assessing the risk of DILI and liver enzymes behavior after exposure. Results: From 931 hospitalized patients with CLD, 291 (31.3%) were exposed to hepatotoxic drugs during their hospitalization. Of those, 244 (83.8%) were cirrhotic. The most frequent causes of liver disease were hepatitis C (41.2%), followed by alcohol (13.2%), hepatitis C/alcohol (11.7%) and non-alcoholic fatty liver disease (5.8%). Decompensated cirrhosis (46.7%) was the main reason for hospital admission. The most often prescribed PHD were antibiotics (67.7%), cardiovascular drugs (34.4%), neuromodulators (26.1%) and anesthetics (19.9%). After exposure, 113 patients (38.8%) presented significant elevated liver enzymes. Surprisingly, PHD were more often prescribed in GI/Liver unit (48.8%) followed by emergency/intensive care unit (28.5%). A total of 65 patients (22%) died, however in neither case was it possible to safely infer causal relationship among PHD, liver enzymes and death. Conclusion: PHD prescription is frequent in patients with CLD even in a tertiary university hospital and in the gastroenterology and hepatology department, exposing these patients to an additional risk.


2021 ◽  
Vol 14 (5) ◽  
pp. e240408
Author(s):  
Himmat Singh Brar ◽  
Rachana Marathi

Drug-induced liver injury is an uncommon yet fatal cause of liver injury. Black cohosh is a herbal supplement that is derived from Actaea racemosa. It has been used for vasomotor symptoms in postmenopausal women, but it can cause liver injury. A 50-year-old Afro-American woman presented with a 2-month history of malaise, itching and severe jaundice. The labs showed elevation of bilirubin and alkaline phosphatase. The patient had a history of black cohosh use for postmenopausal symptoms before she developed her current symptoms. The extensive workup for infective and autoimmune pathology was negative. Black cohosh was discontinued. The patient improved clinically, and her liver enzymes normalised 6 months after the discontinuation of black cohosh. This report emphasises the need to recognise black cohosh as a potential hepatotoxic agent and to monitor the liver enzymes for a patient on black cohosh.


Pathogens ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 430 ◽  
Author(s):  
Katie Morgan ◽  
Kay Samuel ◽  
Martin Vandeputte ◽  
Peter C. Hayes ◽  
John N. Plevris

A novel strain of coronoviridae (SARS-CoV-2) was reported in Wuhan China in December 2019. Initially, infection presented with a broad spectrum of symptoms which typically included muscle aches, fever, dry cough, and shortness of breath. SARS-CoV-2 enters cells via ACE2 receptors which are abundant throughout the respiratory tract. However, there is evidence that these receptors are abundant throughout the body, and just as abundant in cholangiocytes as alveolar cells, posing the question of possible direct liver injury. While liver enzymes and function tests do seem to be deranged in some patients, it is questionable if the injury is due to direct viral damage, drug-induced liver injury, hypoxia, or microthromboses. Likely, the injury is multifactoral, and management of infected patients with pre-existing liver disease should be taken into consideration. Ultimately, a vaccine is needed to aid in reducing cases of SARS-CoV-2 and providing immunity to the general population. However, while considering the types of vaccines available, safety concerns, particularly of RNA- or DNA-based vaccines, need to be addressed.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Paula Iruzubieta ◽  
Maria Teresa Arias-Loste ◽  
Lucía Barbier-Torres ◽  
Maria Luz Martinez-Chantar ◽  
Javier Crespo

Drug-induced liver injury (DILI) is a potentially fatal adverse event and the leading cause of acute liver failure in the US and in the majority of Europe. The liver can be affected directly, in a dose-dependent manner, or idiosyncratically, independently of the dose, and therefore unpredictably. Currently, DILI is a diagnosis of exclusion that physicians should suspect in patients with unexplained elevated liver enzymes. Therefore, new diagnostic and prognostic biomarkers are necessary to achieve an early and reliable diagnosis of DILI and thus improve the prognosis. Although several DILI biomarkers have been found through analytical and genetic tests and pharmacokinetic approaches, none of them have been able to display enough specificity and sensitivity, so new approaches are needed. In this sense, metabolomics is a strongly and promising emerging field that, from biofluids collected through minimally invasive procedures, can obtain early biomarkers of toxicity, which may constitute specific indicators of liver damage.


2020 ◽  
Vol 8 (T1) ◽  
pp. 154-157
Author(s):  
Gontar Alamsyah Siregar ◽  
Ginanda Putra Siregar ◽  
Darmadi Darmadi ◽  
Riska Habriel Ruslie

Coronavirus Disease (COVID)-19 is a pandemic since March 11, 2020. The total case is more than a half million worldwide. Liver injury is quite common in COVID-19 patients. Direct viral infection is possible due to the presence of angiotensin converting enzyme 2 in cholangiocytes and hepatocytes. Other proposed mechanisms are virus-induced cytopathic effects, inflammation process, hypoxia and shock, increased apoptotic activity, increased positive end expiratory effect, and drug-induced. The manifestation of liver injury is mild and transient with elevated liver enzymes, bilirubin, and gamma-glutamyl transferase levels. Deterioration of liver function can occur in subjects with COVID-19 and underlying liver injury. The management is principally supportive. Hepatoprotective drugs may be administered in severe cases.


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