scholarly journals Chinese Skullcap in Move Free Arthritis Supplement Causes Drug Induced Liver Injury and Pulmonary Infiltrates

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Renumathy Dhanasekaran ◽  
Victoria Owens ◽  
William Sanchez

Herbal medications are being increasingly used by the American population especially for common conditions like arthritis. They have been reported to cause adverse effects, including significant hepatotoxicity, but reporting remains sporadic. We report here a patient who developed drug induced liver injury following the intake of Move Free, which is an over-the-counter arthritis supplement. We propose that Chinese skullcap, which is one of the herbal ingredients of the medication, is responsible for the adverse event. There was a strong temporal association between the intake of supplement and onset of symptoms, and also there have been a few recent case reports implicating the same component. A unique observation in our case is the occurrence of pulmonary infiltrates simultaneously with the hepatotoxicity, and this side effect has not been well documented before. Both the hepatic and pulmonary complications completely resolved over few weeks after the patient stopped taking the medication. Since these supplements are readily available over the counter, we feel that it is important to document possible adverse outcomes to raise awareness in the medical community and also among patients.

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Shurouq H. Alqrinawi ◽  
Nuralhuda Akbar ◽  
Hind AlFaddag ◽  
Shahrazad Akbar ◽  
Lujayn Akbar ◽  
...  

Menotrophin is a protein-based hormonal therapy. It is used as a fertility medication that is given as injection either subcutaneously or intramuscularly. Menotrophin has not been previously reported to cause drug-induced liver injury. Drug-induced liver injury (DILI) is commonly seen nowadays with the expansion of the drug industry. It is associated with prescribed medications, over the counter drugs, herbal and dietary supplements. We report the first case of Menotrophin-induced autoimmune hepatitis in a 26-year-old Caucasian woman who was diagnosed with primary infertility due to failure to conceive after five years of marriage. She had received several cycles of Menotrophin, then developed new onset jaundice and fatigue associated with increase in transaminases. She had normal baseline liver function and enzymes prior to receiving treatment with Menotrophin. Evaluation showed no evidence of viral hepatitis, metabolic, alcoholic or vascular causes of liver injury. Autoimmune screening was positive for antinuclear antibody (ANA) with titer of 1 : 640 fine speckled, immunoglobulin G (IgG) level was 1900 mg/dl. Antimitochondrial antibodies (AMA) and antismooth muscle antibodies were negative. Liver biopsy showed features of chronic hepatitis with interface hepatitis and prominence of plasma cells, which best reflects autoimmune hepatitis. Her liver enzymes and bilirubin completely normalized after discontinuation of further Menotrophin therapy and starting treatment with prednisolone and Azathioprine.


2018 ◽  
Vol 8 (2) ◽  
pp. 167-171
Author(s):  
Masanori Abe ◽  
Morikazu Onji ◽  
Takahide Uehara ◽  
Jiro Miyaike ◽  
Masaki Oomoto ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Mercedes Robles-Díaz ◽  
Lana Nezic ◽  
Vesna Vujic-Aleksic ◽  
Einar S. Björnsson

Introduction: Treatment is generally not available for drug-induced liver injury (DILI) patients except in some specific circumstances. The management of DILI is based on the withdrawal of the responsible drug and monitoring the patients and only a few patients need to be referred to a transplant center. Some studies on the role of ursodeoxycholic acid (UDCA) in DILI have been published. The aim of this study was to perform a systematic review of the role of UDCA in the treatment and prevention of DILI.Methods: A search was undertaken in PubMed, with the key words ursodeoxycholic acid, drug-induced liver injury and hepatotoxicity following the PRISMA guidelines.Results: A total of 33 publications were identified: 25 case reports and 8 case series. In 18 of the 25 cases reports (22 patients), authors reported improvement of liver injury associated with UDCA therapy whereas 7 case reports did not show clinical or biochemical improvement after UDCA treatment. There were 4 studies evaluating the role of UDCA in the treatment of DILI, three prospective (one being a clinical trial) and one retrospective studies. Three studies observed liver profile improvements associated with UDCA. In addition, four studies evaluated UDCA in the prevention of DILI: one pilot study, two randomized clinical trials (RCT) and one retrospective study. Three of these studies observed a lower percentage of patients with an increase in transaminases in the groups that used UDCA for DILI prevention.Conclusion: According to available data UDCA seems to have some benefits in the treatment and prevention of DILI. However, the design of the published studies does not allow a firm conclusion to be drawn on the efficacy of UDCA in DILI. A well designed RCT to evaluate the role of UDCA in DILI is needed.


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.


Kanzo ◽  
2009 ◽  
Vol 50 (3) ◽  
pp. 139-144
Author(s):  
Minoru Ayada ◽  
Tetsuya Ishikawa ◽  
Akihiko Okumura ◽  
Naoki Hotta ◽  
Akinori Hirose ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Can Tu ◽  
Yuan Gao ◽  
Di Song ◽  
Ming Niu ◽  
Run-ran Ma ◽  
...  

Early identification of individuals susceptible to idiosyncratic drug-induced liver injury (IDILI) is a challenging unmet demand. Diclofenac, one of the most widely available over-the-counter drugs for pain management worldwide, may induce liver dysfunction, acute liver failure, and death. Herein, we report that diclofenac-related hepatobiliary adverse reactions occurred more frequently in cases with immune activation. Furthermore, experiments with rats demonstrated divergent hepatotoxicity responses in individuals exposed to diclofenac, and modest inflammation potentiated diclofenac-induced liver injury. Susceptible rats had unique plasma metabolomic characteristics, and as such, the metabolomic approach could be used to distinguish susceptible individuals. The 23 identified susceptibility-related metabolites were enriched by several metabolic pathways related to acute-phase reactions of immunocytes and inflammatory responses, including sphingolipid, tyrosine, phenylalanine, tryptophan, and lipid metabolism pathways. This finding implies a mechanistic role of metabolic and immune disturbances affects susceptibility to diclofenac-IDILI. Further nine metabolite biomarkers with potent diagnostic capabilities were identified using receiver operating characteristic curves. These findings elucidated the potential utility of metabolomic biomarkers to identify individuals susceptible to drug hepatotoxicity and the underlying mechanism of metabolic and immune disturbances occurring in IDILI.


2015 ◽  
Vol 54 (4) ◽  
pp. 395-399 ◽  
Author(s):  
Takao Watanabe ◽  
Masanori Abe ◽  
Fujimasa Tada ◽  
Kanako Aritomo ◽  
Hironori Ochi ◽  
...  

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.


Molecules ◽  
2019 ◽  
Vol 24 (12) ◽  
pp. 2256 ◽  
Author(s):  
Laura E. Ewing ◽  
Mitchell R. McGill ◽  
Eric U. Yee ◽  
Charles M. Quick ◽  
Charles M. Skinner ◽  
...  

The goal of this study was to investigate the potential for a cannabidiol-rich cannabis extract (CRCE) to interact with the most common over-the-counter drug and the major known cause of drug-induced liver injury–acetaminophen (APAP)–in aged female CD-1 mice. Gavaging mice with 116 mg/kg of cannabidiol (CBD) [mouse equivalent dose (MED) of 10 mg/kg of CBD] in CRCE delivered with sesame oil for three consecutive days followed by intraperitoneally (i.p.) acetaminophen (APAP) administration (400 mg/kg) on day 4 resulted in overt toxicity with 37.5% mortality. No mortality was observed in mice treated with 290 mg/kg of CBD+APAP (MED of 25 mg/kg of CBD) or APAP alone. Following CRCE/APAP co-administration, microscopic examination revealed a sinusoidal obstruction syndrome-like liver injury–the severity of which correlated with the degree of alterations in physiological and clinical biochemistry end points. Mechanistically, glutathione depletion and oxidative stress were observed between the APAP-only and co-administration groups, but co-administration resulted in much greater activation of c-Jun N-terminal kinase (JNK). Strikingly, these effects were not observed in mice gavaged with 290 mg/kg CBD in CRCE followed by APAP administration. These findings highlight the potential for CBD/drug interactions, and reveal an interesting paradoxical effect of CBD/APAP-induced hepatotoxicity.


Praxis ◽  
2010 ◽  
Vol 99 (21) ◽  
pp. 1259-1265 ◽  
Author(s):  
Bruggisser ◽  
Terraciano ◽  
Rätz Bravo ◽  
Haschke

Ein 71-jähriger Patient stellt sich mit Epistaxis und ikterischen Skleren auf der Notfallstation vor. Der Patient steht unter einer Therapie mit Phenprocoumon, Atorvastatin und Perindopril. Anamnestisch besteht ein langjähriger Alkoholabusus. Laborchemisch werden massiv erhöhte Leberwerte (ALAT, Bilirubin) gesehen. Der INR ist unter oraler Antikoagulation und bei akuter Leberinsuffizienz >12. Die weiterführenden Abklärungen schliessen eine Virushepatitis und eine Autoimmunhepatitis aus. Nachdem eine Leberbiopsie durchgeführt werden kann, wird eine medikamentös-toxische Hepatitis, ausgelöst durch die Komedikation von Atorvastatin, Phenprocoumon und Perindopril bei durch Alkohol bereits vorgeschädigter Leber diagnostiziert. Epidemiologie, Pathophysiologie und Klink der medikamentös induzierten Leberschäden (drug induced liver injury, DILI), speziell von Coumarinen, Statinen und ACE-Hemmern werden im Anschluss an den Fallbericht diskutiert.


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