Thyrotoxic hepatitis

2017 ◽  
Vol 63 (1) ◽  
pp. 46-50
Author(s):  
Dmitrij V. Pikulev ◽  
Aleksej V. Klemenov
Keyword(s):  
Liver Injury ◽  
Clinical Symptoms ◽  
Correct Diagnosis ◽  
Clinical Signs ◽  
Rare Condition ◽  
Liver Function Tests ◽  
Biliary Cirrhosis ◽  
Liver Pathology ◽  
Drug Induced ◽  
Clinical Variants

In most cases, liver pathology in hyperthyroidism is confined to asymptomatic changes in laboratory indices, while clinical signs are much rarer. Three clinical variants of liver pathology in patients with hyperthyroidism can be differentiated: drug-induced hepatitis that develop in response to administration of thyrostatic agents (mainly propylthiouracil); concomitant autoimmune liver diseases (autoimmune hepatitis, primary biliary cirrhosis), and hepatopathies as a direct manifestation of thyrotoxicosis (thyrotoxic hepatitis). Thyrotoxic hepatitis is a rare condition difficult to diagnose. The variety of etiological factor of liver pathology in hyperthyroidism, universal clinical symptoms, and the lack of specific histological markers make it difficult to make a correct diagnosis. A clinical case of Graves’ disease complicated with severe thyrotoxic hepatitis, the edema-ascites syndrome and hyperbilirubinemia is reported. The patient was diagnosed with thyrotoxic hepatitis after all other reasons for liver pathology have been ruled out. The concomitant thyrogenic myocardiodystrophy, cardiomegaly and atrial fibrillation required ruling out the diagnosis of cardiogenic liver injury and made diagnosing more difficult. Normalization of the thyroid status in patients receiving mercazolyl therapy was accompanied by alleviation of clinical symptoms of hepatitis and the positive dynamics of the indices of liver function tests. A brief review of the data on clinical variants and mechanisms of liver injury in patients with thyrotoxicosis is presented.

scholarly journals Drug-Induced Liver Injury Caused by Adalimumab: A Case Report and Review of the Bibliography

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Bernardo Frider ◽  
Andres Bruno ◽  
Marcelo Ponte ◽  
Marcelo Amante
Keyword(s):  
Liver Injury ◽  
Liver Biopsy ◽  
Clinical Symptoms ◽  
Liver Function Tests ◽  
Virus Genotype ◽  
Drug Induced ◽  
The Third ◽  
Interferon Alpha 2B ◽  
Metavir Score ◽  
Score Pattern

The most serious adverse drug reaction of adalimumab (ADR) is tuberculosis reactivation. We describe a case of a 35-year-old man, with rheumatoid arthritis (RA) and hepatitis C virus genotype 1a with a liver biopsy in 2001 with a METAVIR score pattern A1 F0; he received interferon alpha 2b for six months, but treatment was suspended because of reactivation of RA. Liver function tests after treatment were similar to previous ones showing a minimal cholestatic pattern. In 2008, methotrexate was prescribed, but the drug was withdrawn at the third month because of the appearance of pruritus and Ggt rise. Viral load at that moment was 9300000 UI/mL, log 6,9. The liver biopsy showed a Metavir Score A2 F1. Adalimumab was started in 2010, and at the third month of treatment, Ggt showed a rise of 23 times normal value (NV), alkaline phosphatase 2,5 times NV with AST and ALT with no change. A new liver biopsy showed portal inflammation with eosinophils and a METAVIR A1 F2. We think that adalimumab appears to be responsible for the liver injury, because of temporal relationship, liver biopsy findings, other clinical conditions being discarded, and the improvement of clinical symptoms and biochemical abnormalities when adalimumab was suspended.

A case of statin-induced liver injury with positive rechallenge with a second statin. Is there a class effect?

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Giovanna Onfiani ◽  
Fabio Nascimbeni ◽  
Francesca Carubbi
Keyword(s):  
Liver Injury ◽  
Clinical Symptoms ◽  
High Risk Population ◽  
Drug Induced ◽  
Case Presentation ◽  
Drug Induced Liver Injury ◽  
Aged Woman ◽  
Cardiovascular Morbidity And Mortality ◽  
Middle Aged Woman

Abstract Objectives Statins have proved to reduce cardiovascular morbidity and mortality in high-risk population and are generally well tolerated, although adverse events can occur. Up to 3% of patients develop aminotransferases elevation, which usually normalizes with continued treatment and hardly is associated with clinical symptoms. Serious statin-related liver injury is exceedingly rare. Furthermore, literature regarding rechallenge with a second statin is extremely poor. Some authors caution that re-exposure to these drugs is associated with a more serious liver injury but safe switching to a second statin after drug-induced liver injury (DILI) is also reported. Case presentation We describe a case of a middle-aged woman who developed hepatocellular liver injury after simvastatin dose escalation; a rechallenge with low dose rosuvastatin caused rapid recurrence of DILI. Conclusions In our opinion, clinicians should be very cautious upon rechallenge and closely follow-up patients who experienced statin-induced liver injury when trying re-exposure to another statin.

scholarly journals Chemotherapy induced liver toxicity in children with malignant diseases

2018 ◽  
Vol 91 (1) ◽  
pp. 37-41
Author(s):  
Horváth Adrienne ◽  
Papp Zsuzsanna Erzsébet
Keyword(s):  
Liver Injury ◽  
Maintenance Therapy ◽  
Esophageal Varices ◽  
Liver Toxicity ◽  
Lymphoblastic Leukemia ◽  
Treatment Options ◽  
Clinical Signs ◽  
Treatment Strategies ◽  
Malignant Diseases ◽  
Drug Induced

Abstract A broad spectrum of chemotherapy is being used in the therapy of childhood cancers, which may induce liver injury, impairing quality of life and efficacy of the treatment. History of, especially viral, liver diseases may increase toxicity. The aim of the paper is to assess the incidence, type and grade, predisposing factors and treatment options of drug-induced liver injury in children with malignant diseases under cytostatic therapy at the Hemato-Oncology Department of the Pediatric Clinic 2 from Targu-Mures, over a time period spanning from 2012 to 2017. The results of the study may serve as a foundation for such treatment strategies which would enable optimal outcomes with fewer cases of liver toxicity. During this period, we treated 26 patients with acute lymphoblastic leukemia (ALL), two patients with acute myeloblastic leukemia (AML), one patient with lymphoma and seven with solid tumors. We found liver toxicity in 77% of the patients treated for ALL, mainly during the maintenance therapy (65%) with oral 6-mercaptopurine and methotrexate. The most common clinical signs were anorexia, nausea, vomiting, abdominal pain and faltering weight gain. Cholestasis developed in two patients, while hepatocytolysis was the most common observed event (n = 24). Liver fibrosis, hypersplenism, portal hypertension and esophageal varices were found in two patients. One patient required endoscopic ligation of esophageal varices. Elevation of serum bilirubin appeared in two patients, while hypoproteinemia was observed in nine patients. None of the patients developed acute liver failure. We treated liver toxicity with hydration, alkalinization, i.v. Aspatofort, Aminosteril-N Hepa 8%, oral acetylcysteine, silymarin, ursodeoxycholic acid, Liv-52, Sargenor, and Essentiale forte. We found hepatotoxicity in 77% of the ALL patients undergoing chemotherapy, similar results have been published by other authors. Hepatotoxicity may develop through direct hepatic effects of cytostatics, or a preexisting liver disease impairs the metabolism and excretion of the drug, increasing its toxic effects. In our patients hepatotoxicity can be explained mainly by direct liver-injury, previous infections with hepatotropic viruses, such as cytomegalovirus, were detected only in three patients. Liver injury appeared in 77% of our ALL patients; 65% occurred during maintenance therapy with oral 6-mercaptopurine and methotrexate. Close followup of liver function during chemotherapy is mandatory for optimal results.

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
Keyword(s):  
Liver Injury ◽  
Liver Function ◽  
Liver Failure ◽  
Acute Liver Injury ◽  
Early Recognition ◽  
Antibiotic Use ◽  
Liver Function Tests ◽  
The United States ◽  
Drug Induced ◽  
Drug Induced Liver Injury

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.

scholarly journals Etiology and Outcome of Acute Liver Failure: Experience from a Liver Transplantation Centre in Montreal

2002 ◽  
Vol 16 (10) ◽  
pp. 672-676 ◽  
Author(s):  
Geneviève Tessier ◽  
Edith Villeneuve ◽  
Jean-Pierre Villeneuve
Keyword(s):  
Liver Transplantation ◽  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Rapid Development ◽  
Significant Proportion ◽  
Rare Condition ◽  
Unknown Origin ◽  
The United States ◽  
Drug Induced

BACKGROUND: Acute liver failure is a rare condition in which massive liver injury is associated with the rapid development of hepatic encephalopathy. Although viral hepatitis and drug-induced liver injury are the most common causes, no specific etiology is found in a substantial proportion of cases reported from Europe and the United States.AIM: To determine the etiology and outcome of patients with acute liver failure in the authors’ institution.PATIENTS AND METHODS: The charts of 81 consecutive patients admitted to Saint-Luc between 1991 and 1999 were reviewed.RESULTS: The etiology was viral in 27 cases (33.2%), toxic or drug-induced in 22 (27.2%), of unknown origin in 22 (27.2%) and due to various causes in 10 (12.3%) (autoimmune, vascular, cancer). Of the 81 patients, 16% survived without liver transplantation, and 84% died or underwent liver transplantation. Survival without liver transplantation differed according to the mode of presentation: the survival rate was 27% in patients with hyperacute liver failure, 7% in those with acute liver failure and 0% in those with subacute liver failure. Among the 38 patients who underwent liver transplantation, survival one year after transplantation was 71%. In the 30 patients who died without liver transplantation, the main causes of death were cerebral edema and sepsis.CONCLUSIONS: Acute liver failure is associated with a high mortality, and liver transplantation is the treatment of choice. In a significant proportion of cases, the etiology remains undetermined and is probably related to yet unidentified hepatotropic viruses.

Quercetin Modulates Nrf2 and NF-κB/TLR-4 Pathways to Protect against Isoniazid and Rifampicin Induced Hepatotoxicity in vivo

2021 ◽  
Author(s):  
Sukumaran Sanjay ◽  
Chandrashekaran Girish ◽  
Pampa Ch Toi ◽  
Zachariah Bobby
Keyword(s):  
Liver Injury ◽  
Liver Function Tests ◽  
Treated Group ◽  
Hepatic Necrosis ◽  
Drug Induced ◽  
Rifampicin Treatment ◽  
Nrf2 Activation ◽  
Ifn Γ ◽  
Endogenous Antioxidant

Isoniazid and rifampicin are crucial for treating tuberculosis (TB); however, they can cause severe hepatotoxicity leading to liver failure. Therapeutic options are limited and ineffective. We hypothesized that prophylaxis with quercetin attenuates isoniazid and rifampicin induced liver injury. We randomly divided Wistar rats into seven groups (n=6). The animals received isoniazid and rifampicin or were co-treated with quercetin or silymarin for 28 days. The protective effect of quercetin was assessed using liver function tests and liver histology. NRF2 and NF-κB pathways were explored to elucidate the mechanism of action. Quercetin co-administration prevented the elevation of ALT, AST, ALP and bilirubin compared to isoniazid and rifampicin treatment alone. In the histological analysis, we observed that quercetin prophylaxis lessened the severity of hepatic necrosis and inflammation compared to the anti-TB drug treated group. Quercetin attenuated anti-TB drug induced oxidative stress by increasing NRF2 activation and expression, boosting endogenous antioxidant levels. Additionally, quercetin blocked inflammatory mediators HMGB-1 and IFN-γ, inhibiting activation of the NF-κB/TLR-4 axis. Quercetin protects against anti-TB liver injury by activating NRF2 and blocking NF-κB/TLR-4.

Prednisolone: role in amoxicillin–clavulanate-induced cholestatic liver injury

2021 ◽  
Vol 14 (4) ◽  
pp. e239488
Author(s):  
Melvin Qiyu Lee ◽  
Royale Chigozie ◽  
Irfan Khan ◽  
Gerard O'Mara
Keyword(s):  
Liver Injury ◽  
Liver Function Tests ◽  
Hepatocellular Injury ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
The Us ◽  
Common Causes ◽  
Amoxicillin Clavulanate ◽  
The Common ◽  
Cholestatic Liver Injury

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.

scholarly journals Optimizing diagnostic approach to drug-induced liver injury

2018 ◽  
Vol 12 (3) ◽  
pp. 180-189 ◽  
Author(s):  
Maria Giovanna Minissale ◽  
Maurizio Soresi ◽  
Massimo Galia ◽  
Francesco Agnello ◽  
Lydia Giannitrapani ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Damage ◽  
Transient Elastography ◽  
Liver Stiffness ◽  
Abdominal Ultrasound ◽  
Liver Function Tests ◽  
Accurate Method ◽  
Focal Lesions ◽  
Drug Induced ◽  
Drug Induced Liver Injury

Drug-induced liver injury (DILI) is often a trial even to expert clinicians, because sometimes diagnosis is not easy to be made. Guidelines of the American College of Gastroenterology (ACG) yielded in 2014, help to better understand the problem. The diagnosis of DILI is made through a detailed evaluation of clinical, serological, radiological and histological aspects. Biochemical data include liver function tests that allow to assess the pattern of damage, such as hepatocellular, cholestatic and mixed liver injury; serological data include testing for major and possibly minor hepatotropic viruses, non-organ specific autoantibodies. Clinical scenario might include jaundice, nausea, vomiting and extra-hepatic manifestations such as fever, pruritus, rash and eosinophilia. Investigation of the potential culprit drugs should involve firstly the temporal relationship between intake of the medication and onset of symptoms, thus the improvement after drug withdrawal. Overall, to complete the diagnostic evaluation, an abdominal ultrasound can be performed, as well as measurement of liver stiffness by transient elastography, and finally liver biopsy, which still represents the most accurate method to definitely assess liver damage. Sometimes, in such cases, computed tomography scan and magnetic resonance could help in the diagnosis of cases presenting with focal lesions of the liver, with cholestatic-like disease or vascular alterations, such as veno-occlusive disease. DILI diagnostic criteria help clinicians thinking of liver injury induced by drug, excluding other causes of liver disease. According to severity of liver damage and type of drug, it is possible to carefully predict the patient’s outcome.

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