Tolterodine-Associated Acute Mixed Liver Injury

2002 ◽  
Vol 36 (5) ◽  
pp. 817-819 ◽  
Author(s):  
Raymond G Schlienger ◽  
Martin J Keller ◽  
Stephan Krähenbühl
Keyword(s):  
Liver Injury ◽  
White Woman ◽  
Hypersensitivity Syndrome ◽  
Eye Drops ◽  
Laboratory Examination ◽  
Internal Organs ◽  
Drug Induced ◽  
Case Summary ◽  
First Case ◽  
Close Temporal Relationship

OBJECTIVE: To report a patient with an acute mixed liver injury associated with tolterodine therapy. CASE SUMMARY: An 81-year-old white woman with urge incontinence experienced malaise, fever, and gastrointestinal disturbances 18 days after starting tolterodine 2 mg twice daily. The patient's concurrent medications included flunitrazepam, diclofenac, and dorzolamide/timolol eye drops. Laboratory examination was consistent with the presentation of an acute mixed liver injury with increased transaminase enzymes, alkaline phosphatase, λ-glutamyltransferase, and bilirubin. Additionally, she had mild leukocytosis with eosinophilia. After tolterodine was discontinued, the abnormal liver and hematologic parameters returned to normal within 4 weeks. DISCUSSION: Tolterodine, a muscarinic receptor antagonist, has predominantly anticholinergic effects. To our knowledge, this is the first case published describing tolterodine-associated acute mixed liver injury. However, some of the patient's additional symptoms can also be considered part of a drug-induced hypersensitivity syndrome. This is usually defined by the triad of fever, cutaneous reaction, and involvement of internal organs, mainly affecting the liver. The close temporal relationship between the start of tolterodine therapy and the first symptoms and the reversibility after dechallenge led us to conclude that the adverse reaction was possibly related to tolterodine exposure. CONCLUSIONS: Our case illustrates that tolterodine may rarely be associated with liver injury. This may have been an organ manifestation of tolterodine-induced hypersensitivity syndrome.

scholarly journals Drug-Induced Autoimmune Hepatitis following Treatment with Zoledronic Acid

2017 ◽  
Vol 11 (2) ◽  
pp. 440-445 ◽  
Author(s):  
Jenny Sarah Schneider ◽  
Matteo Montani ◽  
Felix Stickel
Keyword(s):  
Liver Disease ◽  
Zoledronic Acid ◽  
Side Effects ◽  
Liver Injury ◽  
Drug Reactions ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
First Case ◽  
Alternative Drugs

Adverse drug reactions are among the most frequent side effects of synthetic and complementary alternative drugs and represent the premier causes of license revocations and acute liver failure. Drug-induced liver injury can resemble literally any other genuine liver disease and usually responds well to drug dechallenge. However, in some cases autoimmune-like hepatitis can evolve, requiring short- and sometimes long-term immunosuppression. Here, we present the hitherto first case of autoimmune-like hepatitis following treatment with zoledronic acid.

scholarly journals Menotrophin Induced Autoimmune Hepatitis

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Shurouq H. Alqrinawi ◽  
Nuralhuda Akbar ◽  
Hind AlFaddag ◽  
Shahrazad Akbar ◽  
Lujayn Akbar ◽  
...  
Keyword(s):  
Liver Injury ◽  
Autoimmune Hepatitis ◽  
Plasma Cells ◽  
Caucasian Woman ◽  
Drug Induced ◽  
Over The Counter ◽  
Drug Induced Liver Injury ◽  
First Case ◽  
Igg Level ◽  
New Onset

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.

scholarly journals Severe Drug-Induced Liver Injury from Combination Encorafenib/Binimetinib

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Nicholas Gravbrot ◽  
Srinath Sundararajan
Keyword(s):  
Liver Injury ◽  
Liver Function ◽  
Combination Therapy ◽  
Hepatic Injury ◽  
Mek Inhibitor ◽  
New Combination ◽  
Normal Range ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
First Case

Encorafenib/binimetinib is a new combination BRAF/MEK inhibitor used in the treatment of advanced or metastatic BRAFV600-mutant melanoma. Though generally tolerated well, mild to moderate aminotransferase elevations are common. However, significant liver injury has not been demonstrated in the literature. Here, we report the first case of severe hepatic injury associated with encorafenib/binimetinib in a 58-year-old gentleman requiring admission and extensive workup. He was successfully treated by withdrawing the combination therapy, and liver function returned to normal range.

scholarly journals Drug-induced hypersensitivity syndrome caused by minodronic acid hydrate

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yutaka Muto ◽  
Naoyuki Kuse ◽  
Minoru Inomata ◽  
Nobuyasu Awano ◽  
Mari Tone ◽  
...  
Keyword(s):  
Clinical Symptoms ◽  
Laboratory Data ◽  
Human Herpesvirus ◽  
Hypersensitivity Syndrome ◽  
Ground Glass ◽  
Lymphocyte Stimulation Test ◽  
Drug Induced ◽  
First Case ◽  
Minodronic Acid ◽  
Acid Hydrate

Abstract Background Drug-induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is an important adverse reaction caused by a few drugs. Reactivation of human herpesvirus 6 (HHV-6) is known to be associated with its pathogenesis. DIHS occasionally manifests as pulmonary lesions with a variety of imaging findings. Case presentation An 83-year-old woman started taking minodronic acid hydrate 5 years before admission. She noticed a generalized skin rash 44 days before admission and started oral betamethasone-d-chlorpheniramine maleate combination tablets for allergic dermatitis. She developed a fever and cough in addition to the rash, and was referred to our hospital. Laboratory data showed a high level of eosinophils and liver and biliary enzymes. Computed tomography (CT) studies revealed bilateral diffuse ground-glass opacities with ill-defined centrilobular nodules from the central to peripheral regions of the lungs. Transbronchial lung cryobiopsy specimens showed that lymphocyte infiltration was observed in the alveolar walls and fibrinous exudates and floating macrophages in the alveolar lumina. Immunohistochemistry of biopsy specimens showed more CD4+ lymphocytes than CD8+ lymphocytes, while few Foxp3+ lymphocytes were recognized. The serum anti-HHV-6 immunoglobulin G titer increased at 3 weeks after the first test. Based on these findings, we diagnosed her with DIHS. We continued care without using corticosteroids since there was no worsening of breathing or skin condition. Eventually, her clinical symptoms chest CT had improved. Minodronic acid hydrate was identified as the culprit drug based on the positive results of the patch test and drug-induced lymphocyte stimulation test. Conclusions We described the first case of DIHS caused by minodronic acid hydrate. Lung lesions in DIHS can present with bilateral diffuse ground-glass opacities and ill-defined centrilobular nodules on a CT scan during the recovery phase. Clinicians should be aware of DIHS, even if patients are not involved with typical DIHS/DRESS-causing drugs.

Phenazopyridine-Induced Sulfhemoglobinemia

2005 ◽  
Vol 39 (6) ◽  
pp. 1128-1130 ◽  
Author(s):  
Anuradha S Gopalachar ◽  
Venita L Bowie ◽  
Parag Bharadwaj
Keyword(s):  
Emergency Department ◽  
Methylene Blue ◽  
Urinary Tract Infection ◽  
White Woman ◽  
Probability Scale ◽  
Drug Induced ◽  
Over The Counter ◽  
Case Summary ◽  
Counter Medication ◽  
Bluish Discoloration

OBJECTIVE: To report a case of sulfhemoglobinemia in a patient receiving phenazopyridine for a urinary tract infection. CASE SUMMARY: A 63-year-old white woman presented to the emergency department with complaints of fatigue and bluish discoloration of her body that had gradually progressed over the previous 6–8 weeks. About 4 months prior to presenting to the emergency department, she had started taking phenazopyridine, an over-the-counter medication for symptoms of dysuria. Because the cyanosis did not improve after the patient received oxygen and methylene blue, sulfhemoglobinemia was suspected and confirmed by spectrophotometer analysis. DISCUSSION: Sulfhemoglobin is a green-pigmented molecule containing a sulfur atom in one or more of the porphyrin rings. It is a rare cause of cyanosis, which is usually drug induced. Sulfhemoglobinemia is suspected when a cyanotic patient has normal to near-normal oxygen tension, laboratory reports of elevated methemoglobin, and does not respond to methylene blue therapy. Sulfhemoglobinemia is relatively rare, despite the widespread use of drugs that have been reported to cause it. Predisposing factors, such as chronic constipation, present in our patient, have been suggested as a source of hydrogen sulfide. CONCLUSIONS: This case of sulfhemoglobinemia, which occurred after the patient took phenazopyridine, is considered a probable adverse event according to the Naranjo probability scale.

scholarly journals Zanubrutinib-induced liver injury: a case report and literature review

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Edmond Atallah ◽  
Pramudi Wijayasiri ◽  
Nicole Cianci ◽  
Khorrum Abdullah ◽  
Abhik Mukherjee ◽  
...  
Keyword(s):  
Liver Injury ◽  
Kinase Inhibitor ◽  
Liver Toxicity ◽  
Causality Assessment ◽  
Hepatocellular Injury ◽  
Severe Liver ◽  
Drug Induced ◽  
Blood Profile ◽  
First Case ◽  
Clinical Awareness

Abstract Background Zanubrutinib is a Bruton’s tyrosine kinase inhibitor that has been recently licensed in refractory mantle cell lymphoma and under assessment in phase 3 clinical trials for other B cell malignancies. To date, there are no reported cases of hepatotoxicity secondary to zanubrutinib. We report the first case of severe liver injury due to zanubrutinib. Case presentation A 56-year-old Caucasian male with a history of relapsed lymphoplasmacytic lymphoma was admitted to the hospital with new-onset jaundice, choluria, and pruritus for 10 days. He had been on zanubrutinib as part of a clinical trial for 30 months. His blood profile showed a severe hepatocellular injury with jaundice (alanine transaminase 2474 IU/L and total bilirubin 141 umol/L with mild coagulopathy). He had an extensive work-up including virology, autoimmune, and metabolic profiles in addition to abdominal ultrasound with no alternative explanation found for his liver injury. Zanubrutinib-induced liver injury was suspected, and causality assessment by the updated Roussel Uclaf Causality Assessment Method score showed a probable causal relationship with zanubrutinib. His liver histology was also consistent with drug-induced liver injury. His liver biochemistry improved following cessation of zanubrutinib and normalised after 8 weeks. Conclusion We report the first case of severe liver injury secondary to zanubrutinib after 30 months of treatment. This case raises clinical awareness regarding zanubrutinib-induced liver toxicity and the importance of drug withdrawal in the event of liver injury.

Pancreatic Insufficiency Due to Antituberculous Therapy

1997 ◽  
Vol 31 (6) ◽  
pp. 724-726 ◽  
Author(s):  
Barbara A Liu ◽  
Sandra R Knowles ◽  
Lawrence B Cohen ◽  
Marsha R Werb ◽  
Neil H Shear
Keyword(s):  
Acute Pancreatitis ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Hypersensitivity Syndrome ◽  
Secretin Test ◽  
Antituberculous Therapy ◽  
Drug Induced ◽  
Enzyme Replacement ◽  
Case Summary

OBJECTIVE: To describe a case of chronic pancreatic insufficiency related to antituberculous therapy. CASE SUMMARY: A 57-year-old man developed rash, fever, and hepatitis (aspartate aminotransferase 369 IU/L, alanine aminotransferase 506 IU/L), 6 weeks after starting isoniazid, rifampin, ethambutol, and pyrazinamide. He also developed severe metabolic acidosis secondary to diabetic ketoacidosis and lactic acidosis (serum bicarbonate 7 mEq/L, glucose 1778 mg/dL, and lactate 4.0 mEq/L). Acute pancreatitis was diagnosed on the basis of a mildly elevated amylase concentration (392 U/L) and radiologic evidence of pancreatic inflammation. He developed pancreatic insufficiency with steatorrhea and an abnormal secretin test. He continues to require pancreatic enzyme replacement and insulin therapy. Rechallenge was not performed. DISCUSSION: Hypersensitivity syndromes have been reported for various drug therapies, including antituberculous agents. Hypersensitivity syndrome reactions are characterized by fever, rash, and internal organ involvement. Rifampin has been reported to cause acute pancreatitis in up to 2.7% of patients. Drug-induced chronic pancreatitis, however, is reported to be extremely rare. This is the first reported case of chronic pancreatic insufficiency occurring in the setting of a hypersensitivity syndrome reaction to antituberculous drugs. CONCLUSIONS: Chronic pancreatic insufficiency should be considered as a possible long-term sequelae of a hypersensitivity syndrome reaction to antituberculous therapy.

Severe Vaginal Bleeding Associated with Recombinant Interferon Beta-1B

1997 ◽  
Vol 31 (1) ◽  
pp. 50-52 ◽  
Author(s):  
Leslie A Pakulski ◽  
Linda M DiMarco
Keyword(s):  
Blood Cells ◽  
White Woman ◽  
Vaginal Bleeding ◽  
Interferon Beta ◽  
Stable Condition ◽  
Menstrual Disorders ◽  
Recombinant Interferon ◽  
Packed Red Blood Cells ◽  
Case Summary ◽  
First Case

OBJECTIVE: To report a case of severe vaginal bleeding associated with interferon beta-1b (IFN-β). CASE SUMMARY: A 19-year-old white woman diagnosed with multiple sclerosis was treated with IFN-β 4 million IU every other day for 1 month. After 1 month, the dosage was increased to 8 million IU. The patient subsequently experienced severe vaginal bleeding. Because her hemoglobin was 3.9 g/dL, she was admitted to the hospital for treatment and observation. IFN-β was discontinued and she was treated with conjugated estrogens and received 2 units of packed red blood cells. The bleeding ceased and the patient was discharged in stable condition. DISCUSSION: Menstrual disorders of mild-to-moderate severity were reported during clinical trials with IFN-β. This is the first case report regarding severe vaginal bleeding probably associated with IFN-β. The mechanism for development of IFN-β-reiated menstrual disorders is unknown. CONCLUSIONS: Reports of menstrual disorders associated with recombinant IFN-β are rare; however, clinicians should be aware that this complication can occur. Should menstrual disorders occur with no other etiologic factors identified, IFN-β should be discontinued, with improvement expected shortly thereafter.

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