Drug-induced hepatotoxicity linked to zoledronic acid in the treatment of an elderly man with primary osteoporosis

2021 ◽  
Author(s):  
Wenjun Chen ◽  
Mingjin Zhu
Keyword(s):  
Zoledronic Acid ◽  
Primary Osteoporosis ◽  
Drug Induced

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 Zoledronic Acid Once-yearly: What Role in the Prevention of Non-vertebral Osteoporotic Fractures?

2010 ◽  
Vol 2 ◽  
pp. CMT.S4947
Author(s):  
Sheila Anne Doggrell
Keyword(s):  
Zoledronic Acid ◽  
Osteoporotic Fractures ◽  
Primary Osteoporosis ◽  
Mineral Density ◽  
Glucocorticoid Treatment ◽  
Oestrogen Treatment ◽  
Treatment Of Osteoporosis ◽  
Hormone Sensitive ◽  
Low Levels ◽  
Single Intravenous Administration

Osteoporosis is the most common bone disease. Low levels of oestrogens or testosterone are risk factors for primary osteoporosis. The most common cause of secondary osteoporosis is glucocorticoid treatment, but there are many other secondary causes of osteoporosis. Osteoporosis can be secondary to anti-oestrogen treatment for hormone-sensitive breast cancer and to androgen-deprivation therapy for prostate cancer. Zoledronic acid is the most potent bisphosphonate at inhibiting bone resorption. In osteoporosis, zoledronic acid increases bone mineral density for at least a year after a single intravenous administration. The efficacy and safety of extended release (once-yearly) zoledronic acid in the treatment of osteoporosis is reviewed.

scholarly journals ZOLEDRONIC ACID: A MISCHIEVOUS SUSPECT FOR LIVER INJURY

2016 ◽  
pp. 3 ◽  
Author(s):  
Rupam Gill ◽  
Balaji O. ◽  
Meena K. Kumari ◽  
Amberkar Mohan Babu V. ◽  
Karthik S. Udupa
Keyword(s):  
Zoledronic Acid ◽  
Liver Enzymes ◽  
Liver Function Tests ◽  
Assessment Method ◽  
Hepatic Damage ◽  
Drug Induced ◽  
Necrosis Factor Alpha ◽  
Radiographic Images ◽  
Factor Alpha ◽  
Necrosis Factor

<p>ABSTRACT<br />A 47-year-old male diagnosed as adenocarcinoma of the lung and received 8 cycles of chemotherapy comprising intravenous administration of<br />cisplatin 125 mg, pemetrexed 850 mg along with zoledronic acid 4 mg. After the completion of the 8<br /> cycle, the liver enzymes were found to be<br />markedly elevated, evincing zoledronic acid as the cause for hepatotoxicity. The case details were taken from the patient’s medical record along with<br />the biochemical test reports and radiographic images. The causal association was confirmed using Naranjo’s algorithm and Roussel Uclaf Causality<br />Assessment Method (RUCAM). After the uneventful chemotherapy, patient’s liver function tests (LFT) were abnormal. There was an elevation in the<br />aspartate aminotransferase, alanine transaminase, alkaline phosphatase, and direct bilirubin. The causal relationship was established using Naranjo’s<br />algorithm (score-6) and RUCAM (score-5), displayed a “probable” and “possible” association. Hartwig’s severity scale and Thornton’s preventability<br />scale displayed the adverse drug reaction to being moderately severe and not preventable, respectively. The zoledronic acid was stopped and never<br />readministered. The LFTs assumed normal after a span of 2 months. The mechanism underlying hepatotoxicity due to zoledronic acid remains elusive.<br />Zoledronic acid can induce acute phase response mediated by active production of interleukin-6, tumor necrosis factor alpha, and pro-inflammatory<br />cytokines from the T-cells and macrophages. Vigilant monitoring along with timely assessment and management can prevent the occurrence of<br />irreversible liver damage. Henceforth, we would like to report the rare incidence of drug induced hepatic damage due to zoledronic acid. Henceforth,<br />we would like to report the rare incidence of drug induced hepatic damage due to zoledronic acid.<br />Keywords: Bisphosphonate, Dechallenge, Hepatotoxicity, Rechallenge.<br />th</p>

Drug-induced dermatomyositis after zoledronic acid

2011 ◽  
Vol 53 (4) ◽  
pp. e73-e75 ◽  
Author(s):  
Philip L Tong ◽  
Lawrence L Yu ◽  
Jonathan J Chan
Keyword(s):  
Zoledronic Acid ◽  
Drug Induced

scholarly journals Effect of different hydration doses on renal function in patients with primary osteoporosis treated with zoledronic acid

Medicine ◽  
2020 ◽  
Vol 99 (25) ◽  
pp. e20831 ◽  
Author(s):  
Xin Dai ◽  
Yongtao Deng ◽  
Yetao Luo ◽  
Jianghong Xie ◽  
Houxun Ma
Keyword(s):  
Renal Function ◽  
Zoledronic Acid ◽  
Primary Osteoporosis

scholarly journals SAT0456 REAL-LIFE RISK OF FRACTURE AND TREATMENT PREVALENCE IN DRUG-INDUCED OSTEOPOROSIS IN ITALY USING A NEW ALGORITHM

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1185.1-1186
Author(s):  
G. Adami ◽  
A. Fassio ◽  
A. Giollo ◽  
G. Orsolini ◽  
O. Viapiana ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Zoledronic Acid ◽  
Fracture Risk ◽  
Hormone Therapy ◽  
Osteoporotic Fracture ◽  
Real Life ◽  
Drug Induced ◽  
Adjuvant Hormone Therapy ◽  
Risk Of Fracture ◽  
Increased Risk

Background:Glucocorticoid-induced osteoporosis and osteoporosis induced by adjuvant hormone therapy for breast cancer are the most common forms of secondary osteoporosis.Objectives:The exact real-life prevalence of treatment with anti-osteoporotic drugs in women with drug-induced osteoporosis is not known. In the present study, using a new mathematical and computerized algorithm, we investigate the profile of risk of fracture of women with drug-induced osteoporosis and the prevalence of treatment with anti-osteoporotic drugs.Methods:We have retrospectively analyzed the 10-year risk of major osteoporotic fracture calculated with the DeFRAcalc79 tool in postmenopausal women aged over 50 years that were initiating an anti-osteoporotic treatment (fully reimbursed according to the Nota 79). DeFRAcalc79 is a new web-based fracture risk-assessment tool (https://defra-osteoporosi.it) that arithmetically adjusts the risk based on multiple risk factors contemplated by the Nota 79, which regulates the reimbursability for osteoporosis medications in Italy (Italian Agency for Drugs, AIFA), including demographic and anthropometric data, femoral and/or lumbar spine BMD T-score, family history of femoral or vertebral fractures, number and site of previous osteoporotic fracture (including vertebral, femoral, and non-vertebral non-femoral fractures), glucocorticoid treatment (> 3 or > 12 months, ≥5 mg prednisone or equivalent), adjuvant hormone therapy for breast cancer, and comorbidities that induce an increased risk of fracture (rheumatoid arthritis and other connective tissue diseases, chronic obstructive pulmonary disease, inflammatory bowel diseases, Parkinson’s disease, multiple sclerosis, human immunodeficiency virus infection, diabetes, or severe physical handicap). This is a sub-analysis of the cross-sectional observational study to validate and further develop the DeFRA algorithm for the estimation of the risk of osteoporotic fractures, promoted by Verona hospital with the unconditional support of Amgen Srl.Results:Among 208 women, 116 (55.8%) were treated with adjuvant hormone therapy for breast cancer and 92 (44.2%) were on glucocorticoid ≥5 mg/day. Women on glucocorticoids had a greater mean 10-year risk of fracture compared to women on adjuvant hormone therapy for breast cancer (67.0% vs 39.1% p<0.01). 50.7% of women on adjuvant hormone therapy for breast cancer used denosumab, 28.0% zoledronic acid and 17.3% alendronate. In glucocorticoid-induced osteoporosis, 17.6% of the women used teriparatide, 37.3% alendronate, 29.4% zoledronic acid and 13.7% denosumab.Conclusion:In our cohort of patients, treatment with adjuvant hormone therapy for breast cancer was slightly more common than glucocorticoids. Women with glucocorticoid-induced osteoporosis had a greater risk of fracture compared to patients treated with adjuvant hormone therapy for breast cancer. Half of the patients on adjuvant hormone therapy for breast cancer were prescribed with denosumab. One-fifth of the patients with glucocorticoid-induced osteoporosis was treated with teriparatide. DeFRAcalc79 is a useful and practical tool for the integrated evaluation of fracture risk in drug-induced osteoporosis.Disclosure of Interests:Giovanni Adami: None declared, Angelo Fassio Speakers bureau: Angelo Fassio reports personal fees from: Abiogen and Novartis, outside the submitted work., Alessandro Giollo: None declared, Giovanni Orsolini: None declared, Ombretta Viapiana: None declared, Davide Gatti Speakers bureau: Davide Gatti reports personal fees from Abiogen, Amgen, Janssen-Cilag, Mundipharma, outside the submitted work., Maurizio Rossini Speakers bureau: AbbVie, Abiogen, Amgen, BMS, Eli-Lilly, Novartis, Pfizer, Sanofi, Sandoz and UCB

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

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