Hepatic Cirrhosis Caused by Low-Dose Oral Amiodarone Therapy

Puli, Srinivas R.; Fraley, Matthew A.; Puli, V; Kuperman, Aaron B.; Alpert, Martin A.

doi:10.1097/00000441-200511000-00012

Cited by 42 publications

(18 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the context of drug-induced steatohepatitis, fat accumulates usually as large vacuoles, although microvesicular steatosis can also be present in some hepatocytes. Inflammation and fibrosis can be of variable severity and occasionally cirrhosis occurs with drugs, such as amiodarone, perhexiline, and didanosine [116,149,[190][191][192]. Importantly, drug-induced steatohepatitis shares many pathological and clinical features with alcoholic steatohepatitis and nonalcoholic steatohepatitis (NASH).…”

Section: Mechanisms Involved In the Progression Of Steatosis Into Stementioning

confidence: 99%

Drug-induced toxicity on mitochondria and lipid metabolism: Mechanistic diversity and deleterious consequences for the liver

Begriche¹,

Massart²,

Robin³

et al. 2011

Journal of Hepatology

466

413

View full text Add to dashboard Cite

Numerous investigations have shown that mitochondrial dysfunction is a major mechanism of drug-induced liver injury, which involves the parent drug or a reactive metabolite generated through cytochromes P450. Depending of their nature and their severity, the mitochondrial alterations are able to induce mild to fulminant hepatic cytolysis and steatosis (lipid accumulation), which can have different clinical and pathological features. Microvesicular steatosis, a potentially severe liver lesion usually associated with liver failure and profound hypoglycemia, is due to a major inhibition of mitochondrial fatty acid oxidation (FAO). Macrovacuolar steatosis, a relatively benign liver lesion in the short term, can be induced not only by a moderate reduction of mitochondrial FAO but also by an increased hepatic de novo lipid synthesis and a decreased secretion of VLDL-associated triglycerides. Moreover, recent investigations suggest that some drugs could favor lipid deposition in the liver through primary alterations of white adipose tissue (WAT) homeostasis. If the treatment is not interrupted, steatosis can evolve toward steatohepatitis, which is characterized not only by lipid accumulation but also by necroinflammation and fibrosis. Although the mechanisms involved in this aggravation are not fully characterized, it appears that overproduction of reactive oxygen species by the damaged mitochondria could play a salient role. Numerous factors could favor drug-induced mitochondrial and metabolic toxicity, such as the structure of the parent molecule, genetic predispositions (in particular those involving mitochondrial enzymes), alcohol intoxication, hepatitis virus C infection, and obesity. In obese and diabetic patients, some drugs may induce acute liver injury more frequently while others may worsen the pre-existent steatosis (or steatohepatitis).

show abstract

Section: Mechanisms Involved In the Progression Of Steatosis Into Stementioning

confidence: 99%

Drug-induced toxicity on mitochondria and lipid metabolism: Mechanistic diversity and deleterious consequences for the liver

Begriche¹,

Massart²,

Robin³

et al. 2011

Journal of Hepatology

466

413

View full text Add to dashboard Cite

show abstract

“…The cases associated with these circumstances are usually fulminant hepatitis or cirrhotic liver disease, respectively. There has, however, been one recorded case of a patient receiving lowdose amiodarone therapy for a period of 22.5 months who presented with ascites and micronodular cirrhosis (10). Our patient received the standard loading dose and was maintained on low-dose therapy for a period of 18 months without medical follow-up.…”

Section: Discussionmentioning

confidence: 83%

Hepatic Dysfunction and Neurotoxicity in a Patient Receiving Long-Term Low-Dose Amiodarone Therapy

Arkun

Deusen

Grau

et al. 2010

The Journal of Emergency Medicine

View full text Add to dashboard Cite

“…Asymptomatic elevation of serum aminotransferases occurs in 25% of those patients who are treated with amiodarone. Micronodular cirrhosis that was clearly due to amiodarone therapy has been confirmed in 12 cases [2] . However, the prevalence of severe liver injury has been estimated at only 1% to 3% [3] .…”

Section: Introductionmentioning

confidence: 91%

Acute hepatitis secondary to parenteral amiodarone does not preclude subsequent oral therapy

Lahbabi

Aqodad²,

Ibrahimi³

et al. 2012

WJH

View full text Add to dashboard Cite

Amiodarone chlorhydrate is a diiodated benzofuran derivative used to treat cardiac rhythm abnormalities�� Hepatotoxicity is a relatively uncommon side effect of amiodarone and symptomatic hepatic dysfunction occurs in less than 1% to 3% of patients taking amiodarone�� We report here on an unusual case of amiodarone-induced hepatotoxicity�� A 29 year old woman with normal liver function was given amiodarone intravenously to treat her atrial fibrillation. She developed acute toxic hepatitis after 24 h�� The intravenous form of amiodarone was immediately avoided and replaced by the oral form, using conventional loading doses as soon as the deranged liver function tests had normalized, without recurrence of the hepatitis�� These observations show that the occurrence of acute hepatic impairment with intravenous amiodarone does not necessarily preclude the use of this drug by mouth and the necessity of monitoring the hepatic function of patients treated with amiodarone��

show abstract

Hepatic Cirrhosis Caused by Low-Dose Oral Amiodarone Therapy

Cited by 42 publications

References 14 publications

Drug-induced toxicity on mitochondria and lipid metabolism: Mechanistic diversity and deleterious consequences for the liver

Drug-induced toxicity on mitochondria and lipid metabolism: Mechanistic diversity and deleterious consequences for the liver

Hepatic Dysfunction and Neurotoxicity in a Patient Receiving Long-Term Low-Dose Amiodarone Therapy

Acute hepatitis secondary to parenteral amiodarone does not preclude subsequent oral therapy

Contact Info

Product

Resources

About