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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-.

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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].

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Thalidomide

Last Update: April 10, 2019.

OVERVIEW

Introduction

Thalidomide and its analogue lenalidomide are immunomodulatory and antineoplastic agents that are used in the therapy of multiple myeloma. Both agents are associated with a low rate of serum aminotransferase elevations during therapy and both have been implicated in causing rare instances of clinically apparent liver injury which can be severe.

Background

Thalidomide (tha lid' oh mide) is a glutamic acid derivative that was introduced in Europe as a sedative in the late 1950s and subsequently withdrawn in 1961 when it was shown to be teratogenic, causing severe infant limb defects (phocomelia) when given to pregnant women. Several decades later, thalidomide was found to have potent activity in erythema nodosum leprosum, and subsequent studies found it beneficial in several autoimmune conditions and cancers. Thalidomide has immunomodulatory, antiinflammatory, antiangiogenic and anticancer properties that underlie its effects in inflammatory and malignant diseases. Thalidomide was approved for therapy of erythema nodosum leprosum (ENL) in the United States in 1998 and was subsequently approved for use in multiple myeloma (in combination with dexamethasone) in 2006. Lenalidomide (len" a lid' oh mide) is a thalidomide derivative that was found to be more potent as an antineoplastic agent, and was approved for use in selected myelodysplastic syndromes in 2005 and for multiple myeloma (combined with dexamethasone) in 2006. Thalidomide has also been used on an experimental basis for graft vs host disease, Kaposi sarcoma, AIDS associated wasting syndrome and several forms of autoimmune disease. Thalidomide is available in capsules of 50, 100, 150 and 200 mg under the brand name Thalomid, and lenalidomide in capsules of 2.5, 5, 10, 15, 20 and 25 mg under the brand name Revlimid. The recommended doses vary by indication, and their use is restricted because of their proven teratogenicity. Side effects of thalidomide and lenalidomide are common and include sedation, dizziness, orthostatic hypotension, neutropenia, peripheral neuropathy, and venous thromboembolism (for which reason they are often given with anticoagulation).

Hepatotoxicity

Serum enzyme elevations occur in 8% to 15% of patients taking thalidomide or lenalidomide and are more frequent with higher doses. The enzyme abnormalities are usually mild and self-limited, and only rarely require drug discontinuation. In addition, both thalidomide and lenalidomide have been implicated in rare instances of clinically apparent, acute liver injury which can be severe and has led to deaths from acute liver failure. The onset of injury is typically within 1 to 8 weeks of starting therapy. The pattern of serum enzyme elevation at the time of presentation can be either hepatocellular or cholestatic; however, the injury tends to be cholestatic and can be prolonged. Immunoallergic and autoimmune features are not common. Several instances of acute liver injury associated with thalidomide and lenalidomide therapy have occurred in patients with other apparent causes of liver disease or with preexisting chronic hepatitis B or C. If performed during the acute injury, liver biopsy shows hepatocellular necrosis and inflammatory cell infiltration, consistent with acute drug induced injury. In some instances there is bile duct injury and loss resulting in progressive cholestatic liver injury suggestive of vanishing bile duct syndrome.

Likelihood score: B (well known but rare cause of clinically apparent liver injury).

Mechanism of Injury

The mechanism of thalidomide and lenalidomide hepatotoxicity is not clear, but it may be related to their activity in reducing TNF-α production, a potent inflammatory cytokine that activates T cells and promotes inflammation, but is also necessary for normal liver regeneration. Several of the reported cases of hepatotoxicity have occurred in patients with underlying chronic liver disease (hepatitis B, C or nonalcoholic fatty liver), and another possibility is that thalidomide or lenalidomide may worsen preexisting hepatic conditions.

Outcome and Management

The severity of thalidomide and lenalidomide induced liver injury ranges from transient, asymptomatic elevations in serum enzymes to acute liver injury with jaundice to severe acute liver failure and death. The liver injury usually starts to resolve within a week of stopping the medication, but prolonged jaundice with bile duct injury and possible vanishing bile duct syndrome have also been reported. Rechallenge should be reserved for cases of mild liver injury in which the agent is considered very necessary and done with caution and careful monitoring. Nevertheless, instances of reinitiation of therapy without subsequent recurrence of liver injury have been reported.

Drug Class: Antineoplastic Agents, Miscellaneous

Other Related Drugs: Pomalidomide

CASE REPORT

Case 1. Acute hepatitis due to thalidomide.

[Modified from: Hanje AJ, Shamp JL, Thomas FB, Meis GM. Thalidomide-induced severe hepatotoxicity. Pharmacotherapy 2006; 26: 1018-22. PubMed Citation].

A 76 year old woman with multiple myeloma developed jaundice 5 weeks after starting thalidomide combined with warfarin and intermittent dexamethasone. She had no previous history of liver disease or risk factors for viral hepatitis. She did not drink alcohol. Her only other medications were metoprolol and furosemide for hypertension and insulin for diabetes. Routine liver tests had been normal in the past. Routine monitoring of serum enzymes demonstrated rises in ALT and AST after 4 weeks of treatment. Thalidomide was continued, and one week later she developed nausea, fatigue, abdominal discomfort and jaundice. On physical examination, she was jaundiced but had no fever, rash or signs of chronic liver disease. Laboratory tests showed bilirubin 5.6 mg/dL, ALT 2206 U/L, and international normalized ratio (INR) of greater than 15. She was admitted to the hospital for management and both thalidomide and the warfarin were stopped. Tests for hepatitis A, B and C were negative as were autoantibodies. Imaging of the liver showed evidence of diffuse fatty liver, but no masses or biliary obstruction. She was treated with fresh frozen plasma to correct the INR and underwent transjugular liver biopsy which was interpreted as compatible with acute drug induced liver injury superimposed upon an underlying nonalcoholic steatohepatitis. After thalidomide was stopped, she began to improve rapidly (Table). She was discharged after a week in the hospital and, when seen three months later, her liver tests were normal.

Key Points

Medication:Thalidomide
Pattern:Hepatocellular (R value could not be determined)
Severity:3+ (jaundice and hospitalization)
Latency:4 to 5 weeks
Recovery:Complete within 30 days
Other medications:Furosemide, metoprolol, insulin, warfarin, dexamethasone

Laboratory Values

Time After StartingTime After StoppingALT*
(U/L)
Alk P*
(U/L)
Bilirubin* (mg/dL)Other
PreNormal
4 weeks218179
5 weeks0220523765.6INR >15, admission
1 day22502425Thalidomide stopped
4 days15001050
6 weeks12 days165865.5INR 1.1: Discharged
4 months3 monthsNormalNormalNormalOutpatient follow up
Normal Values<34<35<1.2

* Some values estimated from Figure 1.

Comment

This woman developed jaundice within 5 weeks of starting an experimental regimen of cancer chemotherapy including thalidomide, warfarin and dexamethasone. Typical of thalidomide hepatotoxicity was the latency to onset (1 to 3 months), the hepatocellular pattern of injury (although no alkaline phosphatase values were provided in this case), the presence of an underlying liver disease, and the rapid improvement with stopping the medication.

PRODUCT INFORMATION

REPRESENTATIVE TRADE NAMES

Thalidomide – Thalidomid®

Lenalidomide – Revlimid®

DRUG CLASS

Antineoplastic Agents

COMPLETE LABELING

Product labeling at DailyMed, National Library of Medicine, NIH

CHEMICAL FORMULAS AND STRUCTURES

DRUGCAS REGISTRY NUMBERMOLECULAR FORMULASTRUCTURE
Thalidomide50-35-1C13-H10-N2-O4
Thalidomide Chemical Structure
Pomalidomide19171-19-8C13-H11-N3-O4
Image clip_image002_006.jpg
Lenalidomide191732-72-6C13-H13-N3-O3
Lenalidomide Chemical Structure

ANNOTATED BIBLIOGRAPHY

References updated: 10 April 2019

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  • Bonkovsky HL, Kleiner DE, Gu J, Odin JA, Russo MW, Navarro VM, Fontana RJ, et al.; U.S. Drug Induced Liver Injury Network Investigators. Clinical presentations and outcomes of bile duct loss caused by drugs and herbal and dietary supplements. Hepatology 2017; 65: 1267-77. [PMC free article: PMC5360519] [PubMed: 27981596]
    (Among 363 patients with drug induced liver injury who underwent liver biopsy, 26 [7%] had bile duct loss, including 1 case attributed to lenalidomide and 1 to thalidomide both marked by severe, and relentlessly progressive cholestatic liver injury resulting in death from liver failure within 3 months of onset).

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