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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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Quinidine

Last Update: May 10, 2018.

OVERVIEW

Introduction

Quinidine is a natural cinchona alkaloid which has potent antiarrhythmic activity and has been used for decades in the treatment of atrial and ventricular arrhythmias. Quinidine has been associated with fever, mild jaundice and clinically apparent liver injury in up to 2% of treated patients.

Background

Quinidine (kwin' i deen) and its stereoisomer quinine (kwye' nine) are natural cinchona alkaloids found in the powdered bark of the American cinchona tree. The bark powder was used for centuries in the prevention and therapy of malaria, but was also known to decrease heart palpitations. Quinidine was found to be the most potent of the antiarrhythmic substances extracted from the cinchona plant and was introduced into medical practice in the 1940s. Quinidine acts by depressing action potentials and is considered a myocardial depressant. It was formally approved for use in the United States in 1950 and was widely used to treat ventricular arrhythmias and to suppress the frequency of premature ventricular contractions. However, careful prospective studies demonstrated that suppression of ventricular arrhythmias can be associated with a decrease in survival and use of quinidine has fallen out of favor and now used largely for therapy of atrial flutter or fibrillation. Quinidine is also approved for intravenous use in treatment of life threatening Plasmodium falciparum malaria. Quinidine is available in multiple generic forms in tablets of 200 and 300 mg as well as in sustained release formulations and as a solution for intravenous administration. A typical maintenance dose of standard formulations in adults is 200 to 400 mg three to four times daily. Common side effects include dizziness, headache, tinnitus, blurred vision, gastrointestinal upset, diarrhea, nausea and skin rash.

Hepatotoxicity

Chronic therapy with quinidine is associated with a low rate of serum enzyme elevations, which are usually mild, asymptomatic and self limited even without alteration in dose. In addition, there have been many reports of acute hypersensitivity reactions to quinidine that include hepatic involvement. The reactions usually arise after 1 to 2 weeks of therapy, but can appear within 24 hours of restarting quinidine or with rechallenge. The clinical features are marked by fatigue, nausea, vomiting, diffuse muscle aches, arthralgias and high fever. Blood testing at an early stage shows increases in serum aminotransferase and alkaline phosphatase levels as well as mild jaundice, which can deepen for a few days even after stopping quinidine. The pattern of serum enzymes elevations is typically cholestatic or mixed. Rash is uncommon and eosinophilia is not typical, despite the presence of other signs of hypersensitivity (fever, arthralgias). Autoantibodies are not typically found. Liver biopsies usually show mild injury and small epithelioid granulomas, as are often found in many organs during systemic hypersensitivity reactions. A similar clinical signature of liver injury occurs with quinine, an optical isomer of quinidine that is used predominantly as an antimalarial agent. In recent years, there have been few reports of liver injury attributed to quinidine, probably because it is now rarely used.

Likelihood score: A (well established cause of clinically apparent liver injury).

Mechanism of Injury

The hepatotoxicity of quinidine is clearly due to a hypersensitivity reaction and there is no evidence for a direct hepatotoxic effect of the drug. There is likely to be a genetic predisposition to this hypersensitivity.

Outcome and Management

The hepatotoxicity of quinidine is clearly a part of a hypersensitivity reaction and is usually mild, resolving within 1 to 4 weeks of stopping. In many instances, jaundice and liver test abnormalities may worsen for a few days after stopping, but fatalities have not been reported and recovery is usually rapid. Because of the rapidity of recovery, therapy with corticosteroids is usually best avoided. There is cross reactivity to quinine (the optical isomer of quinidine which is used as an antimalarial agent) and other exposures to quinidine should be avoided.

Drug Class: Antiarrhythmic Agents

See also: Quinine

CASE REPORT

Case 1. Acute hypersensitivity and cholestatic liver injury due to quinidine.

[Modified from: Koch MJ, Seeff LB, Crumley CE, Rabin L, Burns WA. Quinidine hepatitis: a report of a case and review of the literature. Gastroenterology 1976; 70: 1136-40. PubMed Citation]

A 47 year old man developed nausea, fever and right upper quadrant pain 10 days after starting quinidine for supraventricular tachycardias. He had a history of cardiac disease and was treated with furosemide, digoxin and nitroglycerin tablets chronically. He had no history of liver disease, alcohol abuse, risk factors for liver hepatitis or previous history of drug-allergies. Physical examination revealed a temperature of 101.6 oF, but normal white blood cell count and differential. Quinidine was continued and he continued to have fever. While serum bilirubin levels remained normal, ALT, AST and alkaline phosphatase levels were elevated starting a few days after the onset of fever (Table). Oral and intravenous cholangiograms were negative as were tests for hepatitis B. A liver biopsy was done which showed centrizonal hepatocellular necrosis and inflammation with prominent eosinophils suggestive of drug induced liver injury. Quinidine was stopped and the fevers and liver test abnormalities rapidly resolved. Because of recurrent arrhythmias despite use of procainamide, the patient was readmitted for a monitored rechallenge with quinidine. A day after taking four doses of quinidine (200 mg every 6 hours), he developed nausea and fever. Serum ALT levels rose from 18 to 52 U/L, while eosinophil counts, alkaline phosphatase levels and bilirubin values remained normal. Symptoms and ALT elevations resolved within two days.

Key Points

Medication:Quinidine (200 mg every 6 hours)
Pattern:Cholestatic-mixed-hepatocellular (R=1.4→12.0)
Severity:1+ (symptoms and enzyme elevations without jaundice)
Latency:10 days to symptoms
Recovery:1-2 weeks
Other medications:Digoxin, furosemide, nitroglycerin

Laboratory Values

Days After StartingDays After StoppingALT* (U/L)Alk P* (U/L)Bilirubin* (mg/dL)Other
Pre26810.4Admission
1004090NormalFever and nausea
140110225
200150150
240370100Liver biopsy
300680190NormalQuinidine stopped
322925170
366345
388270110
Two months later rechallenged with quinidine 200 mg every 6 hours
1011
2118
3252NormalNormalFever and nausea
5420
Normal Values <40 <103 <1.2

* Some values estimated from Figure 1.

Comment

This patient developed signs of hypersensitivity to quinidine (fever) which resolved rapidly with stopping therapy. With continuation of the medication, liver test abnormalities arose that were initially cholestatic but eventually hepatocellular. The injury was mild in that there was no jaundice or hepatic synthetic dysfunction. Reexposure led to a more rapid onset of symptoms and liver test abnormalities, but they were still mild and rapidly reversible.

PRODUCT INFORMATION

REPRESENTATIVE TRADE NAMES

Quinidine – Generic

DRUG CLASS

Antiarrhythmic Agents

COMPLETE LABELING

Product labeling at DailyMed, National Library of Medicine, NIH

CHEMICAL FORMULA AND STRUCTURE

DRUGCAS REGISTRY NUMBERMOLECULAR FORMULASTRUCTURE
Quinidine 56-54-2 C20-H24-N2-O2
Chemical Structure for Quinidine

ANNOTATED BIBLIOGRAPHY

References updated: 10 May 2018

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    (Expert review of hepatotoxicity of antiarrhythmics published in 1999; among the antiarrhythmics, only amiodarone and quinidine are common causes of hepatotoxicity; quinidine has been associated with many cases of clinically apparent, but mild liver injury usually with signs of hypersensitivity and hepatic granulomas).
  • De Marzio DH, Navarro VJ. Cardiovascular drugs. Hepatotoxicity of cardiovascular and antidiabetic drugs. In, Kaplowitz N, DeLeve LD, eds. Drug-induced liver disease. 3rd ed. Amsterdam: Elsevier, 2013, pp. 520-1.
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    (47 year old man developed fever and abdominal pain 10 days after starting quinidine [normal bilirubin, ALT 910 U/L, Alk K 210 U/L], resolving rapidly when quinidine was stopped, and with recurrence of symptoms and mild ALT elevation within days of rechallenge: Case 1).
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    (74 year old man developed fever, abdominal pain and jaundice one month after starting quinine for leg cramps [bilirubin 7.2 mg/dL, ALT 241 U/L, Alk P 314 U/L, ESR 65], biopsy showing granulomas and rapid resolution upon stopping).
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    (57 year old woman developed fever, nausea and myalgias within 24 hours of starting quinine for leg cramps with temperature 39.5 oC [bilirubin 0.7 mg/dL, ALT 184 U/L, Alk P 192 U/L], resolving within 3 weeks of stopping).
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    (Four women developed quinine induced thrombocytopenia with other systemic manifestations, including prominent AST [131, 992, 741 and 3735 U/L] and mild Alk P [74-170 U/L] elevations and 2 with jaundice [bilirubin 4.3 and 16.1 mg/dL], often due to inadvertent quinine use from over-the-counter pills).
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  • Chalasani N, Fontana RJ, Bonkovsky HL, Watkins PB, Davern T, Serrano J, Yang H, Rochon J; Drug Induced Liver Injury Network (DILIN). Causes, clinical features, and outcomes from a prospective study of drug-induced liver injury in the United States. Gastroenterology 2008; 135: 1924-34. [PMC free article: PMC3654244] [PubMed: 18955056]
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    (Among 1198 patients with acute liver failure enrolled in a US prospective study between 1998 and 2007, 133 were attributed to drug induced liver injury, none of which were attributed to quinidine or quinine).
  • Björnsson ES, Bergmann OM, Björnsson HK, Kvaran RB, Olafsson S. Incidence, presentation and outcomes in patients with drug-induced liver injury in the general population of Iceland. Gastroenterology 2013 ; 144: 1419-25. [PubMed: 23419359]
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  • Hernández N, Bessone F, Sánchez A, di Pace M, Brahm J, Zapata R, A Chirino R, et al. Profile of idiosyncratic drug induced liver injury in Latin America. An analysis of published reports. Ann Hepatol 2014; 13: 231-9. [PubMed: 24552865]
    (Systematic review of literature of drug induced liver injury in Latin American countries published from 1996 to 2012 identified 176 cases, none of which were attributed to quinidine or quinine).
  • Chalasani N, Bonkovsky HL, Fontana R, Lee W, Stolz A, Talwalkar J, Reddy KR, et al.; United States Drug Induced Liver Injury Network. Features and outcomes of 899 patients with drug-induced liver injury: The DILIN Prospective Study. Gastroenterology 2015; 148: 1340-52.e7. [PMC free article: PMC4446235] [PubMed: 25754159]
    (Among 899 cases of drug induced liver injury enrolled in a US prospective study between 2004 and 2013, none were attributed to quinine or quinidine).

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