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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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Last Update: March 24, 2018.



Hydralazine is a commonly used oral antihypertensive agent that acts by inducing peripheral vasodilation. Hydralazine has been linked to several forms of acute liver injury as well as a lupus-like syndrome.


Hydralazine (hye dral' a zeen) is a phthalazine derivative and antihypertensive agent which acts by direct relaxation of arteriolar smooth muscle, probably by alteration in intracellular calcium signaling. Hydralazine was one of the first oral antihypertensive medications introduced into clinical medicine and was first used in the late 1950s, but was officially approved for use in the United States in 1984. The vasodilation caused by hydralazine is followed by reflex sympathetic response that may partially reverse its antihypertensive effects. Nevertheless, when combined with other antihypertensive medications, hydralazine is effective in lowering blood pressure and it is still widely used, with more than 2 million prescriptions for hydralazine being filled yearly in the United States. Hydralazine is available in generic forms and under the brand name of Apresoline in tablets of 10, 25, 50 and 100 mg as well as in parenteral forms. The typical dose is 10 mg four times daily initially, with subsequent increases to a maximum of 200 mg daily. Common side effects include dizziness, headache, tachycardia, orthostatic hypotension, flushing, nausea and gastrointestinal upset.


Serum aminotransferase elevations during hydralazine therapy are considered uncommon. However, hydralazine has been clearly linked to cases of acute liver injury with jaundice as well as a delayed lupus-like syndrome. Two clinical patterns of hepatic injury have been described, associated with either a short (2 to 6 weeks) or long (2 months to more than a year) latency period. The clinically apparent liver injury is usually hepatocellular, although cholestatic forms have also been reported (Case 1). In cases with a short latency period, rash, fever and eosinophilia are common and the onset is typically abrupt and severe, and recovery is rapid. In cases with a longer latency (Case 2), the onset is more typically insidious, liver biopsy may resemble chronic hepatitis and demonstrate fibrosis, and autoantibodies are often present. The late form of hepatitis may also accompany the lupus-like syndrome that occurs with hydralazine, particularly in high doses when given for 6 months or more. Recovery can be prolonged. Autoantibodies to isoforms of the P450 system (CYP 1A2) have been identified in patients with hepatotoxicity due to the structurally related antihypertensive agent dihydralazine (available in Europe, but not the United States) and which is associated with a higher rate of hepatotoxicity than hydralazine.

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

Mechanism of Injury

The cause of the acute liver injury due to hydralazine appears to be due to its metabolism to an immunologic adduct that can result in an immunoallergic hepatitis or a more delayed lupus- and/or an autoimmune hepatitis-like syndrome. Hydralazine, like isoniazid, is metabolized by N-acetyltransferase (NAT) and hepatic injury may be more frequent with specific genetic variants in NAT activity.

Outcome and Management

Fatal instances of liver injury due to hydralazine have been reported, but most cases begin to resolve within a few days of stopping the medication. In patients with signs and symptoms of hypersensitivity, corticosteroids are often used and anecdotal results suggest that they are beneficial in speeding recovery. The duration of therapy with corticosteroids, however, should be kept to a minimum and careful follow up after stopping is prudent. While liver histology can resemble chronic hepatitis and include hepatic fibrosis, persistent injury and vanishing bile duct syndrome have not been reported after hydralazine induced liver injury. Reexposure to hydralazine results in prompt recurrence, that can be severe. There does not appear to be cross reactivity of hepatic injury with other medications or antihypertensive agents, but there may be cross reactivity to other phthalazines such as dihydralazine and possibly to isoniazid.

Drug Class: Antihypertensive Agents


Case 1. Rapid onset of acute cholestatic hepatitis due to hydralazine.

[Modified from: Myers JI, Augur NA. Hydralazine-induced cholangitis. Gastroenterology 1984; 87: 1185-8. PubMed Citation]

A 59 year old woman with coronary artery disease and hypertension was started on hydralazine and developed fever, malaise, and right upper quadrant pain 8 days later. She was admitted for suspected cholecystitis, but ultrasound of the abdomen showed no abnormalities of the biliary system. She had no history of alcohol abuse or liver disease and was known to have normal liver tests in the past. On admission, she had leukocytosis, the total serum bilirubin was 5.2 mg/dL, alkaline phosphatase 540 U/L and AST 141 U/L (Table). Hydralazine was stopped and she recovered rapidly. After discharge, she restarted hydralazine on her own and rapidly developed symptoms again with nausea, vomiting, fever and hypotension. She was febrile and jaundiced, but had no rash or eosinophilia. Autoantibodies were negative. She underwent exploratory laparotomy which was unrevealing; the gallbladder was removed but there were no stones and no biliary dilatation by intraoperative cholangiography. A liver biopsy showed intrahepatic cholestasis. She recovered rapidly and three months later, when readmitted for coronary artery bypass surgery, her liver tests were back to baseline values.

Key Points

Pattern:Cholestatic (R=1.1)
Severity:Moderate (3+; jaundice and hospitalization)
Latency:8 days; 2 days on rechallenge
Recovery:Within 1-3 months
Other medications:None mentioned

Laboratory Values

Time After StartingTime After StoppingALT (U/L)Alk P (U/L)Bilirubin (mg/dL)Other
Developed fever and right upper quadrant pain 8 days after starting hydralazine
8 days01415405.2US normal
14 days4 days481411.7
Unintentional rechallenge with hydralazine for 1-2 days
24 (1 day)0922443.5Cholecystectomy
35 (11) days10 days532370.7
3 months3 months231270.6
Normal Values <50 <115 <1.2


An example of hydralazine induced liver injury with a short latency (8 days), mild immunoallergic features (fever) and a cholestatic pattern of liver enzymes. She had immediate recurrence of injury on mistakenly restarting the drug. Patients with drug induced liver injury should be specifically warned about restarting the medication and should specifically search out and discard any residual medication that might still be in home medicine cabinets. The recurrence of jaundice was interpreted as cholecystitis and she underwent an unnecessary cholecystetomy. This example demonstrates how early and accurate diagnosis of drug induced liver injury can help avoid unnecessary, invasive diagnostic or therapeutic interventions.

Case 2. Cholestatic hepatitis due to hydralazine with delayed onset.

[Modified from: Hassan A, Hammad R, Cucco R, Niranjan S. Hydralazine-induced cholestatic hepatitis. Am J Ther 2009; 16: 371-3. PubMed Citation]

A 63 year old woman with hypertension and end-stage renal disease on dialysis developed epigastric pain and jaundice approximately 12 weeks after starting hydralazine. She had no previous history of liver disease and was known to have normal serum aminotransferase and alkaline phosphatase levels. Abdominal CT scans and magnetic resonance cholangiopancreatography were normal and “no other laboratory evidence of cholestatic jaundice was found.” Serum bilirubin levels continued to rise (Table). Hydralazine was suspected as the cause of the liver injury and, indeed, serum enzyme elevations and bilirubin began to fall when it was stopped. Three months later serum bilirubin and alkaline phosphatase had fallen to baseline values.

Key Points

Pattern:Cholestatic (R=1.7)
Severity:Moderate (3+; jaundice and hospitalization)
Latency:10 weeks according to figure, 5 months according to text
Recovery:9 weeks
Other medications:None mentioned

Laboratory Values

Time After StartingTime After StoppingALT* (U/L)Alk P* (U/L)Bilirubin* (mg/dL)Other
5 days0251800.5
Hydralazine (75 mg three times daily) started
10 weeks02108203.5Admitted for jaundice
11 weeks01107404.1Ultrasound normal
12 weeks01007606.2MRCP normal
Hydralazine stopped
13 weeks1 week506402.1
15 weeks3 weeks503901.1
18 weeks6 weeks302100.6
21 weeks9 weeks201200.5
Normal Values <40 <130 <1.2

*Some values estimated from figures 1 and 2.


The onset, clinical features, course and prompt improvement with stopping therapy are typical of hydralazine induced liver injury presenting after several months of therapy. Typically, cases with a longer latency period are associated with a hepatocellular pattern of serum enzyme elevations, autoantibodies and often present insidiously with fatigue rather than abrupt onset of fever, rash and jaundice. In this case report, the injury pattern was cholestatic and results of autoantibody testing and immunoglobulin levels were not provided.



Hydralazine – Generic, Apresoline®


Antihypertensive Agents


Product labeling at DailyMed, National Library of Medicine, NIH


Hydralazine 86-54-4 C8-H8-N4
Hydralazine chemical structure


References updated: 24 March 2018

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    (63 year old developed abdominal pain and jaundice ~3 months after starting hydralazine [peak bilirubin 6.5 mg/dL, ALT ~400 U/L, Alk P ~825 U/L], resolving within 9 weeks of stopping: Case 2).
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  • 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]
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  • 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, 39 [4.3%] were attributed to antihypertensives including 8 to hydralazine and 11 to methyldopa).
  • deLemos AS, Foureau DM, Jacobs C, Ahrens W, Russo MW, Bonkovsky HL. Drug-induced liver injury with autoimmune features. Semin Liver Dis 2014; 34: 194-204. [PubMed: 24879983]
    (Review of drug induced liver injury with autoimmune features includes a case of hydralazine jaundice arising 3 weeks after stopping a 10 week course of hydralazine [bilirubin 19.8 mg/dL, ALT 1005 U/L, Alk P 239 U/L, INR 2.0, ANA 1:160], with progressive liver injury necessitating liver transplantation 2 months later).
  • Alansari A, Quiel L, Boma N. A one-two punch: hydralazine-induced liver injury in a recovering ischemic hepatitis. Am J Ther 2016; 23: e1094-5. [PubMed: 25423497]
    (77 year old woman with cardiomyopathy and atrial fibrillation had elevations in serum ALT [391 U/L] which improved with control of heart rate but worsened again 4 days after starting hydralazine [peak ALT 359 U/L], ultimately resolving 1 month after stopping).
  • Harati H, Rahmani M, Taghizadeh S. Acute cholestatic liver injury from hydralazine intake. Am J Ther 2016; 23: e1211-4. [PubMed: 26291593]
    (75 year old African American woman developed jaundice 10 weeks after starting hydralazine [bilirubin 22.0 mg/dL, ALT 242 U/L, Alk P 166 U/L, INR 1.23, ANA negative], that improved with prednisone therapy and stopping hydralazine, all tests being normal 5 weeks later).
  • de Boer YS, Kosinski AS, Urban TJ, Zhao Z, Long N, Chalasani N, Kleiner DE, et al.; Drug-Induced Liver Injury Network. Features of autoimmune hepatitis in patients with drug-induced liver injury. Clin Gastroenterol Hepatol 2017; 15: 103-12. [PMC free article: PMC5370577] [PubMed: 27311619]
    (Among 7 patients with hydralazine induced liver injury enrolled in a US prospective database [Chalasani 2015], 5 were women, 4 white and 3 black, ages 42 to 72 years, latency to onset of 2 weeks to 7 months, 5 with jaundice [bilirubin 0.3 to 29.7 mg/dL, ALT 132 to 2018 U/L, Alk P 188 to 607 U/L] and 1 with acute liver failure requiring liver transplantation [deLemos 2014]; 3 had autoimmune features, but ANA levels tended to decrease with recovery).


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